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Background: There are numerous data indicating a significant role of the sympathoadrenal system and the reninangiotensin- aldosterone system in the regulation of blood pressure and the pathogenesis of essential hypertension. However, the genetic background of essential hypertension remains unclear., Aim: To determine the effects of genetic factors on selected indicators of the activity of the sympathoadrenal system and the renin-angiotensin-aldosterone system in twins., Methods: We studied 39 monozygotic twin pairs (age 33+/-7 years) and 37 same-gender dizygotic twin pairs (age 36+/-7 years). We measured blood and urine adrenaline (A), noradrenaline (NA), dopamine (DA) and aldosterone (ALD) levels, as well as plasma renin activity (PRA) and serum angiotensin-converting enzyme (ACE) activity. Parameters of the genetic models for age- and gender-adjusted data were estimated by model fitting and path analysis technique using LISREL 8., Results: The effects of genetic factors on the variability of blood and urine catecholamine levels were 69% and 65% for A, 42% and 76% for NA, and 58% and 40% for DA, respectively. We also found shared environmental components for blood NA (28%) and urine DA (17%). Genetic factors accounted for 36% of the variability of PRA and 80% of the variability of ACE. ALD levels were related only to environmental factors (including a shared environmental component, estimated at 25%, for urine ALD)., Conclusions: We found significant effects of genetic factors on the activity of the sympathoadrenal system, as indicated by blood and urine catecholamine levels. We also found the effect of genetic factors on PRA and ACE, but not on aldosterone levels.

Objective: Assessment of relationship between homocysteine (Hcy) and noradrenaline (NA), adrenaline (A) concentration and left ventricular mass index (LVMI) in patients with essential hypertension (EH)., Design and Methods: Samples obtained from 37 patients (14 female, 23 male) with mild EH (according to WHO criteria) (mean age 43.6 +/- 13.2 years) and 37 healthy volunteers (18 female, 19 male; mean age 38.2 +/- 10.6 years) were evaluated for Hcy (ELISA), NA and A (HPLC). Each patient underwent echocardiographic investigation with LVMI measurement (Penn convention). The examinations were performed in the outpatient clinic., Results: Hcy was significantly higher in patients with EH (8.7 +/- 2.4 vs 6.6 +/- 1.3 micromol/l; p < 0.01). NA and A levels were significantly elevated in the EH group (A: 43.9 +/- 26.4 vs 36.9 +/- 29.4 pg/ml; NA: 428.5 +/- 148.8 pg/ml vs 314.6 +/- 103.4 pg/ml; both p < 0.05). LVMI was also significantly higher in EH group (96.6 +/- 19.5 vs 83.4 +/- 16.0 g/m2; p < 0.01). There was no significant correlation between Hcy and other analysed parameters in the studied groups., Conclusion: High levels of Hcy appear together with increased left ventricular mass and augmented adrenergic activity in patients with EH. Coexistence of high Hcy concentration, left ventricular hypertrophy and increased adrenergic activity increases the risk of atherosclerosis and cardiovascular disease in patients with EH.

Hemorrheological and humoral abnormalities and excessive platelet activity can predict the development of cardiovascular complications in patients with essential hypertension. A study was conducted to assess the influence of gender on these factors and the interrelations between changes in hemorrheology and the sympatho-adrenal system in 54 patients (18 women, 36 men) with essential hypertension (aged 39.6 +/- 9.7 years) and 25 healthy volunteers (10 women, 15 men; aged 36.0 +/- 7.2 years). A decrease in erythrocyte deformability (p < 0.01) was found in the hypertensive men compared with the hypertensive women. Hematocrit (p < 0.01), blood viscosity at the shear rates of 0.3 s-1 (p < 0.01) and 6 s-1 (p < 0.01), plasma viscosity (p < 0.01), erythrocyte aggregation (p < 0.01), and neuropeptide Y (p < 0.02) concentrations were higher in the hypertensive men than in the hypertensive women. A positive correlation between blood fibrinogen and serotonin was found in the pooled hypertensive group and in the hypertensive men (p < 0.01) and between blood viscosity (shear rate 6 s-1) and neuropeptide Y in the pooled hypertensive group (p < 0.01). Neuropeptide Y correlated with filtration time of 1 mL blood in the hypertensive men (p < 0.05) and in the pooled normotensive group (p < 0.01) and with beta-thromboglobulin in the hypertensive women (p < 0.001). A positive correlation was also found in the hypertensive men between erythrocyte and platelet aggregation (p < 0.01) and between beta-thromboglobulin and adrenaline (p < 0.01). Hemorrheological and humoral abnormalities are more pronounced in men than in women with essential hypertension and may contribute to the increased incidence of cardiovascular events in men.

