Enhanced myogenic activation in skeletal muscle arterioles from spontaneously hypertensive rats

JC Falcone, HJ Granger… - American Journal of …, 1993 - journals.physiology.org
JC Falcone, HJ Granger, GA Meininger
American Journal of Physiology-Heart and Circulatory Physiology, 1993journals.physiology.org
The purpose of this study was to determine whether the vascular myogenic response is
enhanced in hypertension. Experiments were conducted in the intact cremaster muscle
microcirculation as well as in isolated arterioles of hypertensive (SHR) and normotensive
(WKY) rats. Increasing venous pressure in vivo by approximately 5 mmHg had no effect on
normotensive first-(1A) or third-order arteriolar (3A) diameters; in contrast, hypertensive 1A
diameter decreased 4%(89+/-2 to 85+/-3 microns) with an 8% decrease in 3A (24+/-2 to 22+ …
The purpose of this study was to determine whether the vascular myogenic response is enhanced in hypertension. Experiments were conducted in the intact cremaster muscle microcirculation as well as in isolated arterioles of hypertensive (SHR) and normotensive (WKY) rats. Increasing venous pressure in vivo by approximately 5 mmHg had no effect on normotensive first- (1A) or third-order arteriolar (3A) diameters; in contrast, hypertensive 1A diameter decreased 4% (89 +/- 2 to 85 +/- 3 microns) with an 8% decrease in 3A (24 +/- 2 to 22 +/- 2 microns). To further examine this enhanced constriction to elevated intravascular pressure in SHR, diameter was monitored in isolated 1A during step increases and decreases in intraluminal pressure. Normotensive arterioles displayed myogenic responses between pressures of 50 and 170 cmH2O; in contrast, hypertensive arterioles demonstrated myogenic responses over an extended pressure range (50–210 cmH2O). In addition, the change in diameter for each step change in pressure was greater in the arterioles from SHR, indicating an increased myogenic responsiveness. The myogenic reactions were unaffected by alpha-receptor blockade with phentolamine (10(-6) M), indicating that adrenergic hypersensitivity was not involved in the enhanced response to stretch. Morphometric analysis of the vascular wall revealed no differences in wall thickness, cross-sectional wall area, or wall-to-lumen ratio between normotensive and hypertensive rats. The length-tension relationships for normotensive and hypertensive rats demonstrated that peak active tension occurred at nearly the same vascular smooth muscle length. In addition, SHR arterioles were capable of maintaining higher levels of active tension that WKY arterioles, indicating an altered length-tension curve in chronic arterial hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
American Physiological Society