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This study attempted to determine whether central magnesium (Mg) influences the regulation of blood pressure (BP). An intracerebroventricular (icv) injection of a high Mg2+ solution (190.0 mEq/L, 10 microL), made by adding MgC12 to artificial cerebrospinal fluid, increased the mean BP in both conscious spontaneously hypertensive rats (SHR; n = 17, p < 0.001) and Wistar Kyoto rats (WKY; n = 8, p < 0.005). Spontaneously hypertensive rats showed a greater pressor response than WKY (+11.7 +/- 0.9 mm Hg versus +3.5 +/- 1.1 mm Hg, p < 0.001). This pressor response to Mg2+ given icv was dose-dependent in the range of Mg2+ concentration between 47.5 and 190.0 mEq/L in SHR. A high Mg2+ solution (190.0 mEq/L), made by adding MgSO4 given icv, also increased the mean BP in SHR (n = 7, p < 0.001) and WKY (n = 6, p < 0.01), whereas the high osmolarity solution (340 mOsm/kg H2O) given icv did not change the mean BP in either SHR or WKY. Also administered was a high Mg2+ solution icv after either hexamethonium bromide (Hx; 50 mg/kg intravenously) or arginine vasopressin antagonist (aAVP, (CH2)5Tyr(Me)AVP, 30 micrograms/kg i.v.). The pressor response to the high Mg2+ solution was abolished by arginine vasopressin antagonist both in SHR and WKY, although it was not canceled by Hx. A high Mg2+ solution administered icv caused a 3.5-fold increase in plasma arginine vasopressin concentration in SHR (n = 5, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

The role of central Ca2+ in the regulation of blood pressure (BP) was investigated in conscious spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY). Ten microliters of a high Ca2+ solution (Ca2+: 32.6 mM) administered intracerebroventricularly (i.c.v.) decreased the mean arterial pressure (MAP) for more than 20 min in SHR (n = 7, P < 0.005), while no change of MAP was observed in the WKY (n = 6). This depressor response to Ca2+ i.c.v. was dose-dependent at Ca2+ concentrations between 16.3 and 65.2 mM. We also investigated the effect of high Ca2+ i.c.v. in SHR after pretreatment with Ca2+ channel blockers, diltiazem (60 micrograms/10 microliters) or nisoldipine (4, 8, 16 and 32 micrograms/10 microliters), administered i.c.v., the autonomic ganglion blocker, hexamethonium (50 mg/kg), administered i.v. and alpha-methyl-p-tyrosine (100 and 400 micrograms/10 microliters) delivered i.c.v. Pretreatment with i.c.v. diltiazem (n = 8) or nisoldipine (n = 5 for 8 micrograms, n = 6 for 4, 16, 32 micrograms) abolished and/or blunted the decrease of MAP due to high Ca2+. Hexamethonium administered i.v. (n = 6) also canceled the depressor action of i.c.v. Ca2+. Pretreatment with 100 micrograms of i.c.v. alpha-methyl-p-tyrosine could not prevent the depressor action of i.c.v. Ca2+; however, 400 micrograms of alpha-methyl-p-tyrosine administered i.c.v. abolished the effect of i.c.v. Ca2+. Furthermore Ca2+ channel blockers administered i.c.v. in themselves increased MAP in SHR (P < 0.05). These results suggest that central Ca2+ is involved in the central regulation of BP in SHR. This effect may be mediated through changes in sympathetic activity.

We performed retrospective study of the relationship between the severity and duration of hypertension and echocardiographically-detected left ventricular hypertrophy (echo-LVH) in patients with untreated essential hypertension. The subjects consisted of 92 untreated essential hypertensives who were observed for more than 5 years from the onset of diastolic hypertension (greater than or equal to 95 mmHg), and whose left ventricular (LV) mass index was measured at the end of the observation period. On the basis of the frequency of diastolic hypertension during the observation period, the population was categorized in 3 groups. In Group I (32 cases), diastolic hypertension was observed in more than 80% of blood pressures obtained throughout the entire observation period. In Group II (38 cases), diastolic hypertension was observed in 33 to 80% of the observation period. In Group III (22 cases), diastolic hypertension was observed in less than 33% of the observation period. The average diastolic blood pressure during the entire observation period in each group were 101.0, 96.0, and 90.7 mmHg in groups I, II, and III, respectively. The LV mass index was significantly higher in groups I (114.6 g/m2) and II (105.3 g/m2) than in group III (90.7 g/m2) (p less than 0.01). The prevalence of echo-LVH (more than 121 g/m2) was 34.4%, 18.4%, and 4.8% in groups I, II, and III, respectively. The average diastolic blood pressure in patients with echo-LVH (99.3 +/- 5.1 mmHg) was significantly higher than in patients without echo-LVH (95.7 +/- 4.7 mmHg). We concluded that the degree and duration of diastolic pressure elevation are closely correlated to the LV mass index.