In phaeochromocytoma, sudden hypertensive or arrhythmic episodes are believed to be associated with excessive free catecholamine excretion. However, lack of correlation between blood pressure (BP) and plasma catecholamine levels has been reported. Therefore an attempt was made to assess the sympathovagal balance before and during episodes of BP elevation or complex cardiac arrhythmias in this disease. Ten patients with phaeochromocytoma and 10 matched controls with essential hypertension underwent simultaneous 24 h Holter ECG and BP monitoring. BP elevation was diagnosed when the BP exceeded the mean 24 h values by 40 mm Hg systolic or 30 mm Hg diastolic, respectively. Heart rate variability (HRV) was measured for 5 min periods 1 h before, 15 min before and during 13 episodes of BP elevation in phaeochromocytoma and 13 episodes in the control group, as well as at 1 h, 15 min and immediately before five arrhythmic events in phaeochromocytoma. In phaeochromocytoma, vagal activity measured 1 h before BP elevation was markedly higher than in control hypertensives. However, in both groups at 15 min before and during the hypertensive events, the vagal tone decreased significantly. In contrast, just before the arrhythmic events HRV remained unaltered with a slight insignificant increase in sympathetic activity. We conclude that in phaeochromocytoma, pronounced BP elevations during daily activities are preceded by a parasympathetic withdrawal, similar to the findings in essential hypertension. Such a sequence does not seem to precede sudden complex arrhythmic events in phaeochromocytoma.

The aim of the study was to investigate endothelin-1 (ET-1) and neuropeptide Y (NPY) plasma concentrations in renal venous blood of hypertensive patients with unilateral renal artery stenosis (URAS). The study was performed in 22 patients with URAS and 18 patients diagnosed as essentially hypertensive. In each subject renal arteriography and renal vein catheterisation was performed. Blood samples for ET-1, NPY and plasma renin activity (PRA) were withdrawn from renal veins and vena cava inferior, and for ET-1 and NPY from the aorta. Patients with URAS were divided in two subgroups according to the renal vein renin ratio. Both in nine patients with URAS and ratio > 1.5 and in 13 patients with URAS and ratio < 1.5, ET-1 and NPY plasma concentrations evaluated in renal venous blood of the ischaemic kidney were not different from those assessed in the contralateral side, in vena cava inferior and in the aorta. In essential hypertension, the mean ET-1 and NPY plasma concentrations of both renal veins were not different from the ET-1 and NPY plasma values assessed in renal vein of stenosed and contralateral side, vena cava and aorta of patients with URAS with and without activation of the renin system. Our study indicates that chronic ischaemia does not affect ET-1 and NPY plasma concentrations in renal venous blood of hypertensive URAS patients both with and without activation of the renin system.

Pheochromocytoma is a unique type of hypertension caused by excessive production of catecholamines by the chromaffin tumor. Pheochromocytoma, a potentially life-threatening disease, is a rare cause of hypertension. The incidence varies from 0.1 to 0.8% of hypertensive population. The author's experience is based on 138 patients treated in one institution from 1956 to 1995. Hormonal activity of pheochromocytoma varies considerably, influencing the pattern, of blood pressure and the clinical symptoms. It is emphasized that different other humoral mechanisms may play a role in the pathophysiology of this type of endocrine hypertension. Biochemical tests and non-invasive localizing methods are essential for the definite diagnosis of pheochromocytoma. A great progress has been made in this respect during the last three decades. Surgical removal of the tumor is the only definite therapy with low morbidity and mortality.

