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The goal of this study was to determine the role of the vascular endothelium in regulating the response of small renal arteries to increased transmural pressure and reduced PO2. Canine small renal arteries (496 +/- 32 microns) were isolated, cannulated with micropipettes, and mounted in an in vitro chamber that allowed transmural pressure, tissue bath PO2, and vessel lumen PO2 to be controlled. In intact arteries, elevation of transmural pressure caused contractile activation and a progressive depolarization (0.17 +/- 0.09 mV/mm Hg pressure increase) of the vascular smooth muscle cells. Endothelial damage by air perfusion caused a 13-14% reduction in resting diameter and an 18 +/- 3 mV depolarization of the vascular smooth muscle, but eliminated the progressive contraction and depolarization that occurred in intact vessels in response to transmural pressure elevation. Reduction of either tissue bath O2 concentration or vessel lumen PO2 significantly enhanced norepinephrine-induced contractions of the arteries. Endothelial damage prevented the enhancement of norepinephrine-induced contractions by reduced PO2 in the vessels. The results of this study suggest that the vascular endothelium regulates both myogenic contraction and the enhancement of norepinephrine-induced contractions by reduced PO2 in small arteries of the dog kidney.

Role of the vascular endothelium in regulating the response of small arteries of the dog kidney to transmural pressure elevation and reduced PO2.