Arteriolar diameter and tissue oxygen tension during muscle contraction in hypertensive rats.

Abstract

This study evaluated the possibility that in hypertension, mechanisms that maintain near normal arteriolar diameters at elevated arteriolar pressures limit the ability of skeletal muscle arterioles to dilate in response to an increase in tissue metabolism. The spinotrapezius muscles of 16- to 20-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were contracted at frequencies of 1, 2, 4, and 8 Hz. The inner diameters of first-order through third-order arterioles were measured at rest and following 3 minutes of contractions. Tissue oxygen tension (PO2) at the venous end of capillaries was monitored during 8-Hz contractions. At rest, following contractions, and after maximum dilation with adenosine, the inner diameters of arterioles of equivalent branch order were not significantly different in SHR and WKY. Opening of closed arterioles during muscle contraction and adenosine application occurred in less than 5% of the observations in both groups. The resting tissue PO2 was 25.5 .+-. 1.3 mm Hg in normal rats and 26.1 .+-. 2.1 mm Hg in SHR. At nearly maximum vasodilation during 8-Hz stimulation, tissue PO2 recovered to 81.9 .+-. 12.7% of control in WKY but only to 41.2 .+-. 13.0% of control in SHR. These observations indicate that the expression of local regulatory mechanisms related to tissue metabolism is virtually normal in the spinotrapezius muscle vasculature of SHR in the context of arteriolar dilation. However, at near maximum performance, factors other than absolute arteriolar diameter preclude the normal preservation of tissue PO2 in the spinotrapezius muscle of SHR.