Search

Objective: Reduced baroreflex sensitivity has been reported in several kinds of human hypertension. However, the nature of the baroreceptor-heart rate reflex in hypertension due to excess mineralocorticoid has never been fully explored., Patients and Methods: Thirty patients with primary aldosteronism, 60 patients with essential hypertension (World Health organization stages I or II) and 45 normotensive subjects were enrolled. The groups did not differ in mean age. Blood pressure was similar between patients with primary aldosteronism and those with essential hypertension. Blood pressure (Finapres) and the RR interval (ECG) were monitored continuously at rest. The closed loop gain between systolic blood pressure and RR interval variabilities was used to measure the sensitivity of the baroreceptor-heart rate reflex., Results: Baroreflex sensitivity in the group with primary aldosteronism was significantly greater than in the essential hypertensive group, but did not differ significantly between the group with aldosteronism and the normotensive group. Three to four weeks after removal of an adrenal adenoma (n = 25), both systolic and diastolic blood pressure were decreased significantly in the aldosteronism group but were still higher than in the normotensive group. The baroreflex sensitivity was reduced by about 40% after adrenalectomy compared to pre-operative values. The decrease in the baroreflex gain following adrenalectomy was correlated negatively with the decrease in systolic blood pressure (r = -4.00, P=0.05)., Conclusion: These results demonstrate that hypertension due to excess mineralocorticoids is characterized by an increase in the gain of the baroreceptor-heart rate reflex. The reduction in baroreflex gain following adrenalectomy may delay the normalization of blood pressure.

Anaesthetized rabbits were used to examine the effects of amiloride (an inhibitor of a conductive sodium channel in the distal tubule) and atrial natriuretic peptide (ANP), both singly and in combination, on renal function and the renal kallikrein-kinin system. The administration of ANP (0.05 microgram/kg per min) produced a natriuresis with increases in renal blood flow and glomerular filtration rate. The administration of ANP superimposed on amiloride infusion (5 mg/kg + 0.04 mg/kg per min) showed an additive effect on the natriuresis, although the renal haemodynamic changes were now absent. The infusion of ANP alone increased the urinary excretion of kallikrein and kinins. Prior infusion of amiloride prevented the expected increases in the urinary excretion of kallikrein and kinins after infusion of ANP was superimposed. These results suggest that the observed renal haemodynamic changes could be mediated through renal kallikrein and kinins. The additive effect on sodium excretion might be elicited by the results of alterations in the tubular handling of sodium, although distal tubular function is not modified by ANP. It seems that the renal kallikrein-kinin system is not causally involved in the increased sodium excretion by ANP.

To examine a possible role of endogenous bradykinin in the regulation of blood pressure (BP) and renal blood flow (RBF), a newly synthesized competitive antagonist of bradykinin (B4147) was studied in anesthetized rats. Also, the question of whether the hypotensive effect of the converting enzyme inhibitor, captopril, is mediated partly by an accumulation of endogenous bradykinin was considered. The intravenous infusion of B4147 (25 micrograms/min) inhibited the depressor effect of exogenous bradykinin (0.5 microgram, i.v.) by 69%. After an intravenous injection of B4147 at doses of 25, 50 and 100 micrograms, BP increased and RBF decreased in a dose-dependent fashion. The increase in BP was not blocked by pretreatment with an angiotensin II antagonist (1-Sar-8-Ile angiotensin II; 20 micrograms/kg per min) or an alpha 1-blocker (prazosin; 0.1 mg/kg). The administration of captopril (1 mg/kg) decreased mean BP from 110 +/- 3.5 to 71 +/- 1.9 mmHg (P less than 0.001). However, the injection of B4147 (50 micrograms) after the administration of captopril elicited an increase in BP of 43% of the initial decrease induced by captopril. These results suggest that the effects of B4147 on BP and RBF are not mediated through angiotensin II or sympathetic alpha 1-stimulation. Endogenous bradykinin could contribute to the maintenance of BP and RBF in anesthetized rats, probably counter-balancing the vasoconstrictor mechanisms. It is also suggested that bradykinin may partly participate in the acute hypotensive effect induced by the converting enzyme inhibitor captopril.