Neuropeptide-Y (NPY) is a peptide proposed to modulate the effect of the sympathetic nervous system on blood pressure control and contribute to the development of essential hypertension. To assess the possible influence of gender on its role, we evaluated plasma NPY, noradrenaline (NA) and adrenaline (A) concentrations in men and women with essential hypertension. No difference in NPY concentration was found between genders, but NPY concentration was elevated in both hypertensive men and women. NA levels were similar in all investigated hyper- and normotensives, while A was increased only in hypertensive men. These results suggest various patterns of sympatho-adrenal activity in gender subgroups of patients with essential hypertension.

Background: Atrial natriuretic peptide (ANP) has been extensively studied in cardiovascular disorders in recent years. Particular attention has been paid to the role of ANP in the pathogenesis of hypertension and congestive heart failure and in the neurohormonal response to myocardial infarction. However, no published data are available on the significance of ANP in hypertensive patients with acute myocardial infarction., Methods: We studied the relationship between plasma ANP concentration and systolic blood pressure, diastolic blood pressure, left atrial dimension, left ventricular diastolic dimension and left ventricular mass index in patients with essential hypertension in the acute phase of myocardial infarction. Plasma ANP concentrations were determined at 0, 4, 8, 16, 24, 48 and 72 h after admission in 40 patients with a first myocardial infarction (18 hypertensive patients, group 1; 22 normotensive patients, group 2). Left atrial dimension and left ventricular diastolic dimension were assessed echocardiographically within the first 48 h of acute myocardial infarction., Results: Maximum and mean plasma ANP values at 0, 4, 8, 16, 24, 48, and 72 h as well as mean ANP concentrations within the 72 h period were higher in group 1 than in group 2 (P < 0.001). Plasma ANP concentration, left atrial dimension (r = 0.59) and left ventricular diastolic dimension (r = 0.56) were positively correlated in both groups., Conclusion: Acute myocardial infarction is characterized by a more pronounced rise in plasma ANP concentration in hypertensive patients than in those without a history of hypertension. Plasma ANP concentration correlates with left heart chamber sizes.

Neuropeptide Y (NPY) is a vasoconstrictor sympathetic cotransmitter and a modulator of adrenergic function whose role in hypertension is yet unknown. We studied the co-release of NPY and noradrenaline (NA) in patients with essential hypertension (13 females, 11 males, age 42 +/- 13 years) by measuring plasma levels of NPY-immunoreactivity (-ir, radioimmunoassay) and NA (radioenzymatic method) following administration of clonidine (CL 300 micrograms, p.o.). At rest, only NPY-ir levels significantly correlated with diastolic blood pressure (DBP, r = 0.42, p < 0.05). Three hours after CL, there were a decrease in mean arterial pressure and plasma NA (by 31 +/- 14 mmHG, p < 0.05 and 92 +/- 10 pg/ml, p < 0.01) but no change in NPY-ir levels. Patients were subsequently subdivided into groups with high (> or = 90 mmHg) or normal DBP (< or = 89 mmHg) and with or without elevated plasma NA levels (above or below 414 pg/ml, a normotensive mean +1 standard deviation). In hypertensives, but not in those with normal DBP, plasma NPY-ir correlated not only with DBP but also with systolic and mean blood pressure (r = 0.53 and r = 0.60, respectively) at rest. Hypertensives with "high" NA had significantly lower resting plasma NPY-ir levels than those with "low" NA (7.1 +/- 3.6 vs 14.7 +/- 6.0 fmol/ml, p < 0.05). In the former group, CL evoked the greatest fall in plasma NA, and also decreased NPY-ir levels by 50% (p < 0.05). Thus, patients with essential hypertension were found to display differential patterns of changes in sympathetic cotransmitters to clonidine. NPY may contribute to the increased blood pressure in hypertensives and together with NA, mediate hypotensive action of clonidine but only in the hyperadrenergic subgroup of hypertensives.

