Signals controlling renin release in aglomerular toadfish

Abstract

The toadfish,Opsanus tau, lacks renal glomeruli and macula densa, but has high renal renin activity and abundant granulated cells in renal arteries and arterioles. Reduction of blood pressure (BP) or blood volume by hemorrhage or vasodilatory drugs causes renin release, indicating that an intrarenal or extrarenal pressure- or volume-sensitive mechanism exists for controlling renin release in the toadfish. Thus, we examined whether 1) β-adrenergic receptor-mediated activation of renin release, and 2) calcium influx which may underlie the baroreceptor mechanism are involved in the cellular control of renin release. Acute injection of isoproterenol (1 μg/kg, n = 6) decreased BP and increased plasma renin activity (PRA) 4–5 fold in unanesthetized toadfish. Propranolol abolished both effects, but did not decrease basal PRA levels.In vitro superfusion of renal slices with bicarbonate Ringer's solution showed a steady secretion of renin, and addition of 50 mM K⁺ (K⁺ methylsulfate replacing NaCl, n = 10) to the superfusate markedly suppressed renin secretion. Nifedipine (10⁻⁵ M, n = 8) completely restored the high K⁺-induced inhibition of renin secretion from renal slices, whereas isoproterenol (10⁻⁴ M, n = 6) neither increased basal renin secretion nor restored K⁺-induced renin suppression. These results suggest that calcium influx may mediate inhibitory messages for renin secretion, while the β-adrenoceptor-mediated activation of granulated cells appears absent in toadfish.