Sodium deprivation increased plasma aldosterone in normotensive (5.8 to 15.3 ng/100ml) and hypertensive patients (5.9 to 14.4 ng/100ml), without correlating with endogenous angiotensin II changes.
Observational (n=25)
How do sodium deprivation and angiotensin II infusion affect the renin-angiotensin-aldosterone system in normotensive and hypertensive patients?
The study demonstrates differential responses of plasma angiotensin II to sodium deprivation between normotensive and hypertensive patients, alongside a potent feedback inhibition of renin release by angiotensin II infusion in both groups.
The responses of plasma renin activity, plasma angiotensin II, plasma aldosterone, cortisol, and corticosterone to sodium deprivation and to angiotensin II infusion (100 ng/min) were measured in 8 normotensive patients and in 17 patients with essential hypertension. Following sodium deprivations, plasma renin activity rose from 0.513 ± 0.100 to 1.029 ± 0.124 ng/ml hour -1 in normotensive patients and from 0.406 ± 0.077 to 0.629 ± 0.059 ng/ml hour -1 in hypertensive patients. Plasma angiotensin II did not parallel changes in plasma renin activity: in normotensive patients plasma angiotensin II was unchanged by sodium deprivation (31.8 ± 6.0 compared with 30.1 ± 4.6 pg/ml), but in hypertensive patients it rose from 22.2 ± 3.4 to 36.4 ± 5.1 pg/ml. Plasma aldosterone rose equally in both groups following sodium deprivation (5.8 ± 1.3 to 15.3 ± 2.4 ng/100 ml for normotensive patients and 5.9 ± 1.4 to 14.4 ± 1.6 ng/100 ml for hypertensive patients) and angiotensin infusion (5.8 ± 1.3 to 10.4 ± 2.1 ng/100 ml in sodium-loaded normotensive patients, 15.3 ± 2.4 to 19.6 ± 3.6 ng/100 ml in sodium-deprived normotensive patients, 5.9 ± 1.4 to 11.4 ± 2.7 ng/100 ml in sodium-loaded hypertensive patients, and 14.4 ± 1.6 to 22.2 ± 2.6 ng/100 ml in sodium-deprived hypertensive patients). However, changes in endogenous plasma angiotensin II did not correlate with the rise in plasma aldosterone caused by sodium deprivation, and, despite much larger increases in plasma angiotensin II during angiotensin II infusion, plasma aldosterone showed smaller rises than those accompanying sodium deprivation. Plasma renin activity fell during angiotensin II infusion, in both groups of patients during both sodium loading and sodium deprivation, and, hence, the infusion constitutes a potent feedback inhibition of renin release in normotensive and hypertensive man. Plasma cortisol and corticosterone were unaltered by sodium deprivation but fell significantly with the angiotensin II infusion.
Mendelsohn et al. (Wed,) conducted a observational in Essential hypertension (n=25). Sodium deprivation and angiotensin II infusion vs. Baseline / sodium loading was evaluated on Responses of plasma renin activity, plasma angiotensin II, plasma aldosterone, cortisol, and corticosterone. Sodium deprivation increased plasma aldosterone in normotensive (5.8 to 15.3 ng/100ml) and hypertensive patients (5.9 to 14.4 ng/100ml), without correlating with endogenous angiotensin II changes.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: