To evaluate whether, in the forearm of hypertensive patients with different circulating renin profiles, local β-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, β-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.