Background: Endothelin-1 (ET-1) may play an important role in the development and maintenance of hypertensive states. In patients with essential hypertension, ET-1 plasma concentration increases or remains unchanged. The aim of the present study was to investigate ET-1 plasma concentration in patients with mild-to-moderate essential hypertension and its interrelationship with catecholamines, neuropeptide Y and atrial natriuretic peptide (ANP)., Methods: The study included 37 patients (mean age 38.2 +/- 1.6 years) with mild-to-moderate essential hypertension. The control group consisted of 21 healthy volunteers (mean age 35.6 +/- 1.4 years). ET-1, neuropeptide Y and ANP were determined by radioimmunoassay methods and catecholamine plasma concentration was determined radioenzymatically., Results: Our study shows that plasma ET-1 and neuropeptide Y levels are elevated in patients with essential hypertension compared with a control group. No correlation was found in either of the groups between plasma ET-1 level and plasma neuropeptide Y, catecholamine or ANP concentrations., Conclusion: Our results suggest that ET-1 is relevant in the development and maintenance of elevated blood pressure.

Ketanserin, a serotonin-2-receptor antagonist, was administered to 16 patients with mild to moderate essential hypertension in randomized single-blind placebo controlled study. After 2 weeks of placebo administration ketanserin 60 mg daily was given for 3 weeks. In 7 patients the normalization of blood pressure was obtained and they were given the same daily dose of ketanserin for another 3 weeks. In the remaining 9 patients the dose of ketanserin was increased to 120 mg daily for the same period; in one additional case blood pressure decreased to normal. In the whole group the decrease of diastolic pressure was statistically significant comparing to placebo period. Ketanserin therapy did not influence serum free serotonin concentration, but the hypotensive effect was greater in patients with lower serotonin blood levels. Serum aldosterone concentration decreased in the initial period of treatment; the decrease was more pronounced in patients who responded to therapy. In this subgroup of patients diastolic blood pressure correlated positively with plasma renin activity. Ketanserin lowered serum adrenaline concentration, particularly in patients with good response to therapy. There was also decrease of total cholesterol concentration without any significant changes in HDL--cholesterol fraction. The authors conclude that oral chronic ketanserin treatment is an effective therapy in essential hypertension and that its effectiveness is greater in patients with lower serum serotonin levels. The hypotensive effect of the drug may be connected with lower sympathetic activity and with changes in renin-angiotensin-aldosterone system. Ketanserin is well tolerated and exerts beneficial effect on lipid metabolism.

We evaluated the effect of captopril treatment on left ventricular mass (LVM) and function in sustained mild-to-moderate primary hypertension. In 16 men aged 34.5 +/- 6.4 yrs. M-mode echo and pulsed wave Doppler recordings were obtained prior to and after 2 months captopril treatment (50-150 mg daily). No significant changes in heart rate, systolic blood pressure, ejection fraction, fractional shortening, cardiac output, LVM and Doppler-derived indices of mitral inflow were observed. Diastolic blood pressure measured during examination fell from 102.2 +/- 13.3 to 90.3 +/- 9 mmHg (p less than 0.026). No consistent correlations between catecholamines and indexes of left ventricular function were found. Two-month captopril therapy in mild-to-moderate hypertension results in diastolic blood pressure lowering with no effect on LVM or left ventricular function.

89 patients were operated upon for pheochromocytoma. 61 patients (37 women and 24 men) were available for follow-up. Mean age at operation was 39 +/- 12.3 yrs. Before operation paroxysmal and sustained hypertension were observed in 34 (55.7%) and 27 (44.3%) patients, respectively. Postoperatively permanent normalization of blood pressure was achieved in 38 cases (62.3%). All patients were divided into four groups. Group I with increased urine excretion of noradrenaline (NA) and adrenaline (A) consisted of 19 (31.1%) patients. Group II (increased NA excretion) included 27 (44.3%) patients. Group III comprised 3 (4.9%) cases with elevated A excretion. 12 (19.7%) patients with normal urinary excretion of catecholamines and increased excretion of methoxycatecholamines were alloted to group IV. Permanent normalization of blood pressure predominantly was observed in group IV--91.6%, whilst in group I, II and III this hypotensive effect was noted in 57.9%, 51.8% and 2/3, respectively. Permanent normalization of blood pressure can be mainly expected in patients with pheochromocytoma in whom catecholamines are rapidly inactivated within the tumor.

