Angiotensin II Blockade in Normal Subjects and Essential Hypertensive Patients

Abstract

1. Saralasin (Sar1-Ala8-angiotensin II), a competitive inhibitor of angiotensin II (AII), has been infused into normal subjects and patients with essential hypertension when deprived of sodium by 5 days of a 10 mmol/day sodium diet. 2. When saralasin was given by an incremental rate of infusion starting at 0·25 μg min—1 kg—1, sodium-deprived normal subjects showed a fall in standing blood pressure with no change in lying blood pressure, sodium-deprived normal-renin hypertensive patients showed no change in lying or standing blood pressure and sodium-deprived low-renin patients showed a significant sustained rise in lying and standing blood pressure. 3. These findings suggest that: (a) standing blood pressure in sodium-deprived normal subjects is angiotensin II dependent; (b) normal-renin hypertensive patients when sodium deprived by diet alone do not appear to be angiotensin II dependent (angiotensin II is unlikely therefore to be directly maintaining their blood pressure on their normal sodium intake); (c) the rise in blood pressure seen in low-renin hypertensive patients with saralasin may be a further way of distinguishing this group of patients.

The myogenic response in uremic hypertension

“…scarred [32] kidneys, and consistent with this is the observation that bilateral nephrectomy in dialysis patients causes a lowering of blood pressure and of peripheral resistance [6,15]. However, in both experimental renal failure [27] and in a proportion of dialysis patients [8], plasma renin activity is not completely autonomous, and can be suppressed by extracellular volume expansion such that inappropriate plasma renin activity and volume expansion do not necessarily co-exist. Third, the sympathetic nervous system is activated in uremia [10,11], which might increase vascular tone through noradrenaline-induced constriction.…”

“…2) despite using the of the renin-angiotensin-aldosterone system inapproprisame anatomical vessel. The animals we studied were ate to the prevailing blood pressure occurs in uremia approximately 26-weeks-old at sacrifice, compared to [8,9] for the hypertension of chronic renal failure.…”

“…These include Oxon, UK). General anesthesia was induced for both sodium retention [6,7], inappropriate activity of the restages of nephrectomy by intramuscular injection of nin-angiotensin-aldosterone system [8,9], and increased HYPNORM 1 mL/kg body weight (fentanyl citrate sympathetic nervous system activity [10,11]. Vascular 0.315 mg/mL plus fluanisone 10 mg/mL; Janssen-Cilag endothelial dysfunction [12] and structural changes of resistance arteries [13,14] in which the appropriate kidney was stripped of its cap-VT, USA).…”

Response of Mineralocorticoid Hypertensive Animals to an Angiotensin I Converting Enzyme Inhibitor

“…The recent development of angiotensin I converting enzyme inhibitors has made possible their use in delineating the role of the renin-angiotensin system in different types of hypertension (1). These inhibitors also block agents responsible for kinin destruction (2).…”