Search

Air pollution causes hypertension, cardiovascular disease, and mortality. Asian dust (AD) reportedly induces asthma or acute myocardial infarction along with air pollution, but its impact on blood pressure (BP) is unknown. We investigated the association between short-term AD exposure and BP fluctuations in 300,952 individuals whose BP was measured during April 2005-March 2015 and divided them into AD and non-AD groups based on visitation for AD-related events. AD's occurrence, air pollutants' concentration (suspended particulate matter, SO 2 , NO 2 , photochemical oxidants), and meteorological variables (mean ambient temperature, relative humidity) were obtained from a monitoring station; AD events correlated with decreased visibility (< 10 km). We observed 61 AD days, with 3897 participants undergoing medical check-ups. Short-term AD exposure at lag day-0 was significantly associated with higher systolic BP (SBP), diastolic BP (DBP), and pulse rate (PR) risk (β = 1.85, 95% confidence interval (CI) 1.35-2.35 for SBP, β = 2.24, 95% CI 1.88-2.61 for DBP, β = 0.52, 95% CI 0.14-0.91 for PR) using multi-pollutant model. Population-attributable fractions exposed to AD were 11.5% for those with elevated SBP (SBP ≥ 120 mmHg) and 23.7% for those with hypertension (SBP ≥ 140 mmHg or DBP ≥ 90 mmHg). This study showed a strong association between short-term AD exposure and increased SBP and DBP.

Background: Hypertension is considered a major risk factor of stroke and systemic embolism (SE) as well as bleeding in patients with atrial fibrillation (AF). The purpose of this study was to investigate the relationship of hypertension and systolic blood pressure (SBP) with the risk of stroke/SE or bleeding in AF patients., Methods: The Fushimi AF Registry, a community-based prospective survey, was designed to enroll all of the AF patients in Fushimi-ku, Kyoto. Fushimi-ku is densely populated with a total population of 283,000. Follow-up data were available for 3,713 patients (follow-up rate 90.0%) as of August 2015, and the median follow-up period was 1,035 days., Results: We compared the clinical backgrounds at baseline, and follow-up outcomes of AF patients between those with hypertension (HTN; n = 2,304, 62.1% of total) and those without (non-HTN; n = 1,409). History of hypertension was neither associated with the incidence of stroke/SE, ischemic stroke, hemorrhagic stroke nor major bleeding. However, when we divided the HTN group by baseline SBP ≥150 mm Hg (HTN-high blood pressure [HBP]: n = 305, 13.3% of HTN group) or <150 mm Hg (HTN-low blood pressure [LBP]: n = 1,983), HTN-HBP group was significantly associated with a higher incidence of both stroke/SE (hazard ratio [HR]: 1.74, 95% confidence interval [CI]: 1.08-2.72) and major bleeding (HR: 2.01, 95% CI: 1.21-3.23) compared with the non-HTN group. In contrast, HTN-LBP group was not associated with the risk of stroke/SE or major bleeding, compared with the non-HTN group., Conclusion: The incidences of stroke/SE and bleeding were higher in AF and hypertension patients with elevated SBP. UMIN Clinical Trials Registry: UMIN000005834., (© American Journal of Hypertension, Ltd 2017. All rights reserved. For Permissions, please email: journals.permissions@oup.com)

Background: The impact of the metabolic syndrome (MS) on cardiovascular events in elderly subjects has not been clarified. We hypothesized that the impact differs between patients with and without strictly controlled blood pressure (BP) and also between early elderly (<75 years) and late (≥75 years) elderly patients., Methods: Elderly hypertensive patients (65-85 years old) were randomly assigned to strict (target systolic BP <140 mm Hg) or mild (140-159 mm Hg) BP target, and were treated for 2 years with efonidipine-based regimen. MS was defined according to the National Cholesterol Education Program Adult Treatment Panel III criteria, except for the use of body mass index (BMI) ≥25 kg/m(2) instead of waist circumference. Primary endpoint was combined incidence of cardiovascular and renal events. Data were obtained from 2,865 patients., Results: The prevalence of MS was 31.4%. The incidence of primary endpoint in patients with and without MS was 4.0% and 3.1%, respectively. MS was a significant risk factor for cardiovascular events in patients <75 years old (adjusted hazard ratio (HR) 2.17, P = 0.01), but not in patients ≥75 years old (adjusted HR 0.98, P = 0.94). In patients with MS, the event rate was significantly lower with strict treatment than with mild treatment among patients aged <75 years (P = 0.0006) but not in those aged ≥75 years (P = 0.82)., Conclusions: MS was associated with cardiovascular risk in elderly hypertensive patients <75 years old, and strict BP control was beneficial for those with MS. However, MS and intensive control of BP may have little effect on cardiovascular events in elderly patients ≥75 years old.

We performed a per-protocol analysis of the Japanese Trial to Assess Optimal Systolic Blood Pressure in Elderly Hypertensive Patients (JATOS) to evaluate the optimal target blood pressure (BP) in elderly hypertensive patients. In JATOS, conducted in elderly (65-85 years) hypertensive patients treated with efonidipine hydrochloride, there were no differences between the strict-treatment group (systolic BP maintained at <140 mm Hg) and the mild-treatment group (systolic BP maintained at ≥140 mm Hg and <160 mm Hg) in the incidence of primary end points (cardiovascular disease and renal failure) for 2 years. The present study analyzed data in subgroups of JATOS in which the average systolic BP was within the range of target values. The average BP levels achieved in the strict-target BP achieved subgroup (n=1191) and the mild-target BP achieved subgroup (n=1531) were 132.3/74.0 mm Hg and 146.6/78.3 mm Hg, respectively. The incidences of primary end points were similar between these subgroups (11.1/1000 patients per year and 13.2/1000 patients per year, respectively, P=0.502), and there were also no differences in the incidences of adverse events. The incidences of cardiovascular events in patients who failed to achieve their respective treatment goals, on the other hand, were significantly higher than in patients who achieved them. These results indicate that strict treatment for elderly hypertensive patients may have little effect in enhancing the suppression of the onset of cardiovascular events as compared with mild treatment, although patients who have difficulties in achieving treatment goals should be given more aggressive treatment as a high-risk population.