Concentration of free serotonin, adrenaline, noradrenaline, aldosterone and plasma renin activity have been assayed in blood of 18 patients with the primary arterial hypertension (WHO stage I) and in 10 healthy volunteers. It was found that blood free serotonin and noradrenaline are increased in hypertensive patient. No difference in adrenaline and aldosterone levels and plasma renin activity was seen. No significant correlation between free serotonin and assayed hormones was noted.

An effect of the long-term prazosin therapy on sympathetic activity, renin plasma activity and beta-endorphin and lipid blood levels was investigated in 23 patients with the primary arterial blood hypertension. Group A included 18 patients treated with prazosin, and group B - 5 patients treated with prazosin combined with propranolol. Mean daily dose of prazosin in group A was 3.0-10.0 +/- 1.3 mg in different phases of therapy whereas in group B mean daily dose of prazosin was 3.0-6.5 +/- 1.8 mg and propranolol 50-80 mg. Significant decrease in diastolic and systolic blood pressure (p < 0.01) was achieved in both groups. Additionally significant decrease in pulse rate (p < 0.01) was seen in group B. It was found that prazosin produced significant increase in plasma noradrenaline in group A and decrease in 4-hydroxy-3-methoxyglycol excretion with the urine (p < 0.05) in both groups. Moreover, negative correlation between a decrease in blood pressure (diastolic) and noradrenaline excretion with the urine (p < 0.05) was noted in group A. No effect of prazosin therapy on plasma renin activity, beta-endorphin and lipids blood levels was observed in both groups. These results suggest that prazosin therapy in patients with the primary blood hypertension exerts an effect on sympathetic activity and does not change plasma renin activity or blood beta-endorphin and lipids levels.

In the face known antihypertensive action of small dopamine (DA) concentrations, serum free and conjugated dopamine levels were determined during orthostatic impulse. It was also estimated, whether correlation between blood pressure changes and serum dopamine concentration existed under those conditions. 9 patients with borderline hypertension, 8 with fixed hypertension and 5 healthy volunteers (control group) underwent the 10 minute passive tilt up test. It caused significant decrease of free DA concentration in healthy men as well as in those with borderline hypertension and conjugated DA level in both groups of patients with primary hypertension. Blood pressure increased only in patients with borderline hypertension. Most expressed changes in dopamine concentration were also observed in those patients and they only had increased serum DBH activity. Blood pressure changes inversely correlated with changes of serum free and/or conjugated DA levels in the control group and in patients with primary hypertension. Authors stated basing on this study results, that serum DA level lowering caused by the orthostatic impulse can be one of phenomenons enable adaptation for a vertical position.

Serotonin appears to play an important part in the pathogenesis of essential hypertension. Various studies have shown, that the metabolism of serotonin may be disturbed in some pathological conditions for example in hypertension. It concerns also the changed mechanisms of uptake and release of serotonin. The certain blood vessels may become more hypersensitive to the vasoconstrictor effects of serotonin in patients with hypertension than in normal subjects. During chronic treatment with ketanserin, S2-serotonergic antagonist, blood pressure is reduced in spontaneously hypertensive rats and in humans. This fact can also indicate indirectly, that that serotonin plays a part in the pathogenesis of essential hypertension. The aim of the study was to determine the concentration of free serotonin (S) in the blood of 15 patients with sustained essential hypertension in the mean age 32.8 +/- 1.8, of 23 patients with borderline essential hypertension in the mean age 29.0 +/- 3.0 and of 10 normal subjects in the mean age 31.1 +/- 1.7 years. Plasma free serotonin was determined by fluorometric method. All patients and controls were investigated at the hospital. They were on normosodium diet, without drugs for last two weeks. The fasting blood samples were collected in the supine position. Free serotonin blood concentration was significantly higher in hypertensive group than in normal subjects. The important difference of serotonin blood concentration between two groups of hypertensive patients was noticed. It was significantly higher in group of patients with sustained hypertension, than in group with borderline hypertension (p less than 0.05). Our results are similar to the observations of other authors.(ABSTRACT TRUNCATED AT 250 WORDS)

