Abstract

Effects of ouabain on the autoregulation of renal blood flow (RBF) and renin release were examined in filtering and nonfiltering kidneys of anesthetized dogs. Autoregulation of RBF was observed in both kidneys; however, autoregulation in the nonfiltering kidney was comparatively less efficient. These findings indicate that both the myogenic mechanism via a sensor element in the afferent arteriole, a so-called baroreceptor, and the tubuloglomerular feedback mechanism via the macula densa are essential for complete autoregulation. In both the control and nonfiltering kidney, intrarenal arterial infusion of ouabain abolished the autoregulation of RBF and glomerular filtration rate, with no change in the renal vascular sensitivity to vasoactive substances or in renin release induced by pressure reduction. Since various vasoactive drugs elicited a normal vascular response, it appears that the site of action of ouabain was not the vascular contractile elements; at least, an impairment of autoregulation during ouabain infusion was apparently not due to a defect in these elements. These results suggest the possible existence of another mediator, a sensor element in the afferent arteriole that is affected by ouabain. Ouabain may abolish the autoregulation of RBF and renin release via a modification of this baroreceptor in the afferent arteriole as well as through inhibition of the macula densa.

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