To evaluate the contribution of beta 1-2-adrenergic receptor stimulation to the regulation of single-nephron glomerular filtration rate (SNGFR), we examined by micropuncture techniques the effects of systemic and intrarenal infusion of isoproterenol on glomerular hemodynamics in plasma volume-expanded Munich-Wistar rats. Isoproterenol infused systemically was consistently associated with an elevation in glomerular capillary hydrostatic pressure difference (delta P) from 44.2 +/- 1.2 to 50.1 +/- 1.3 mmHg, P less than 0.01, the consequence of a 5.9-mmHg fall in Bowman's space hydrostatic pressure, P less than 0.005. The potentially beneficial effect of increased delta P on SNGFR was overcome by a 40% reduction in the glomerular ultrafiltration coefficient (LpA) from 0.043 +/- 0.003 to 0.026 +/- 0.003 nl.s-1.mmHg-1.g kidney wt-1, P less than 0.005, with a net effect of a modest 13% decline in SNGFR, P less than 0.01. In contrast, the intrarenal infusion of isoproterenol did not modify glomerular hemodynamics. Suppression of angiotensin II activity eliminated the influences of systemic isoproterenol infusion on LpA and delta P, the latter was the consequence of lower efferent arteriolar resistance. The findings suggest that systemic infusion of a beta 1-2-adrenergic agonist results in a decrease in LpA via angiotensin II effects and exerts a vasodilatory action on postglomerular vessels during angiotensin II inhibition.