Higher pulse pressure is associated with higher cardiovascular risk. We investigated the relationship between pulse pressure and known metabolic risk factors in hypertensive patients who had not experienced stroke or myocardial infarction. In a multicenter cross-sectional survey made in 1995, we registered 939 hypertensive patients aged > or = 50 years. Of these, 734 had never experienced stroke or myocardial infarction. We divided these 734 patients into two groups based on the value of their pulse pressures: 396 patients with a pulse pressure > or = 60 mmHg, and 338 patients with a pulse pressure<60 mmHg. The average pulse pressure value was 72 +/- 12 mmHg in the former group, and 49 +/- 8 mmHg in the latter group. The former group exhibited advanced age, a higher women-to-men ratio, lower high-density lipoprotein (HDL) cholesterol, and higher systolic and lower diastolic blood pressure. Diabetes mellitus (DM) and left ventricular hypertrophy were more frequently noticed in the former group than in the latter group. The prevalence of hyperlipidemia, however, was similar in the two groups. The association of pulse pressure with DM and low HDL cholesterol was statistically significant by multiple logistic analysis adjusted for age, sex, and other known cardiovascular risk factors. In conclusion, pulse pressure increases with advancing age. DM made a substantially larger contribution to the increase in pulse pressure than hyperlipidemia.

The aim of this study was to analyze the treatment of elderly hypertensive patients by Japanese physicians specializing in hypertension. We enrolled 939 patients with hypertension who were treated in the outpatient clinics of 11 hospitals in 1995; 793 of these patients (388 men and 405 women; mean age, 66.6+/-9.0 years) received follow-up examinations in 1996, and the data on these patients was used for the present analysis. Blood pressure (BP), body mass index, lifestyle, and laboratory data were analyzed in all patients. The average BP was 143+/-16/81+/-10 mmHg in 1995 and 142+/-15/80+/-10 mmHg in 1996. The patients whose baseline BP was at the level of Grade 2 or 3 in the WHO-ISH classification (n=117) were characterized by a higher women-to-men ratio, higher age, a higher serum total cholesterol concentration, and higher QRS voltage. In these patients, from 1995 to 1996, the average BP significantly decreased, whereas fasting plasma glucose, serum total cholesterol and serum creatinine concentrations showed only negligible changes. In 220 patients (28%), BP was <140/<90 mmHg at both the initial and the follow-up examinations, whereas 351 patients (44%) were hypertensive in both 1995 and 1996. Thirty-three percent of the patients were smokers. More smokers than nonsmokers had had prior cardiovascular events, diabetes mellitus, or overt proteinuria. In conclusion, the average BP level among the patients treated by Japanese physicians specializing in hypertension was somewhat higher than that recommended by WHO-ISH Guidelines (1999). Patient education to control lifestyle-related risk factors, particularly to stop smoking, should be emphasized.

Objective: To investigate the relationship between circadian changes in urinary microalbumin excretion (UAE), blood pressure (BP) and physical activity in patients with essential hypertension., Design and Methods: The subjects were 45 patients with essential hypertension (EH group: 26 male and 19 female, age 56+/-12 years (mean +/- SD)) and 25 patients with diabetes mellitus (DM group: 14 male and 11 female, age 61+/-10 years). Their BP and physical activity (acceleration) were measured at 30-min intervals for 24 h by means of a multi-biomedical recorder (TM2425). Urine samples were collected during each of four 4-h daytime periods and one 8-h night-time period. From these samples, per-h UAE (UAE/h) was measured. Mean values for mean blood pressure (MBP) and acceleration were calculated for corresponding time periods. Plasma hormones were measured during an early morning rest period., Results: In the EH group, a significant positive correlation was observed between circadian variation of UAE/h and MBP in 35 (78%) subjects, and the mean coefficient of correlation (r) was 0.86+/-0.12. A significant positive correlation was observed between circadian variation of UAE/h and mean acceleration value (Gh) in 25 (56%) subjects, and the mean r value was 0.70+/-0.26. Multivariate linear regression analysis showed that MBP exerted a greater influence on UAE/h than Gh. Significant positive correlations were observed between UAE/day and plasma human atrial natriuretic peptide and plasma aldosterone concentration (r = 0.50, P < 0.01; r = 0.36, P< 0.05). None of these relations, however, was observed in the DM group., Conclusions: In patients with essential hypertension, circadian changes in activity and variation of BP influence UAE/h, but no definite relationship of this kind was observed in patients with diabetes mellitus. Measurement of circadian changes in UAE or UAE/day may be useful in estimating the degree of daily stress in non-diabetic patients with essential hypertension.

The purpose of this study was to calculate statistically the minimum (base) blood pressure (BP) of nighttime (sleep-time) BP values obtained by ambulatory BP monitoring (ABPM) and to investigate its clinical significance. Twenty-four-hour recording of ECG with ABPM was performed directly (n=89) or indirectly (n=117) in 206 patients with essential hypertension. A telemeter was used for the direct method and a multi-biomedical recorder (TM2425) was used for indirect measurement. First, minimum heart rate (HR0=60/RR0) was determined from sleep-time ECG. The mean product of sleep-time diastolic BP (DBP) and pulse interval (RR) was divided by RR0 to obtain DBP0 [DBP0=(DBPxRR)s/RR0]. The correlation between systolic BP (SBP) and DBP was used to determine SBP0 corresponding to DBP0. Statistical base mean BP (MBP0) was calculated from these values, and its reproducibility and relation to hypertension severity were investigated. MBP0 values were similar to true base values of sleep-time MBP obtained by the direct method (mean+/-SD difference, 2.0+/-4.2 mm Hg). Direct MBP0 criteria predicted hypertension severity (mild, moderate, or severe target organ damage) more accurately (predictive accuracy, 89%) than daytime MBP criteria (53%, P<0.01). Almost the same results were obtained using indirect MBP0 criteria. Day-to-day indirect MBP0 variation (mean absolute difference) was smaller (2.4+/-1.8 mm Hg) than day-to-day daytime and nighttime MBP variation (6.3+/-5.3 and 5.4+/-3.4 mm Hg, respectively; n=61, P<0.01), and the correlation coefficient between day-to-day variations of daytime MBP and physical activity (measured by an acceleration sensor) was 0.38 (P<0.05). In conclusion, statistical base BP was almost equal to true base (minimum) BP of sleep-time BP distribution. It was closely related to the severity of hypertensive organ damage, was highly reproducible, and is considered likely to serve stochastically and physiologically as a representative BP value in an individual subject.

In 10 patients with uncomplicated anterior acute myocardial infarction, within 24 hours after onset, heart rate, plasma renin activity, and the low- to high-frequency power ratio increased and high-frequency power decreased during nitroglycerin infusion; however, both heart rate and plasma renin activity did not change, the low- to high-frequency power ratio decreased, and high-frequency power increased during atrial natriuretic peptide infusion. Atrial natriuretic peptide seems to be more beneficial in its effect on autonomic nervous activity, plasma renin activity, and myocardial oxygen consumption than nitroglycerin for the treatment of anterior acute myocardial infarction.

