MYOGENIC VASOCONSTRICTION IN THE RAT-KIDNEY ELICITED BY REDUCING PERIRENAL PRESSURE

Autoregulation of renal blood flow is generally believed to result from tubuloglomerular feedback and/or a vascular myogenic mechanism, but there is no consensus on the relative importance of these mechanisms. We designed an experiment in which tubuloglomerular feedback would tend to oppose a myogenic response: the denervated kidney in situ was enclosed in an airtight chamber and exposed to a 35 mmHg subatmospheric pressure for 1 to 10 minutes. Renal blood flow recorded by an electromagnetic flowmeter fell by 33% in the course of a few seconds. Renal venous concentration of inulin showed no consistent change, indicating similar reduction in glomerular filtration rate. Since urine flow also fell, it is likely that the tubular flow rate was reduced. The kidney volume expanded by 10-20%, and subcapsular interstitial fluid pressure was reduced from 6.8 to -8.6 mmHg. Arterial pressure remained unchanged, while renal venous pressure inside the chamber fell from 9.4 to 5.8 mmHg. Normalization of perirenal pressure gave rapid normalization of all parameters. Elevation of ureteral pressure attenuated or even prevented the renal blood flow reduction. Renal decapsulation or sympathetic blockade by phentolamine, or infusion of furosemide or 0.9% NaCl to inactive tubuloglomerular feedback, did not prevent the renal blood flow reduction. We interpret the results to indicate that myogenic vasoconstriction greatly overpowered TGF and even surpassed the constriction predicted by a mathematical model based on maintenance of the preglomerular wall tension as estimated from transmural pressure.