Tubular sodium reabsorption and the regulation of renal hemodynamics. The effect of chlorothiazide on renal vascular resistance.

In hydropenic dogs under Nembutal anesthesia chlorotiazide, in parallell with its inhibition of distal tubular Na reabsorption, caused a marked increase in renal vascular resistance and a decrease in total renal blood flow and glomerular filtration rate. The renal vasoconstriction appeared to be both pre- and post-glomerular, since the glomerular filtration rate was reduced in proportion to the total renal blood flow. The vasoconstriction could not be abolished by sympathetic blockade (Dibenzylene). During ureteral obstruction, when formation of glomerular filtrate could be regarded as minimal despite of unimpaired renal blood flow, the vasoconstrictive response to chlorothiazide was much reduced. This excludes a direct constrictive effect of chlorothiazide on the renal vascular bed. The constrictive response of the renal vascular bed was found to be correlated with the inhibition of Na reabsorption rather than with increase in urine flow. The data are interpreted as supporting the hypothesis that Na transfer in the distal tubule is one important mechanism for controlling renal vascular tone. a control that may be mediated by the renin angiotensin system. It is further suggested that the important factor is the intracellular Na concentration in the first part of the distal tubule. lather than intratubular concentration as such at this site. Contrary to previous interpretation the present observations suggest that it is a decrease in Na transfer, rather than an increase, that is directly or indirectly involved.