Objective: Physiological roles of the renin-angiotensin system in maintaining blood pressure and sodium-water balance in angiotensinogen gene-knockout mice were evaluated with special reference to endogenous pressor substances., Methods: Angiotensinogen-gene knockout mice and control mice were fed a 0.3 or 4% NaCl diet for 2 weeks. Systolic blood pressure and urinary excretions of electrolytes, creatinine, aldosterone, adrenaline, noradrenaline, dopamine and vasopressin were measured., Results: About 60% of our angiotensinogen-gene knockout mice did not survive until weaning. These mice presented with hypotension and polyuria. Urinary excretion of aldosterone from such mice was significantly lower (not detected) than that from control mice (2.0+/-0.3 pg/mg creatinine). In contrast, urinary excretion of vasopressin from angiotensinogen-gene knockout mice (0.7+/-0.1 ng/mg creatinine) was greater than that from control mice (0.3+/-0.1 ng/mg creatinine), and those of adrenaline and of noradrenaline were similar for knockout and control mice. After salt loading (a 4% NaCl diet), angiotensinogen-gene knockout mice exhibited a significant increase in systolic blood pressure (from 68.3+/-2.9 to 95.9+/-5.9 mmHg), significant decreases in urinary excretions of adrenaline (from 65+/-8 to 40+/-7 pg/mg creatinine) and noradrenaline (from 467+/-48 to 281+/-41 pg/mg creatinine) and no change in excretion of vasopressin compared with such mice fed a 0.3% NaCl diet, Conclusion: The present results with angiotensinogen-gene knockout mice confirm that the renin-angiotensin system plays fundamental roles in maintaining the blood pressure and sodium-water balance. Because the vasopressin and catecholaminergic systems may be altered by lack of angiotensin in angiotensinogen-gene knockout mice, these systems perhaps are not able to restore blood pressure and sodium-water depletion to normal levels in these mice.

This study compared renal and intestinal handling of sodium in Dahl-Iwai salt-sensitive (S) and salt-resistant (R) rats given a normal-salt diet (0.3% NaCl) and a high-salt diet (4.0% NaCl). Six-week-old female S and R rats (n = 7 each) were given a normal-salt diet for 14 days followed by a high-salt diet for 3 weeks. Systolic blood pressure was significantly higher in the S rats than in the R rats only at the end of the high-salt diet period (170 +/- 5, mean +/- SEM, vs 152 +/- 1 mmHg, p < 0.01). Daily sodium intake, water intake, urine volume, and urinary and fecal excretions did not significantly differ between the R and the S rats during the normal- and high-salt diets, except for a slight, although significant, decrease in fecal sodium excretion in the S rats as compared with the R rats in the 2nd week of the high-salt diet period. After switching from the normal-salt diet to the high-salt diet, urinary sodium excretion increased by 17- to 18-fold and fecal sodium excretion increased by about 5-fold in the 1st week of salt loading. The changes in urinary and fecal sodium excretions did not differ significantly between the groups. Cumulative sodium retention was similar in the two groups. The aldosterone/creatinine ratio in 24-hr urine, which was significantly lower in the S than in the R rats during the normal-salt diet, decreased to similar levels in both groups after salt loading, indicating a blunted response of aldosterone in the S rats. Thus, there were no discernible differences in renal and intestinal handling of sodium between the S and the R rats, except for a slight, but significant, difference in fecal sodium excretion in the 2nd week of the high-salt period. The results indicate that inappropriate suppression of aldosterone or some other mechanism induced by salt loading may be involved in blood pressure elevation in Dahl-Iwai S rats.

To investigate the effects of doxazosin on blood pressure and sympathetic nervous activity, we analyzed the circadian variation of blood pressure and the power spectrum of R-R intervals using an ambulatory multibiomedical monitoring system (TM2425) in 10 untreated outpatients with essential hypertension. After a 2-wk placebo period (P-period), we administered 1 to 4 mg of doxazosin mesilate to the patients for 2 to 6 wk (T-period). We measured systolic and diastolic blood pressure (SBP, DBP), heart rate, R-R intervals, posture, and activity with the use of TM2425. Power spectral analysis of R-R intervals was used to calculate the ratio of low to high frequency components (LF/HF). The values were compared between the P-period and T-period. Although daytime blood pressure significantly decreased during the T-period (SBP, 148.1 +/- 5.9 vs. 130.3 +/- 4.4 mmHg; DBP, 92.3 +/- 3.2 vs. 83.6 +/- 2.6 mmHg, p < 0.01), nighttime DBP did not. The LF/HF of R-R intervals in the daytime (5.8 +/- 2.0 vs. 4.9 +/- 1.2, p < 0.01) and the morning rise in blood pressure also decreased significantly (SBP, 17.5 +/- 9.4 vs. 12.1 +/- 6.5 mmHg; DBP, 12.5 +/- 6.5 vs. 8.3 +/- 5.3 mmHg, p < 0.05). We conclude that doxazosin may suppress the morning rise in blood pressure in association with a decrease in sympathetic nervous activity.

A close relationship between obesity and hypertension has been recognized, and plasma angiotensinogen concentrations (p-AGT) have been reported to correlate with blood pressure (BP). However, little is known about AGT in obese patients with hypertension. To define the role of AGT in obese hypertension, we measured p-AGT in obese patients. The subjects were 42 obese patients diagnosed on the basis of a body mass index (BMI) of more than 25 kg/m2, and 21 sex- and age-matched nonobese patients, whose BMI was less than 25 kg/m2. The hypertensive patients had not previously received antihypertensive drugs. P-AGT (P < .05) and mean BP (P < .0001) was increased in the obese patients as compared with the nonobese patients. Positive correlations were observed between BMI and p-AGT, mean BP and p-AGT, and BMI and mean BP (all P < .05). However, after adjustment for blood pressure, p-AGT was not different between groups, and after adjustment a positive correlation remained only between BMI and mean BP. These results suggested the possible involvement of increased p-AGT in hypertension in obese patients, although this may be a secondary change to hypertension or obesity.

