Arteriolar closure mediated by hyperresponsiveness to norepinephrine in hypertensive rats.

This study was designed to determine if a mechanism exists to cause abnormally large number of arterioles to be closed to blood flow in spontaneously hypertensive rats (SHR). The contributions to vessel closure by neural control and constrictor response to norepinephrine were investigated. Normal rats (WKY) and SHR were studied at age 18--20 wk. Their respective mean arterial blood pressures were 100 +/- 4 (SE) and 154 +/- 7 mmHg when anesthetized with 10% urethan and 2% alpha-chloralose (0.6 mg/100 g ip). The number of arterioles open to blood flow was counted in a large portion of the cremasteric muscle before and after denervation. The percent change in control diameter of denervated arterioles was measured during iontophoretic application (2 min) of norepinephrine at dose currents of 10--300 nA. Following denervation, a 22.2 +/- 6.3% (SE) and 61.8 +/- 12 increase in the number of third-order arterioles open to flow occurred in WKY and SHR. The diameters, wall thicknesses, and cross-sectional areas of vessel walls were not significantly (P less than 0.05) different for comparable types of denervated arterioles in WKY and SHR. The percent changes in diameters of arterioles in SHR were 3--5 times greater at all dose currents than for vessels of WKY. These data indicate arteriolar closure occurs with higher incidence in SHR than WKY and is mediated by hyperresponsiveness of arterioles to norepinephrine.