RT Journal Article
SR Electronic
T1 Beta-1 receptor mediation of renin secretion elicited by low-frequency renal nerve stimulation.
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 265
OP 269
VO 216
IS 2
A1 J L Osborn
A1 G F DiBona
A1 M D Thames
YR 1981
UL http://jpet.aspetjournals.org/content/216/2/265.abstract
AB The purpose of this study was to determine if renin secretion resulting solely from low-frequency renal nerve stimulation (no change in renal blood flow or urinary sodium excretion) is mediated by activation of beta-1 (beta-1) or beta-2 (beta-2) adrenergic receptors. Beta-1 and beta-2 adrenergic receptor blockade were produced with atenolol and butoxamine, respectively. Low-frequency renal nerve stimulation (0.5 Hz) increased renin secretion without altering mean arterial pressure, renal blood flow, glomerular filtration rate or urinary sodium excretion. The increase in renin secretion in response to renal nerve stimulation was blocked by beta-1 blockade with intrarenal atenolol (2.0 micrograms/kg/min) infusion. This dose of atenolol reduced the renal vasodilator response to intrarenal isoproterenol by only 48%, thus indicating modest beta-2 receptor blockade. A lower dose of atenolol (30 micrograms/kg i.v.) markedly decreased the tachycardia in response to i.v. isoproterenol (2 micrograms) but had no effect on the renal vasodilator response to intrarenal isoproterenol injection (2 micrograms), thus indicating selective beta-1 blockade. This dose of atenolol abolished the increase in renin secretion during renal nerve stimulation. In contrast, beta-2 receptor blockade with butoxamine (20 micrograms/kg/min) did not alter the renin secretion response to renal nerve stimulation. This dose of butoxamine decreased the renal vasodilator response to intrarenal isoproterenol by 73%, thus demonstrating significant beta-2 receptor blockade. These results indicate the low-frequency renal nerve stimulation (0.5 Hz) increases renin secretion without altering renal hemodynamics or urinary sodium excretion. This neurally mediated renin secretion resulted from activation of beta-1 adrenergic receptors.