This study assessed the accuracy of indirect blood pressure (BP) measurements by simultaneously performing three kinds of indirect BP measurement on the left arm (auscultatory, microphone and oscillometric methods) and a direct BP measurement on the left arm. The subjects were 34 hospitalized patients, ranging in age from 18 to 73 years (average 47.5 years). Highly significant correlations in systolic or diastolic BP between a given pair of the three indirect methods. The indirect methods underestimated systolic BP and overestimated diastolic BP compared with the direct method, with differences of -12.2 +/- 10.5/+4.6 +/- 7.6 (systolic/diastolic BP) with the oscillometric method, -8.1 +/- 9.7/+1.2 +/- 8.9 with the microphone method and -10.6 +/- 8.1/+3.7 +/- 6.5 mmHg with the auscultatory method. The difference in systolic BP between the auscultatory and direct methods was greater and the difference in diastolic BP was smaller in subjects older than 50 years than in those aged 50 years or less (p < 0.001 for systolic BP, p < 0.05 for diastolic BP). The auscultatory method revealed greater systolic BP in subjects with increased carotid arterial wall stiffness assessed by echoarteriography. Thus, it is concluded that there are inherent differences in BP between the indirect and direct methods which can be attributed to the changes in arterial wall physical properties partly due to aging.

Blood pressure (BP) values (systolic BP = Ps, diastolic BP = Pd, heart rate = HR) fluctuate widely throughout the day, and are at their lowest levels during sleep (sleep-Ps = PS0, sleep-Pd = Pd0, sleep-HR = HR0). We analyzed the relationships among these values using the Windkessel model (logarithmic gradient of diastolic pressure decay A = E/R, E = elastic modulus, R = vascular resistance). Intra-arterial BP and ECG were recorded throughout 24 hours in 23 patients with mild essential hypertension (EH) by telemetry, and EEG was monitored during the night. The waveform of each BP pulse was analyzed by computer. The dye-function method was used to obtain the cardiac output while the subjects were awake, recumbent and during slow-wave sleep on the EEG. A high correlation coefficient (r) was observed between mean BP and square root of E x square root of R during sleep (r = 0.88, p < 0.001). Sleep-HR was determined from the waveform that most effectively permitted peripheral blood flow. Furthermore, the simple algebraic relationships Pd not equal to phi x Pd0 and phi not equal to FI + a1(BI) + b1 (a1, b1 = constant) were observed between Pd0 and different 24 h Pd values [FI = eA(RR0-RR); BI = baroreflex index = RR x Pd(RR0 x Pd0)-1, which was significantly correlated with the baroreflex sensitivity, r = 0.79; RR0 and RR are the RR intervals in Pd0 and Pd waves]. The mean r between Pd0 x phi and the actual Pd over 24 h was 0.91 +/- 0.02 (SD). We conclude that sleep-BP and sleep-HR depend mainly on square root of E x square root of R, m [m = log(e)(Ps/Pd)] and E/R, whereas BP variability (phi) over a 24 h period is related to HR variation, the baroreflex index and E/R in mild EH patients.

Blood pressure varies in relation to factors such as physical activity, body position, ambient temperature, and autonomic nervous system activity. Therefore, we have developed a portable multibiomedical (PMB) recorder that monitors five parameters: indirect blood pressure, physical activity, body position, ambient temperature, and RR interval of the electrocardiogram. In the present study, we applied the PMB recorder over a 24-hour period to study the effect of insufficient sleep on blood pressure in subjects doing extensive overtime work. The parameters listed above were measured by the PMB recorder throughout a normal workday (mean period of sleep, 8 hours) and throughout a day with insufficient sleep (mean period of sleep, 3.6 hours) in 18 male technical workers aged 23 to 48 years old. Blood pressure (mean systolic/diastolic pressure +/- SD) significantly increased the day after a sleep-insufficient night (129 +/- 8/79 +/- 6 mm Hg) compared with the day after a normal night (123 +/- 8/76 +/- 7 mm Hg, P<.05). However, ambient temperature, mean number of steps per minute, and percentage of time spent in a standing position showed no significant difference between these days. Spectral analysis of RR intervals showed that the ratio of the low-frequency component on the RR power spectrum (0.05 to 0.15 Hz) to the high-frequency component (0.15 to 0.40 Hz) was higher on the sleep-insufficient day (2.17 +/- 0.37 versus 1.81 +/- 0.37), as was the urinary excretion of norepinephrine (P<.05). Heart rate was significantly higher on the sleep-insufficient day (81 +/- ll versus 76 +/- 8 beats per minute), after the data of two subjects with abnormal levels of physical activity were excluded (P<.Ol). These data suggest that lack of sleep may increase sympathetic nervous system activity on the following day, leading to increased blood pressure. The PMB recorder was useful for precisely evaluating the relationship between blood pressure and environmental factors.

1. We investigated the effects of direct blockade of angiotensin II (AngII) by a potent, non-peptide angiotensin II toff 1 (AT1) receptor antagonist, TCV 116, on the development of cardiac hypertrophy in salt-loaded Dahl salt-sensitive rats. 2. Six week old male Dahl salt-sensitive rats (n = 44) were fed a 4% salt diet and were simultaneously given various doses of TCV 116 orally for 7 weeks. Each control group received vehicle alone. 3. Dietary high salt intake elevated blood pressure continuously and caused left ventricular hypertrophy in rats treated with vehicle. TCV 116 had a minor effect on the rise in blood pressure. Left ventricular mass (left ventricular weight/body-weight) decreased slightly but not significantly, in rats treated with 3 mg/kg per day of TCV 116 (n = 8). Higher doses of TCV 116 (6 and 10 mg/kg per day; n = 8 each) did not show a decrease in left ventricular mass compared with the vehicle control. 4. These results suggest that AngII blockade has only minor effects on hypertension and on cardiac hypertrophy in salt-loaded Dahl salt-sensitive rats and that the renin-angiotensin system may not contribute to the development of cardiac hypertrophy in Dahl salt-sensitive rats on a moderately high-salt diet.

