Indirect evidence for vascular uptake of circulating renin in hypertensive patients.

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