Conditions for humoral α-adrenoceptor stimulation of renin release in anaesthetized dogs

Abstract

To examine whether an α-adrenergic agonist, methoxamine, influences renin release solely by its haemodynamic effect, experiments were performed in anaesthetized dogs with denervated kidneys. Methoxamine was infused intrarenally at rates which reduced renal blood flow (RBF) by 30—40%. At control blood pressure, renin release rose during infusion of methoxamine from 1.4 ± 0.7 to 31 ± 11 μg/min. A β-adrenergic stimulator, isoproterenol, did not increase renin release significantly when administered alone into the renal artery, but doubled the effect of methoxamine infusion: at control blood pressure renin release rose from 0.5 ± 0.3 to 71 ± 17 μg/min during combined infusion of isoproterenol and methoxamine. Mechanical constriction of the renal artery left RBF unaltered down to a renal perfusion pressure of 90 ± 4 mmHg during methoxamine infusion, whereas the lowest autoregulating pressure in control experiments averaged 60 ± 5 mmHg. At renal perfusion pressure below the range of autoregulation, renin release was not further increased by intrarenal infusion of methoxamine. Isoproterenol infusion at low renal perfusion pressure doubled renin release, which was not significantly altered by additional infusion of methoxamine. The stimulatory effect of methoxamine on renin release at control blood pressure could be diminished but not prevented by infusing 2.9 % NaCl intravenously in large amounts. These data indicate that methoxamine induces autoregulated dilation of afferent arterioles by disproportionate vasoconstriction on pre-afferent arteries. Thereby afferent arterioles are conditioned for stimulation of renin release by isoproterenol.

Key Words:

• afferent arterioles
• isoproterenol
• methoxamine
• renal autoregulation