We studied the effect of high salt intake on blood pressure in two cases with renovascular hypertension. They had hypertension with hyperreninemia and marked difference in plasma renin activity between both renal veins. Blood pressure significantly decreased after single oral administration of captopril. Renal arteriogram revealed significant stenosis in the main artery to the left (case 1) and right (case 2) kidney. Blood pressure response was evaluated after seven (case 1) and five (case 2) days of low salt and seven days (both cases) of high salt intake. Mean blood pressure in two patients was significantly decreased (case 1; 118 +/- 5.5 to 108 +/- 6.1 mmHg and case 2; 150 +/- 3.8 to 138 +/- 3.1 mmHg). Plasma renin activity was also decreased (case 1; 6.25 to 0.77 ng/ml/hr and case 2; 22.8 to 6.3 ng/ml/hr). In case 2, blood pressure elevated markedly during low salt intake, compared with blood pressure level during normal salt intake. The results suggest that excessive salt intake in patients with unilateral renovascular hypertension produces blood pressure reduction because of suppression of renin-angiotensin system. We concluded that in patients with unilateral renovascular hypertension dietary sodium depletion may be harmful, whereas salt supplement may have a beneficial effect.

The contribution of the renin-angiotensin system (RA) and of prostaglandins (PG) to the acute depressor effect of captopril (Capt) was studied in 13 hypertensive patients suppressing either RA by propranolol (Prop) or PG by indomethacin (Indo). Four patients showed abolition of the depressor effect of Capt by pretreatment with both Prop and Indo (Group 1). Indo, but not Prop, cancelled the depressor effect in another 4 patients (Group 2). In the remaining 5 patients, either Prop or Indo did not alter the depressor response to Capt (Group 3). Patients in Group 3 were older than patients in Group 1 and 2 and showed lower plasma volume value. Several mechanisms might contribute to the acute depressor effect of Cap, including not only the suppression of RA and the enhancement of PG, but perhaps other undetermined factor(s), especially in older patients.

We examined the effect of centrally administered aprotinin, a serine protease inhibitor, on blood pressure (BP) in conscious spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Twenty-two gauge needles and polyethylene catheters were implanted into lateral cerebroventricle and femoral artery, respectively, at 48 hours before the experiments. In Group 1 (8 SHR, 6 WKY), rats received a bolus intracerebroventricular injection (i.c.v.) of aprotinin (1,000 KIU/kg/10 microliters). A prompt increase of BP was observed in SHR after aprotinin and this elevation of BP was persisted for over 30 minutes (mean BP: 158.8 +/- 2.9 mmHg at control to 168.7 +/- 3.2 at 15 min., p less than 0.01; to 168.3 +/- 3.4 at 30 min., p less than 0.01). On the other hand, BP of WKY decreased gradually after aprotinin (mean BP: 143.0 +/- 3.3 at control to 136.8 +/- 2.7 at 15 min., n.s.; to 134.2 +/- 5.1 at 30 min., p less than 0.05). The intravenous injection (i.v.) of aprotinin (Group 2: 7 SHR, 5 WKY) and the i.c.v. of artificial cerebrospinal fluid (CSF) (Group 3: 5 SHR, 6 WKY) did not affect BP in both SHR and WKY except for the minor transient increase of BP in WKY immediately after artificial CSF i.c.v.. We performed additional experiments to study the contributions of sympathetic nervous system and vasopressin to these changes in BP.(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormality of the circulatory reflexes has been reported in patients with primary aldosteronism. However, changes in blood pressure, heart rate, plasma renin activity (PRA), and plasma aldosterone concentration (PAC) after head-up tilting in primary aldosteronism have not yet been reported. Seven patients with primary aldosteronism were tilted to a 65 degree head-up position which was maintained for 30 min. Systolic blood pressure decreased significantly 5 min after tilting and remained at this level during the period of tilting. Diastolic blood pressure did not change during the tilting. Heart rate increased after 5 min of tilting and this level of heart rate was maintained for 30 min. Plasma renin activity was low and did not change during tilting. However, plasma aldosterone concentration increased significantly 20 min after tilting. Plasma cortisol concentration and plasma ACTH concentration also increased significantly. These results suggest that primary aldosteronism causes abnormalities of the circulatory reflexes. The increase of endogenous ACTH may increase plasma aldosterone concentration in patients with primary aldosteronism.

