The role of α‐adrenoceptors in the regulation of renal tubular sodium reabsorption and renin secretion in the rabbit

Abstract

1 A study was undertaken in the anaesthetized rabbit to classify the α-adrenoceptor subtypes responsible for increasing renal tubular sodium reabsorption and renin secretion. Intrarenal administration of noradrenaline, at doses which did not change renal blood flow or glomerular filtration rate, significantly decreased urine flow, absolute and fractional sodium excretion by between 26% and 29%. These renal responses to noradrenaline were abolished by the selective α₁-adrenoceptor antagonist, prazosin, but not by the selective α₂-adrenoceptor antagonist, idazoxan. 2 Noradrenaline, given intrarenally, increased renin secretion between two and three fold and this response was not modified by either prazosin or idazoxan. 3 Intrarenal administration of the selective α-adrenoceptor agonists, phenylephrine and methoxamine, at dose rates which did not change renal haemodynamics, significantly reduced urine flow, absolute and fractional sodium excretion by 15% to 33%, but at doses which reduced blood flow and filtration rate, by between 11% and 26%, urine flow, absolute and fractional sodium excretion decreased between 42% and 49%. 4 Infusion of guanabenz (selective α₂-adrenoceptor agonist), at doses with no renal haemodynamic action, increased urine flow, absolute and fractional sodium excretion by 11% to 15%, while at doses which decreased blood flow by 7%, these other variables did not change. 5 Administration of UK 14304 (selective α₂-adrenoceptor agonist) reduced blood flow and filtration rate by 3% and 9% respectively but had no other measurable action. At higher doses, which decreased blood flow by 14% and filtration rate by 24%, urine flow, absolute and fractional sodium excretion fell by between 27% and 50%. 6 Renin secretion was significantly increased by the high doses of phenylephrine and UK 14304 but not by the low doses of these drugs. 7 These studies show that adrenergic stimulation of renal tubular sodium reabsorption involves the activation of α₁- but not α₂-adrenoceptors. Further, adrenergic activation of the juxtaglomerular cells to release renin does not appear to involve either α₁- or α₂-adrenoceptors.