M. Oppes

Comparison of Sublingual and Oral Captopril in Hypertension

The use of sublingual captopril has been recently suggested in hypertensive crisis on the assumption of a faster absorption and thus a more rapid effect on blood pressure than with the oral route. To verify this hypothesis we have compared the hypotensive effect of oral and sublingual captopril in 40 essential hypertensives who were randomly allocated to either route of administration. Captopril was administered orally dissolved in water or allowed to dissolve under the tongue. After 5, 10, 20, 30, 40, 60 and 90 minutes blood pressure, Plasma Renin Activity (PRA) and Angiotensin Converting Enzyme (ACE) were measured. No significant differences were found between the two groups in the time course of blood pressure decrease, PRA increase and ACE inhibition. The changes of the parameters studied was superimposable irrespective of the route of administration thus not supporting the hypothesis that sublingual captopril might be absorbed more rapidly.

Natriuretic effect of acute nifedipine administration is not mediated by the renal kallikrein-kinin system

Despite their vasodilating action, calcium antagonists increase renal sodium excretion. To ascertain whether renal kallikrein plays a role in the renal effects of calcium antagonists, nifedipine (N) (10 mg orally) or placebo (P) was given to 17 male patients with mild to moderate essential hypertension during a 6-h infusion of either saline (S) or aprotinin (A) (2 x 106 KIU in 200 ml of saline). Blood pressure (BP) and heart rate (HR) were measured every 10 min, and blood samples were taken at - 10, 0, 30, 60, 120, 240, 360 min for plasma renin activity (PRA), creatinine, and osmolarity determinations. Urinary kallikrein, aldosterone, creatinine, and electrolytes were measured in 6-h urine collections. The acute administration of N induced a significant systolic BP (SBP) and diastolic (DBP) fall and a transient PRA increase that peaked at 30 min and were not modified by A infusion. Urinary volume ( + 47|X%), Na+ ( + 54|X%) and C1- ( + 58|X%) excretion were significantly enhanced by N. There were less pronounced and statistically not significant increases in urinary excretion of Ca2+ ( + 38|X%) and K+ ( + 29|X%). Infusion of A did not interfere with the natriuretic effect of N. Our data do not support the hypothesis that the kallikrein-kinin system plays an important role in mediating the renal effects of nifedipine in humans.

Active and Inactive Renin During Acute Reduction of Renal Perfusion Pressure in Essential Hypertensives

Arterial and renal venous active and inactive renin were studied in 5 patients with long established moderate hypertension following unilateral acute reductions of renal perfusion pressure (15% and 70% of control) by inflating a balloon catheter introduced into the right renal artery. This procedure failed to induce the expected release of active renin; total and inactive renin levels were also unchanged. On the contrary in a single normotensive patient smaller reductions of the renal perfusion pressure (-15% and -30%) were able to acutely increase the release of active renin with a concurrent conversion of inactive renin but without inducing blood pressure changes. These findings show that the renin pattern typical of unilateral renovascular hypertension, including the intrarenal activation of inactive renin, could be reproduced acutely in a normotensive subject. Moreover, a complete reversal of the above mentioned active and inactive renin pattern was observed in a recent onset renovascular hypertensive patient within 30 min from successful percutaneous transluminal dilation. The negative results observed in our hypertensive patients suggest that structural changes induced by the long duration of hypertension might have reduced the sensitivity of the baroceptors involved in renin release.