Renal adrenoceptor mediation of antinatriuretic and renin secretion responses to low frequency renal nerve stimulation in the dog

We evaluated renal adrenoceptor mediation of the renin secretion and antinatriuretic responses to low frequency (1.0 Hz) electrical stimulation of the renal nerves in the dog using renal α-adrenoceptor blockade with phentolamine (α₁/α₂), prazosin (α₁), yohimbine (α₂), and rauwolscine (α₂), and β-adrenoceptor blockade with d,l-propranolol (β₁/β₂) and atenolol (β₁). In all animals studied, renal blood flow and glomerular filtration rate remained constant throughout the experiment. In 11 dogs, low frequency renal nerve stimulation decreased urinary sodium excretion (119 ± 13 to 86 ± 18 μEq/min) and increased renin secretion (79 ± 22 to 348 ± 73 ng/min). Renal arterial infusion of phentolamine (2-10 μg/kg per min) prevented the antinatriuresis but did not change the response of renin secretion (96 ± 46 to 412 ± 93 ng/min). In six dogs, renal arterial infusion of prazosin (0.7 μg/kg per min) similarly blocked the antinatriuretic but not the renin secretion responses to low frequency renal nerve stimulation. Renal arterial infusion of either yohimbine or rauwolscine did not affect the antinatriuretic or renin secretion responses to low frequency renal nerve stimulation. Intrarenal β₁-adrenoceptor blockade with low dose atenolol (0.5 μg/kg per min, n = 9) had no effect on the antinatriuretic responses to low frequency renal nerve stimulation (-47 ± 12 vs. -37 ± 8 μEq/min) but significantly decreased the increment in renin secretion during low frequency renal nerve stimulation (636 ± 249 vs. 305 ± 157 ng/min; P < 0.05). Renal arterial infusion of d,l-propranolol (0.5 μg/kg per min, n = 4) or a high dose of atenolol (5.0 μg/kg per min, n = 8) abolished the renin secretion but not the antinatriuretic responses to low frequency renal nerve stimulation. These results demonstrate that: antinatriuresis during 1.0 Hz renal nerve stimulation (where renal blood flow and glomerular filtration rate are unchanged) is mediated by renal α₁-adrenoceptors and not by α₂- or β-adrenoceptors, that renin secretion elicited by low frequency renal nerve stimulation is mediated by renal β₁-adrenoceptors and not by α-adrenoceptors, and that the renin secretion response to low frequency renal nerve stimulation is evoked by direct stimulation of juxtaglomerular granular cell β₁-adrenoceptors and not indirectly by stimulation of the macula densa receptor through decreased urinary sodium excretion.