Authors assessed correlation between venous blood catecholamines and prostaglandins concentrations before and after inhibition of sympathetic activity by clonidine in patients with primary hypertension or pheochromocytoma. 30 patients with essential uncomplicated hypertension and 11 with pheochromocytoma underwent the study. The control group consisted of 6 healthy volunteers. Serum norepinephrine (NA), epinephrine (A), prostaglandins: PGE2 PGF2 alpha and prostacyclin metabolite -6-keto-PGF1 alpha were determined before and 3 hours after oral administration of 0.3 mg clonidine. Negative correlation was stated between basic serum norepinephrine and 6-keto-PGF1 alpha concentrations in patients with pheochromocytoma, which could indicate prostacyclin metabolism disorders during persistent hypercatecholaminemia . There was no correlation between catecholamines and prostaglandins during the inhibition of sympathetic activity in patients with pheochromocytoma as well as essential hypertension. The positive correlation was observed between changes in serum NA and PGF2 alpha levels in patients with borderline hypertension. Thus, one may suppose, that correlation between na excretion and vasoconstrictive PGF2 proved in acute experiments, becomes evident within the early stage of hypertension also during sympathetic activity inhibition.

The study included 30 patients with borderline essential hypertension (HPT) (21 with a positive family history of hypertension, mean age 24.6 years, 9 with a negative family history, mean age 27.2 years) and 10 normotensive controls (mean age 27.5 years). In all of them 24-hour urinary noradrenaline (NA) and adrenaline (A) excretion was assayed. Blood levels of NA, A and dopamine, the prostacycline metabolite 6-keto-PGF1 alpha, beta-thromboglobulin, cholesterol, triglycerides and HDL cholesterol were measured, LDL cholesterol was calculated according to the Friedewald equation. Besides, lecithin cholesterol acyltransferase activity was assayed. Patients with HPT and a positive family history had elevated sympathetic and platelet activity and diminished 6-keto-PGF1 alpha blood levels. Their HDL cholesterol level was significantly lower than that of healthy controls. In patients with HPT and a positive family history of HPT the atherogenic index (total cholesterol to HDL cholesterol ratio) was highest, but did not differ significantly from that in other groups. The assessment of the examined humoral factors indicates that patients with borderline HPT with genetic predisposition to high blood pressure have a humoral profile different from that of patients without genetic predisposition. These findings suggest the importance of genetic factors in the development of essential HPT.

The arterial pressure, the pulse frequency, the concentration of arterial natriuretic peptide (ANP), the aldosterone++ concentration and the plasma renin activity were determined in patients with primary hypertension after administration of furosemide in conditions of active assuming of erect position. The ANP concentration was lowered in that conditions both in the patients and in healthy subjects.

1. Urinary excretion of dopa, catecholamines and their metabolites (vanillylmandelic acid, methoxycatecholamines, 3-methoxy-4-hydroxyphenylglycol and homovanillic acid) were studied in eighty patients with essential hypertension and in twenty-five healthy control subjects. 2. Increased urinary excretion of catecholamines, dopa and catecholamine metabolites was found in a proportion of cases. 3. The relationship between urinary excretion of catecholamine metabolites and the excretion of dopa and noradrenaline was studied. 4. In view of the suggested significance of 3-methoxy-4-hydroxyphenylglycol as an index of brain catecholamine metabolism, particular attention was paid to urinary excretion of this metabolite in the subjects under study.

The metabolism of 3H-catecholamines after i.p. injection of 3H-tyrosine was studied in the heart and adrenals of spontaneously hypertensive (SHR) and normotensive Wistar (NCR) rats at rest and following running stress. In the heart of 8-week-old NCR a sharp stress-induced increase of the levels of 3H-A and 3H-DA with an elevation of the levels of their metabolites was observed. In contrast, there was no stress-related change in the levels of 3H-NA, 3H-A and 3H-VMA in the hearts of young SHR, while the 3H-DA level, though increased after stress, remained still lower than in the age-matched NCR. In the phase of established hypertension (24 weeks) lower levels of 3H-NA and 3H-A in the heart already present at rest, as compared with NCR, remained lower after stress but the elevation of the level of their metabolites 3H-VMA and 3H-MA, was similar in both strains. In the adrenals of 8-week-old SHR the basal 3H-A level was already higher than in NCR. Stress provoked a marked decrease of adrenal 3H-A accompanied by increased formation of 3H-MA and an increase in the levels of 3H-NA and 3H-DA, more pronounced in SHR than NCR. In the phase of advanced hypertension a further elevation of 3H-A and 3H-MA and an increase of basal 3H-DA level in the adrenals were found at rest. The decreased levels of 3H-catecholamines in the heart of stressed young and non-stressed older SHR may indicate an increase in their rate of release and/or their impaired synthesis. An increased basal level of 3H-A in the adrenals of SHR concomitant with the development of hypertension, may reflect an increased synthesis and/or decreased release, as evidenced by the proportionally lower increase of its extraneuronal metabolite 3H-MA. The adrenal response to stress, more intense in SHR than in NCR, may be considered as due to enhanced release of 3H-A from the gland.

