Effects of beta 1-adrenergic blockade on glomerular dynamics and angiotensin II response

Adrenergic activity regulates renal function by several mechanisms. Renal nerves not only exert vasoconstrictor functions but also may influence glomerular hemodynamics by beta-adrenergic activity, especially via the effects on renin angiotensin activity. Little is known of the specific glomerular hemodynamic alterations resulting from beta 1-adrenergic blockade. Current studies examined the effects of 4-6 days of treatment with atenolol (50 mg/kg), a beta 1-selective adrenergic antagonist, on glomerular hemodynamics in plasma volume-expanded Munich-Wistar rats. Atenolol treatment reduced blood pressure both in the awake state and during micropuncture. This reduction in blood pressure contributed to a decrease in nephron filtration rate (48 +/- 1 in untreated rats vs. 40 +/- 1 nl.min-1.g kidney wt-1 in the atenolol-treated group, P less than 0.05) by reduction in nephron plasma flow (182 +/- 2 vs. 154 +/- 4 nl.min-1.g kidney wt-1 in the atenolol-treated rats). No other determinant of glomerular ultrafiltration was influenced by atenolol treatment. Since beta 1-adrenergic blockade may influence the generation of angiotensin II, the response to angiotensin II infusion was assessed and found not to differ from control untreated animals. These studies demonstrate that beta 1-receptor blockade reduced nephron filtration rate by decreasing mean arterial blood pressure and nephron plasma flow without significant modifications in vascular resistance and the glomerular hydrostatic pressure gradient.