The clinical efficacy and safety of bevantolol hydrochloride, a newly developed beta-blocker, used in combination with other types of antihypertensive agents, were evaluated in patients with severe hypertension by multicenter open-label trials. A total of 28 patients were studied at 20 medical centers. Four patients (14.3%) were excluded for some reasons, and the remaining 24 patients (22 outpatients and 2 inpatients) were analyzed. Following the initiation of therapy, blood pressure decreased from 181 +/- 15 (SD)/114 +/- 3 mmHg to 170 +/- 17/102 +/- 8 mmHg (p < 0.01) on the 14th day of the therapy and gradually lowered further thereafter. At the end of the trial (8th week), blood pressure was stabilized at the level of 160 +/- 14/96 +/- 10 mmHg. The antihypertensive efficacy rated by the changes in mean blood pressure was 79.2% (19/24). Pulse rate decreased slightly but significantly from 75 +/- 10 beats/min to 70 +/- 7 (p < 0.05) on the 14th day of the therapy and stabilized at the similar level thereafter. As abnormal laboratory data were detected in 3 patients and 1 patient complained of a mild headache, the safety ratio was 83.3% (20/24 patients). When the usefulness was assessed in terms of antihypertensive efficacy and safety profiles, bevantolol hydrochloride was considered useful in 75.0% of the patients studied. In conclusion, bevantolol hydrochloride, used in combination with other classes of antihypertensive agents, appears to be an excellent drug for the management of patients with severe hypertension.

gamma-Aminobutyric acid (GABA) is known to be involved in the regulation of blood pressure by modulating the neurotransmitter release in the central and peripheral sympathetic nervous systems. This study investigated the antihypertensive effect of green tea rich in GABA (GABA-rich tea) in young and old Dahl salt-sensitive (S) rats. GABA-rich tea was made by fermenting fresh green tea leaves under nitrogen gas. In experiment 1, 21 11-month-old rats, fed a 4% NaCl diet for 3 weeks, were given water (group W), an ordinary tea solution (group T), or a GABA-rich tea solution (group G) for 4 weeks. The average GABA intake was 4.0 mg/rat per day. After 4 weeks of the treatment, blood pressure was significantly decreased in group G (176 +/- 4; P < .01) compared with group W (207 +/- 9) or group T (193 +/- 5 mm Hg). Plasma GABA levels were more elevated in group G (111 +/- 54) than in group W (not detectable) or group T (14 +/- 8 ng/mL; P < .01 v G). In experiment 2, 21 5-week-old rats, fed a 4% NaCl diet, were divided into groups W, T, and G. The average GABA intake was 1.8 mg/rat per day. Body weight or chow and beverage consumption did not differ significantly among the three groups. After 4 weeks of the treatment, although blood pressure was comparable in groups W and T (165 +/- 3 v 164 +/- 5 mm Hg, mean +/- SE), it was significantly lower in group G (142 +/- 3 mm Hg) than in the other groups (P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)

We studied the roles played by the renin-angiotensin system in inducing hypertension in nine patients with Cushing's syndrome (CS) resulting from adrenocortical adenoma, and compared them with those in patients with primary aldosteronism (PA), renovascular hypertension (RVH) and essential hypertension (EH). In the CS group, each parameter, including serum potassium, plasma renin activity, plasma aldosterone, deoxycorticosterone and corticosterone concentrations, is within the normal range. However, plasma renin activity in the CS group was lower than that in the RVH group but higher than that in the PA group, and plasma aldosterone concentration was lower than that in each RVH or PA group. These findings indicated that the CS group had a different type of hypertension from that in either RVH or PA, in which the renin angiotensin system or mineralocorticoids play an important role in hypertension. Meanwhile, captopril (50 mg) administration either with or without indomethacin pretreatment decreased the mean blood pressure in the CS group, although captopril failed to change it in the PA group or in normal subjects. Furthermore, the pressor response to exogenous angiotensin II in the CS group was higher than that in the RVH or EH group, but was not different from that in the PA group. Thus, the hypertension in patients with CS due to adrenocortical adenoma appears to be mediated through a change in the renin-angiotensin system in the form of exaggerated pressor responses to angiotensin II.

Objective: A pathogenetic role of altered alpha 2-adrenoceptors in essential hypertension has been suggested, based on studies in humans and animals. To examine the role of the alpha 2-adrenoceptor in genetically hypertensive rats, we compared the alpha 2-adrenoceptor genes of stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto (WKY) rats by restriction fragment length polymorphism analysis using human alpha 2-adrenoceptor probes (alpha 2-C10) and Dde I restriction endonuclease, and conducted a genetic cosegregation study., Method: Five female WKY rats were bred with five male SHRSP. Eight pairs of F1 rats were mated in brother-sister pairs to yield an F2 population of 84 rats. Systolic blood pressure was determined by tail-cuff sphygmomanometry. Direct arterial blood pressure was taken under ether anaesthesia just before the rats were killed. Southern blots were performed using alpha 2C10 as a probe and the DNA from the F2 generation., Results: A restriction fragment length polymorphism of the SHRSP allele of a 1.6-kb fragment and a WKY rat allele of a 0.9-kb fragment with a common band of 1.3 kb in SHRSP and WKY rats was found, as reported previously. The distribution of the genotype based on restriction fragment length polymorphism conformed to a 1:2:1 ratio in F2 rats, as expected for a Mendelian trait. There was no significant difference in the blood pressure of F2 rats with respect to alpha 2-adrenoceptor genotype., Conclusion: This study demonstrated that the alpha 2-adrenoceptor gene restriction fragment length polymorphism distribution is a Mendelian trait in the F2 rats of crossed SHRSP and WKY rats, but failed to show genetic cosegregation of this restriction fragment length polymorphism with blood pressure in this generation.

Blood pressure (BP) and heart rate (HR) (BP waveforms) are affected by external stress during waking and BP is reduced to its lowest level (base BP) during sleep. This study investigated the relationship between BP waveforms while awake and base BP waveforms during sleep. The intra-arterial BPs of 64 inpatients (34 males and 30 females, age: 42 +/- 11, mean +/- SD) with mild essential hypertension were measured for 24 h by the telemetry method. The average ln (SBP/DBP) (m) while awake and the m at base BP (ln: natural logarithm, SBP: systolic BP, DBP: diastolic BP) had approximately the same values in each patient (mean difference: -0.02 +/- 0.07). The product of the RR interval (60/HR) and DBP (RR x DBP) while awake and at base BP had almost the same value (mean difference: -3.2 +/- 10 mmHg.sec). According to the Windkessel model, the RR interval during which blood-flow volume in relation to the m value is at its highest can be inferred as S (em-1)/(em-m-1) (S: systolic time). Using this formula, we developed a formula to estimate base RR from waking m, BP, and RR. Calculations with this estimate formula produced a very slight difference (0.0 +/- 0.1 sec) between estimated and actual values for base RR. For the most part, it was possible to infer the base DBP value from the estimated base RR using RR x DBP while awake (mean difference: -3.7 +/- 7.0 mmHg). These results suggest that the base BP waveform may be the most efficient pattern, and that waking BP waveforms change based on the base BP waveform during sleep.

