We tested the hypothesis that in the absence of changes in arterial blood pressure (BP) and glomerular filtration rate (GFR), renin secretion is controlled by renal sympathetic nerve activity via ß1-adrenoceptors. Eight normal subjects on a sodium intake of 30 mmol NaCl day-1 received a modest saline load intravenously (NaLoad: 12 mmol Na+*kg-1*min-1 for 4 h) with (metoprolol) and without (control) concomitant infusion of metoprolol, 1 mg*kg-1* min-1. Measurements included BP and central venous pressures (CVP), cardiac output (CO, by impedance cardiography), plasma hormones and renal function including GFR (51Cr-EDTA).

Metoprolol decreased renin activity (58 ± 3 to 25 ± 10 mIU/l) and tended to reduce plasma aldosterone. The NaLoad did not change BP from values 81 ± 9 mmHg (control) and 73 ± 6 mmHg (metoprolol) or CO from values of 6.5 ± 1.4 l/min (control) and 6.6 ± 0.5 l/min (metoprolol); a trend towards an increase in CVP remained insignificant. Nevertheless, the NaLoad decreased plasma renin activity and plasma aldosterone also during blockade by metoprolol (25 ± 10 to10 ± 2 mIU/l and 159 ± 29 to 89 ± 11 pg/ml, respectively). Concomitantly, sodium excretion increased irrespective of blockade by metoprolol (control: 14 ± 3 to 59 ± 3 mmol/min; metoprolol: 18 ± 2 to 72 ± 23 mmol/min).

In conclusion, renin suppression and natriuresis in response to a modest sodium load are controlled by factors other than BP, GFR and ß1-mediated sympathetic tone.