To evaluate whether, in the forearm of hypertensive patients with different circulating renin profiles, local beta-adrenergic receptor-induced production of active renin, plasma renin activity, angiotensin I (Ang I), and angiotensin II (Ang II) was or was not related to the renin profile, we studied four groups of patients: 1) hypertensive patients with primary aldosteronism and suppressed circulating plasma renin activity values (0.15-0.1 ng Ang I/mL per hour; n=7), 2) essential hypertensive patients with low (0.47 +/- 0.1 ng Ang I/mL per hour; n=8) circulating plasma renin activity values, 3) essential hypertensive patients with normal (2.48 +/- 0.52 ng Ang I/mL per hour; n=8) circulating plasma renin activity values, and 4) renovascular hypertensive patients with high circulating plasma renin activity values (4.16 +/- 2.1 ng Ang I/mL per hour; n = 10). Isoproterenol was infused into the brachial artery, and active renin, plasma renin activity, and Ang I and Ang II forearm balance (venous-arterial differences corrected for forearm blood flow by strain-gauge plethysmography) were measured. Despite a comparable vasodilation, beta-adrenergic stimulation failed to release active renin, plasma renin activity, and Ang I and Ang II in primary aldosteronism. It slightly increased them (except for Ang I) in low renin patients but determined a local production in normal renin and renovascular hypertensive patients. The individual increments in plasma renin activity and Ang II release induced by isoproterenol showed a correlation with the renin profile. In another group of essential hypertensive patients (n = 6), isoproterenol was infused for 60 minutes, and we observed that despite a stable forearm vasodilation, both plasma renin activity and Ang II reached maximum values between 5 and 10 minutes; after that, they immediately started to decline and returned to basal levels. These data suggest the possibility that in hypertensive patients, vascular tissue renin originates from plasma uptake.
Indirect evidence for vascular uptake of circulating renin in hypertensive patients.
TADDEI, STEFANO;VIRDIS, AGOSTINO;SALVETTI, ANTONIO
1993-01-01
Abstract
To evaluate whether, in the forearm of hypertensive patients with different circulating renin profiles, local beta-adrenergic receptor-induced production of active renin, plasma renin activity, angiotensin I (Ang I), and angiotensin II (Ang II) was or was not related to the renin profile, we studied four groups of patients: 1) hypertensive patients with primary aldosteronism and suppressed circulating plasma renin activity values (0.15-0.1 ng Ang I/mL per hour; n=7), 2) essential hypertensive patients with low (0.47 +/- 0.1 ng Ang I/mL per hour; n=8) circulating plasma renin activity values, 3) essential hypertensive patients with normal (2.48 +/- 0.52 ng Ang I/mL per hour; n=8) circulating plasma renin activity values, and 4) renovascular hypertensive patients with high circulating plasma renin activity values (4.16 +/- 2.1 ng Ang I/mL per hour; n = 10). Isoproterenol was infused into the brachial artery, and active renin, plasma renin activity, and Ang I and Ang II forearm balance (venous-arterial differences corrected for forearm blood flow by strain-gauge plethysmography) were measured. Despite a comparable vasodilation, beta-adrenergic stimulation failed to release active renin, plasma renin activity, and Ang I and Ang II in primary aldosteronism. It slightly increased them (except for Ang I) in low renin patients but determined a local production in normal renin and renovascular hypertensive patients. The individual increments in plasma renin activity and Ang II release induced by isoproterenol showed a correlation with the renin profile. In another group of essential hypertensive patients (n = 6), isoproterenol was infused for 60 minutes, and we observed that despite a stable forearm vasodilation, both plasma renin activity and Ang II reached maximum values between 5 and 10 minutes; after that, they immediately started to decline and returned to basal levels. These data suggest the possibility that in hypertensive patients, vascular tissue renin originates from plasma uptake.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