In order to investigate the effects of manidipine, a newly developed long-acting calcium antagonist, on the diurnal variation of arterial pressure and systemic hemodynamics in patients with essential hypertension, we examined 24-h arterial pressure using a direct arterial pressure monitoring method and cardiac output using the cuvette method before and during manidipine treatment. Once-a-day administration of manidipine at daily doses of 10 to 40 mg decreased systolic and diastolic arterial pressures at almost all measurement points. The arterial pressure reductions were not significantly different between daytime and nighttime. Arterial pressure variability expressed in terms of the standard deviation of values was not affected by manidipine treatment. Thus, it appears that patients treated with manidipine can avoid the excessive decrease in arterial pressure during nighttime that may occur with the use of some other calcium antagonists. Heart rate and its variability were unaffected by manidipine treatment. A hemodynamic study revealed that manidipine did not change cardiac output, but significantly decreased total peripheral vascular resistance at rest. It is concluded that once-a-day administration of manidipine at daily doses of 10 to 40 mg brings about a safe and stable antihypertensive effect over a 24-h period, without affecting the diurnal variation of arterial pressure and heart rate. Dilation of the resistance vessels underlies the antihypertensive effect of the agent.

To determine the feasibility of the non-invasive determination of systolic pressure of the pulmonary artery and the right ventricle in pediatric patients, the velocity of tricuspid regurgitation was measured in 30 patients using a contrast enhanced Doppler echocardiography. After sonicated albumin injection, trivial tricuspid regurgitation signals were enhanced in 27 patients (90%). Peak systolic velocity was not altered by before and after sonicated albumin injection in 2 patients. Right ventricular (RV) systolic pressure obtained by continuous wave Doppler during sonicated albumin enhancement corresponded very closely to that measured by catheter in 27 patients (r = 0.96). In 27 patients, difference of estimation of RV systolic pressure by non-enhanced Doppler and enhanced Doppler with sonicated albumin was statistically significant (32.3 +/- 27.6 mmHg versus 2.9 +/- 7.7 mmHg p < 0.001). Systolic pressure of pulmonary artery was estimated by RV systolic pressure measurement (by enhanced Doppler method) minus peak pressure gradient across the pulmonary valve (non-enhanced Doppler method). Pulmonary arterial systolic pressure measured by enhanced Doppler method and that by catheter method were highly significant (sonicated albumin method, r = 0.95). This technique may be a valuable non-invasive method for determining an accurate right ventricular and pulmonary arterial systolic pressures in this setting.

We attempted to investigate the alterations in the vasoconstrictor thromboxane (TXA2) system in the kidney when spontaneously hypertensive rats (SHR) were treated subchronically with atenolol, a beta 1-adrenoceptor antagonist. Atenolol treatment (30 mg/kg body weight per day for 2 weeks) reduced systolic blood pressure by 11%, being accompanied by a decrease in heart rate. This treatment strikingly decreased thromboxane content in the renal cortex by 48% (p less than 0.05), whereas the tissue content was unaltered for prostaglandin E2 (PGE2) or slightly decreased for prostacyclin (PGI2). These alterations in the eicosanoid system led to an increase in the ratio of PGE2/TXA2 and of PGI2/TXA2. Similarly, thromboxane content in the renal papilla was lowered significantly with atenolol treatment, which raised the ratio of PGE2 to TXA2. Thromboxane reduction was not observed in the aortic walls and heart. However, in the vascular walls, PGI2 synthesis was markedly stimulated with atenolol treatment, resulting in an increase in the ratio of PGI2 to TXA2. Thus, these data indicate that subchronic atenolol-treatment inhibits the thromboxane system in the kidney, thereby shifting the eicosanoid system towards a vasodilator state. These alterations contribute, in part, to the anti-hypertensive properties of atenolol in genetic hypertension.

To determine whether the baroreflex control of sympathetic nerve activity is altered in patients with essential hypertension, muscle sympathetic nerve activity (MSNA) was recorded microneurographically from the tibial nerves of 23 normotensive subjects and 23 patients with essential hypertension. When phenylephrine (2 micrograms/kg) was injected intravenously, although the pressor response of mean arterial blood pressure (MAP) was significantly enhanced in the hypertensives as compared with the normotensives, the reflex decrease in MSNA was significantly smaller in the hypertensives. Furthermore, the baroreflex slope for MSNA, used as an index of baroreflex sensitivity and calculated by relating the change in MSNA to the change in MAP, was significantly less in the hypertensives. Following the injection of nitroglycerin (2 micrograms/kg), there were no significant differences between the normotensives and hypertensives in the depressor response, the reflex increase in MSNA or the baroreflex slope for MSNA. These observations suggest that the baroreflex change in sympathetic nerve activity is reduced during phenylephrine-induced blood pressure elevation but not during nitroglycerin-induced hypotension in the hypertensives, and that the blunted response of sympathetic nerve activity occurring during hypertension in these hypertensive patients may underlie the maintenance of high blood pressure in essential hypertension.

To investigate whether excessive reduction of blood pressure (BP) by antihypertensive medications correlates with myocardial infarction, especially during sleep in elderly patients, we used telemetry and cuvette dye-dilution methods to assess the direct BP and the hemodynamics of 68 inpatients with essential hypertension during wakefulness and sleep. There were 25 patients greater than or equal to 60 years old (OH-group) and 43 were less than or equal to 59 years old (YH-group). Of the OH-group, 36% showed high BP during the day, with marked decreases (minimum BP less than 110/70 mm Hg) during sleep. Average cardiac index (CI) of the OH-group was low during wakefulness and extremely low during slow-wave sleep. Changes of mean BP in the OH-group correlated with changes in total peripheral vascular resistance index (TPRI) during sleep, but this correlation was not observed in the YH-group. The antihypertensive effects on nocturnal BP of the various medications was: central adrenergic inhibitors less than or equal to beta blockers with intrinsic sympathomimetic activity less than or equal to alpha (alpha beta) blockers less than or equal to angiotensin-converting enzyme inhibitors less than or equal to calcium antagonists. Because BP and CI were found to be very low and TPRI seems to play an important role in BP regulation in sleeping elderly patients, excessive antihypertensive medication may be harmful to this subgroup. However, because the effects on nocturnal BP differ among various antihypertensive treatments, further research is required on the relation between antihypertensive medication and the hemodynamics of sleeping elderly hypertensive patients.

In order to investigate the effect of delapril, a new angiotensin converting enzyme inhibitor, on the diurnal variation of arterial pressure in patients with essential hypertension, this study examined 24 h arterial pressure using an indirect or a direct monitoring system. When the effect of twice-a-day administration of delapril at daily doses of 30 to 90 mg was examined using the indirect monitoring system in 12 outpatients, delapril decreased systolic and diastolic arterial pressures significantly only at limited points during the day. However, each of the averaged 24 h daytime and nighttime arterial pressures showed significant reductions. The 24 h intraarterial pressure monitoring demonstrated that delapril decreased systolic and diastolic arterial pressure at most of the measurement points. The arterial pressure reductions during daytime and nighttime were not significantly different, that is, there was no excessive reduction in nighttime arterial pressure. Heart rate and its variability were virtually unaffected by the delapril treatment in either monitoring study. No adverse reactions were observed in the indirect or direct monitoring studies. Thus, it is concluded that twice-a-day administration of delapril at daily doses of 30 to 90 mg brings about a safe and stable antihypertensive effect, without affecting the diurnal variation of arterial pressure.

Purpose: On the assumption that renal tubular cells are more important as the target cells for a natriuretic factor than blood cells, we used a well-characterized cultured renal tubular cell line, Madin-Darby canine kidney (MDCK), cells to monitor the circulating digitalis-like factor in human plasma and examine its role in the regulation of blood pressure and sodium balance., Subjects and Methods: We investigated the effects of plasma on binding of radioactive ouabain to monolayered MDCK cells in order to determine the level of a circulating digitalis-like factor. First, we measured specific 3H-ouabain binding to MDCK cells in the presence of plasma from 71 outpatients (34 normotensive subjects and 37 hypertensive patients) after incubation for 4 hours. Second, we measured specific 3H-ouabain binding after incubation of cells with plasma from 16 hospitalized subjects (eight normotensive subjects and eight hypertensive patients) receiving low and high sodium diets., Results: In Study 1, ouabain binding was lower by 30% with plasma from hypertensive patients than with plasma from normotensive subjects (p less than 0.01). There was a significant negative correlation between individual subject's systolic or mean blood pressure and ouabain binding (r = -0.34, p less than 0.01 or r = -0.29, p less than 0.01). In Study 2, ouabain binding was also significantly reduced by 25% in the presence of plasma from hypertensive subjects as compared with plasma from normotensive subjects irrespective of sodium intake (p less than 0.01). A significant negative correlation was also found for all subjects between either systolic, diastolic, or mean blood pressure and ouabain binding (r = -0.58, p less than 0.01, r = -0.51, p less than 0.01, or r = -0.55, p less than 0.01, respectively). With the changes from low to high sodium intake, there was a corresponding decrease in ouabain binding (p less than 0.01) and an increase in sodium excretion (p less than 0.01). A significant negative correlation was observed between these two parameters (r = -0.47, p less than 0.05)., Conclusions: These findings suggest that a circulating digitalis-like factor, which may act on renal tubular cells as the ouabain-displacing compound, is increased in patients with essential hypertension and also demonstrate that plasma levels may be influenced by changes in dietary sodium intake.

We followed the changes in blood pressure (BP) after discharge from the hospital in 32 patients with essential hypertension whose BP was normalized on a diet containing 7g/day of NaCl during hospitalization. They were divided into two groups on the basis of BP changes: 18 patients whose BP values were elevated by more than 10% after discharge (group I; mean +16.9%, P less than .01) and the remaining 14 patients (group II; -3.6%, P = NS). Urinary Na excretion (UNaV) in Group I patients increased markedly after discharge (83 v 189 mu Eq/min, P less than .001) while it did not change in Group II (122 v 102 mu Eq/min, P = NS), resulting in a greater postdischarge UNaV in group I than in group II (P less than .01). The changes in BP were positively correlated with the overall changes in UNaV (r = 0.45, P less than .01). Plasma epinephrine after discharge was higher in group I than in group II (31 v 18 pg/mL, P less than .05). Thus, increases in NaCl intake seem to play an important role in BP elevation after discharge. Adrenal medullary function may partly contribute also to the BP elevation.

The chronic effects of oral administration of an angiotensin converting enzyme inhibitor (captopril, 63-80 mg/Kg/day) on blood pressure and the renin-angiotensin-aldosterone system were-studied in normotensive male Wistar rats. Blood pressure (BP), plasma renin activity (PRA), plasma renin concentration (PRC), plasma renin substrate concentration (PRS), plasma aldosterone concentration (PAC) and renal renin content (RRC) were measured after 2, 9, 19, 29 and 58 days of captopril administration. BP was determined in awake rats and blood samples were obtained by decapitation. In addition, BP responses to bolus injections of angiotensin I (AI, 80 ng/Kg), angiotensin II (AII, 80 ng/Kg) and bradykinin (BK, 10 micrograms/Kg) were examined in conscious rats which had received captopril for 20 days. The BP of the rats which had been given captopril for 9 days or longer was significantly lower than that of the control rats. PRA and PRC were markedly increased, and both PRS and PAC were decreased in the captopril-treated rats. RRC, which was reduced after 2 days of captopril administration, was substantially increased thereafter. Although the pressor responses to AII were similar in the captopril treated and the control rats, the responses to AI were reduced to 50% of those to AII in the former. The depressor responses to BK in the captopril-treated rats were 2.3 times as large as those in the control rats. Our results show that long-term use of captopril lowers BP in normotensive rats on a normal sodium intake.(ABSTRACT TRUNCATED AT 250 WORDS)

In order to evaluate both the hypotensive and uric acid-retaining effects of thiazide diuretics in an animal model with hypertension, the effects of trichlormethiazide were studied using spontaneously hypertensive rats (SHR) under dietary sodium restriction. Trichlormethiazide was dosed daily for two weeks at 0.05, 0.5, 3 and 10 mg/kg, p.o. All doses caused obvious natriuresis, while an increase of urine volume was observed only at 3 and 10 mg/kg. The hypotensive effect, which was estimated at day 6 and 13, was recognized at doses of more than 0.5 mg/kg. At the end of the dosing, the hematocrit value of all medicated groups rose, and both the uric acid excretory capacity, estimated by the clearance values of inulin and uric acid, and the plasma potassium level clearly decreased at 3 and 10 mg/kg. A detailed study using a dose of 3 mg/kg showed shifts of the cumulative sodium and potassium balances to negative directions against the control group. Thus, trichlormethiazide-treated SHR under dietary sodium restriction showed both a hypotensive effect which might be due to the natriuresis and a tendency toward undesirable side effects such as hypokalemia and hyperuricemia. As there is no practical method in animal studies for simultaneously proving hypotensive and uric acid-retaining effects of diuretic antihypertensives, the findings of the present study might aid in the evaluation of diuretics more useful than the thiazides.