Plasma atrial natriuretic factor (ANF) and catecholamine concentrations were determined in 11 untreated patients with uncomplicated essential hypertension and seven normotensive subjects during graded submaximal exercise on a treadmill (loads: I 40%, II 60%, III 80% of maximal oxygen consumption). No significant differences in plasma ANF and catecholamine concentrations were found between the hypertensive and the normotensive subjects. The results do not support the presence of significant differences in the release of ANF and catecholamines during dynamic exercise between patients with uncomplicated essential hypertension and normotensive subjects.

1. The effect of physical exercise on blood pressure, plasma catecholamines and plasma renin activity was studied in fourteen patients with essential hypertension and in eight healthy subjects. 2. Resting plasma noradrenaline and adrenaline and plasma renin activity of the hypertensive patients did not differ from those of the control subjects. 3. In response to graded exercise producing successive heart rates of 120, 140 and 160 beats/min, significantly greater increases of blood pressure were found in the patients than in the control subjects. 4. Plasma noradrenaline increased significantly in both groups at all levels of exercise, the responses being significantly greater in the hypertensive patients. 5. The mean arterial blood pressure was significantly correlated with plasma noradrenaline concentration in the control subjects but not in the hypertensive patients. 6. In the hypertensive group plasma adrenaline increased significantly after exercise at all work loads whereas, in the control group, significant increase occurred only at the highest work load. The differences in the response of the two groups were significant at each work load. 7. Plasma renin activity increased significantly after exercise at the heart rate of 120 beats/min, both in the hypertensive patients and in the control subjects. The magnitude of the response was similar in the two groups.

An effect of the treatment with guanfacine on the activity of the adreno-sympathetic system, beta-thromboglobulin, beta-endorphin, and blood lipids was studied in 30 patients with the primary arterial blood hypertension. It was found that guanfacine significantly decreases plasma noradrenaline, adrenaline, and dopamine. Moreover, it decreases the excretion of noradrenaline, adrenaline and 4-hydroxy-3-methoxy-phenylglycol. These effects correlate with the drop in both systolic and diastolic blood pressure. A decrease in plasma renin activity was also observed. It correlated with the blood pressure drops. Guanfacine increased beta-endorphin levels while beta-thromboglobulin, total cholesterol and triglycerides levels remained unaffected. The authors suggest that the hypotensive effect of guanfacine is related to the decrease in adreno-sympathetic system activity and plasma renin activity and no effect on the erythrocyte activity and lipids metabolism.

Plasma and urinary catecholamines and their metabolites were estimated in 18 patients with borderline hypertension (BH), 27 patients with established hypertension (EH) and 15 healthy subjects in basal conditions and after 20-min standing. Patients with EH differed from the remaining groups, showing decreased urinary excretion of noradrenaline (NA). In patients with BH, in comparison with controls, an augmented plasma NA in basal conditions as well as a more pronounced increment of plasma NA in response to upright posture was observed. Moreover, in BH increased urinary excretion of dopamine, homovanillic acid and 3-methoxy-4-hydroxyphenylglycol has been found. In patients with BH the increase of diastolic blood pressure in response to upright posture was associated with an exaggerated increase of plasma NA and adrenaline. The results of the study show that patients with BH are characterized by sympathetic overactivity and suggest that in this type of hypertension this factor may play a role in response of blood pressure to physiological stimuli.