At the Radiation Effects Research Foundation, medical examinations have been conducted biennially since 1958 on a fixed population of approximately 20,000 individuals. Blood pressure measurements and electrocardiographic (ECG) recordings are available for 6,569 individuals who were monitored for at least 11 of the 13 2 year intervals between 1958 and 1984. Data from 601 individuals who had satisfied the Foundation's ECG diagnostic criteria of left ventricular hypertrophy ("Kagan-Yano code") on at least one occasion were reviewed. Both the development and the regression of ECG left ventricular hypertrophy were ascertained in 61 subjects (17 men and 44 women). During the course of development of ECG left ventricular hypertrophy, hypertension (including borderline cases) was noted in 83.3% of the subjects. The most common pattern of ECG left ventricular hypertrophy development was high voltage, followed by ST-T changes. In about half of these cases, the condition of hypertrophy regression was associated with lowering of blood pressure, marked by the disappearance of high voltage ECG readings.

A sixty-six-year-old man with severe aortic stenosis, in whom simultaneous and continuous monitoring of the electrocardiogram and arterial blood pressure was performed immediately before, during, and following recovery from exercise-induced syncope, is reported. During exercise the patient developed anginal pain associated with a gradual fall of arterial blood pressure followed by syncope. At the onset of the syncope, arterial blood pressure was extremely low, and the electrocardiogram showed sinus tachycardia. It was assumed from these findings that profound hypotension, induced by peripheral vasodilatation and ischemic myocardial depression leading to inappropriately low cardiac output, was the underlying factor mainly responsible for the occurrence of exercise-induced syncope in the present case.

The biological actions of angiotensin III (AIII) in animals have been reported to be stimulation of aldosterone secretion and vasoconstriction. However, the biological actions of AIII in human essential hypertension (EH) have not been evaluated. Twenty ng/Kg/min of AIII was infused intravenously for 30 min into 6 normal subjects and 24 patients with EH. The systolic blood pressure was elevated significantly, from 116 +/- 5 (mean +/- SD)/68 +/- 4 to 137 +/- 9/74 +/- 5 mmHg in normal subjects and from 155 +/- 29/95 +/- 17 to 176 +/- 26/106 +/- 20 mmHg in EH patients. The elevation in systolic BP of low-renin EH patients was significantly larger than that of normal-renin EH patients. Plasma renin activity (PRA) decreased significantly from 1.64 +/- 1.07 to 1.21 +/- 1.05 ng/ml/hr in normal subjects and from 0.88 +/- 0.66 to 0.76 +/- 0.63 ng/ml/hr in EH. Plasma aldosterone concentration (PAC) increased significantly from 57 +/- 34 to 116 +/- 34 pg/ml in normal subjects and from 66 +/- 56 to 91 +/- 24 pg/ml/ in EH. There was no significant difference between the increase of PAC in low-renin EH and in normal-renin EH. Plasma cortisol concentration (PCC) did not change in these subjects. There were no significant relationships between the changes of PRA and PAC or PRA and blood pressure. These results suggest that the pressor action of AIII appeared in relation to the basal PRA in EH. In EH, PRA is suppressed by the direct action of AIII in the kidney and neither by increased PAC nor by increased blood pressure. The small changes in blood pressure caused by AII infusion suggest that a test using an AIII infusion for aldosterone stimulation would be preferable to an angiotensin II infusion.