The renal and hormonal effects of the alpha 1-adrenoceptor blocker bunazosin were examined in 6 patients with essential hypertension. Oral bunazosin for 4 to 12 weeks significantly decreased mean blood pressure by 10%, increased effective renal blood flow and creatinine clearance by 34% and 37%, respectively, the plasma norepinephrine concentration was elevated by 60%, and the plasma atrial natriuretic peptide level was lowered by 22%. The plasma renin activity and aldosterone concentration were unchanged. Thus, a moderate reduction in blood pressure was produced by bunazosin treatment while maintaining renal perfusion.

Intravenous infusion of graded doses of alpha-human atrial natriuretic polypeptide (alpha-hANP) resulted in a dose-dependent decrease in blood pressure and an increase in heart rate in 11 healthy male volunteers. However, there were no significant changes in urine output or in the urinary excretion rate of sodium. Glomerular filtration rate did not change, while renal blood flow decreased, leading to significant increases in filtration fraction and renal vascular resistance. Although plasma renin activity (PRA) and plasma concentration of norepinephrine (PNE) increased during infusion of alpha-hANP (both p less than 0.001), plasma concentrations of aldosterone (PA) and cortisol (PC) decreased (both p less than 0.001). Plasma concentration of arginine vasopressin (PAVP) did not change during the infusion, but greatly increased after cessation of the infusion. The hematocrit increased slightly, but significantly, during the infusion. These results show that, although alpha-hANP has a potent hypotensive action and inhibits the secretion of aldosterone, cortisol, and probably arginine vasopressin, it does not dilate renal vessels in normotensive persons, and likely increases vascular permeability. The lack of consistent diuretic and natriuretic responses to alpha-hANP may be related to the predominance of the hypotensive effect over the renal effects of the peptide in normotensive persons, or a diurnal change may have served to obscure such a response.

The effect of ramipril on diurnal variations of blood pressure was studied in patients with mild to moderate essential hypertension in groups given once- (n = 18) and twice-daily (n = 21) administration with daily dosages ranging from 2.5 to 10 mg. After ramipril treatment, the blood pressure of patients in both groups was significantly reduced, and no significant differences in diurnal variation of blood pressure were observed between the 2 groups. The pulse rate did not change after administration of ramipril and no serious side effects were observed. In consideration of patient compliance, once-daily administration of ramipril seems to be optimal for the treatment of essential hypertension.

The effect of once daily low-dose carvedilol on circadian variations of blood pressure (BP) was studied in Japanese patients with mild or moderate essential hypertension. Thirty-one patients were admitted to hospital whose BP was 150/90 mm Hg/day or greater and they participated in the study. After a placebo period of 1 week, 5 or 10 mg carvedilol was given once daily in the morning for 3 to 7 days, and if BP reduction was not sufficient, the dose was increased to 20 mg daily. The blood pressure variation was monitored before and 1, 2, 4, 6, 8, 10, 12, and 24 h after administration of the drug on the last day of placebo and final dose of carvedilol. Of the 31 cases receiving carvedilol once daily, cumulative effectiveness (13 mm Hg reduction in mean BP) was 48.4% at 10 mg/day and 54.8% at 20 mg/day. Both systolic and diastolic pressures decreased significantly and heart rate decreased slightly. There was no significant difference between the standard deviations of BP on the last days of the control period and the carvedilol treatment. The difference between maximum and minimum BP during the day was not significant between the two periods. Circadian variations of heart rate were also not significantly different for the two periods. This indicates that carvedilol did not have any effect on circadian variations of BP and heart rate. The present study also suggests that low-dose carvedilol once daily may be effective in the treatment of hypertension.

The role of endothelin (ENT) in the control of systemic blood pressure (BP) was examined in conscious rats. Intracerebroventricular (i.c.v.) administration of ENT (0.002 or 0.2 micrograms, i.e., 0.78 or 78 pmol/2 microliters 0.9% saline) to conscious rats had complicated effects on BP. A significant fall in BP occurred in the initial 2-4 min after administration; and then after recovery toward the control level, BP decreased again within 17 min, following which a constant rise in BP occurred. In addition to the changes in BP, 3 of 9 rats which received 0.2 micrograms lapsed into severe barrel rotation-like behavior only to die 6-8 min after i.c.v. injection. It was therefore assumed that ENT had central effects on BP regulation and motor activity.

The mechanism of natriuresis following administration of atrial extract is not fully understood. This study related the changes in urinary excretion of electrolytes induced by atrial or ventricular extract to those in urinary excretion of prostaglandin E2 (PGE2) in rats. Both atria were removed from Wistar rats and homogenized in a 1 N acetic acid solution. After centrifugation, the supernatant was lyophilized and then resolved in a 0.1 N acetic acid solution. The apical portions of heart ventricles were similarly prepared, and served as controls. One hundred microliter of the solution containing the extract of 10 mg of tissue were injected intravenously into assay rats, the carotid artery and the urinary bladder of which were cannulated to measure blood pressure and urinary output, respectively. Urinary PGE2 was determined by radioimmunoassay. The atrial extract rapidly lowered blood pressure without changing heart rate. This hypotensive effect was maintained for at least 30 minutes. When the urinary samples obtained before and 10 minutes after the injection of the atrial extract were compared, urinary volume and excretion of sodium (UNaV) and potassium (UKV) were increased by 8, 24 and 3-fold, respectively. Urinary excretion of PGE2 (UPGEV) was increased from 5.3 +/- 0.9 (SE) to 16.3 +/- 2.9 ng/kg/10 min (p less than 0.001). There was a significant positive correlation between UNaV and UPGEV in all the samples (r = 0.72, p less than 0.001), and between the changes in UNaV and those in UPGEV after administration of the atrial extract (r = 0.62, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

The renal and hormonal effects of the α-adrenoceptor blocker bunazosin were examined in 6 patients with essential hypertension. Oral bunazosin for 4 to 12 weeks significantly decreased mean blood pressure by 10%, increased effective renal blood flow and creatinine clearance by 34% and 37%, respectively, the plasma norepinephrine concentration was elevated by 60%, and the plasma atrial natriuretic peptide level was lowered by 22%. The plasma renin activity and aldosterone concentration were unchanged. Thus, a moderate reduction in blood pressure was produced by bunazosin treatment while maintaining renal perfusion. [ABSTRACT FROM AUTHOR]