Excretion of noradrenaline (NA), adrenaline (A), dopamine (DA) and their metabolites vanillylmandelic acid (VMA), methoxycatecholamines (MNA + MA) as well as 3-methoxy-4-hydroxy-phenylglycol (MHPG) was studied in 95 patients with essential hypertension and in 25 normal subjects on normal and low sodium diets. The patients were divided into 3 groups according to NA excretion under basal conditions. NA excretion was increased during sodium intake restriction, the highest values of this increase being found in patients whose basal NA excretion was diminished. At low sodium intake the high and the low NA excretors responded with significant increases of DA excretion. The mean excretion of VMA increased significantly on low sodium diet in all 3 groups of patients. The MNA + MA excretion decreased significantly during sodium intake restriction in patients with normal NA excretion. At low sodium intake the excretion of MHPG was highest in patients with low basal NA excretion. These data suggest that in patients with essential hypertension subjected to sodium restriction the excretion and metabolism of catecholamines are related to basal sympathetic activity.

1. Ten patients with essential hypertension and ten healthy men were submitted to mental stress consisting of Kraepelin's arithmetic test combined with noise. Concentrations of plasma and urine catecholamines and of their metabolites as well as plasma renin activity before and after the test were studied. 2. In both groups a significant increase of noradrenaline and adrenaline in blood and noradrenaline in urine was observed. The urinary excretion of dopamine fell significantly in both groups after stress. 3. After mental stress a significant increase in urinary excretion of 3-methoxy-4-hydroxyphenylglycol was observed in both groups. The excretion of vanillylmandelic acid decreased significantly only in healthy subjects. 4. The plasma renin activity rose significantly in both groups but the increase was more pronounced in healthy subjects.

Plasma renin activity, aldosterone and cortisol levels, as well as renal blood flow were studied in borderline and established hypertensive patients and in healthy control subjects at rest and following graded dynamic upright exercise. Resting plasma renin activity was elevated in established hypertension, renal blood flow at rest was decreased in patients with borderline hypertension but its per cent decrease during exercise was similar in all groups. Following exercise, plasma renin activity increased in all groups but a step-wise increase with graded exercise occurred only in borderline hypertension. Resting plasma aldosterone and cortisol levels were similar in all groups. In the hypertension patients physical exercise was associated with disproportional changes of plasma renin activity and aldosterone levels. Plasma cortisol displayed patterns which were roughly similar to those or aldosterone in the control group an in established hypertension, but not in the borderline group, where the most pronounced increased of aldosterone level was associated with the lowest level of cortisol. It is concluded that the physiological response of the renin-angiotensin-aldosterone system to physical exercise is altered in essential hypertension.

To investigate the possible release of beta-endorphins (beta EN) from tumors and to investigate their possible involvement in the hypotensive mechanism of clonidine (CLO) in pheochromocytoma (PHEO), as compared with essential hypertension (EH), we studied 12 patients with PHEO, 17 patients with uncomplicated stable EH (SEH), nine patients with borderline EH (BEH), and seven healthy volunteers (N). All subjects were hospitalized and excreted normal amounts of sodium. Mean blood pressure (MAP) and plasma beta EN, norepinephrine (NE), epinephrine (E), and dopamine (DA) were measured before and 180 min after an oral dose of 0.3 mg CLO. Following CLO, a significant (p less than 0.01) decrease in MAP was present in all groups. Plasma NE and E decreased (p less than 0.02 to p less than 0.01) in N, BEH, and SEH, but not in PHEO. DA did not change in any group. Pretreatment beta EN did not differ significantly between the groups, and following CLO it did not change in N or PHEO, while it increased significantly in BEH (p less than 0.01) and in SEH (p less than 0.02). Absolute changes in MAP correlated with those of beta EN only in the SEH group. Changes in NE or E did not correlate with changes in MAP in either group. Likewise, changes in NE or E were not correlated with those of beta EN, in N or EH, but a correlation between resting plasma E and resting beta EN concentrations was demonstrated in PHEO. These results support a role of beta EN in the hypotensive action of CLO in EH, but not in N or PHEO.(ABSTRACT TRUNCATED AT 250 WORDS)