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(Hypertension. 2000;35:925.)
© 2000 American Heart Association, Inc.

Scientific Contributions

Shear Stress–Induced Release of Prostaglandin H₂ in Arterioles of Hypertensive Rats

An Huang; Dong Sun; Akos Koller

From the Department of Physiology, New York Medical College, Valhalla.

Correspondence to Akos Koller, MD, PhD, Department of Physiology, New York Medical College, Valhalla, NY 10595. E-mail Koller{at}nymc.edu

Abstract—The nitric oxide–mediated portion of shear stress–induced dilation of rat gracilis muscle arterioles was shown to be impaired in spontaneously hypertensive rats (SHR). Because shear stress–induced dilation is primarily mediated by endothelium-derived prostaglandins in rat cremasteric arterioles, we hypothesized that in the cremasteric vascular bed the mediation of shear stress–induced dilation by prostaglandins is altered in hypertension. At a constant intraluminal pressure of 80 mm Hg, the active diameters of isolated rat cremasteric arterioles of normotensive 30-week-old Wistar-Kyoto rats (WKY) and SHR were 58.0±3.1 and 51.7±3.6 µm, respectively, whereas their passive diameters were 109.4±4.4 and 101.9±6.7 µm, respectively. Dilations to increases in shear stress elicited by increases in intraluminal flow (from 0 to 25 µL/min) were significantly less (P<0.05) in cremasteric arterioles isolated from SHR than from WKY. Arachidonic acid (10^-5 mol/L) elicited constrictions in SHR arterioles but dilations in WKY arterioles. The prostaglandin H₂/thromboxane A₂ (PGH₂/TxA₂) receptor antagonist SQ 29,548 (10^-6 mol/L) significantly increased basal diameter by 11% and normalized the attenuated shear stress–induced dilation in SHR, whereas it did not affect basal diameter and arteriolar responses of WKY. Furegrelate, a specific inhibitor of TxA₂ synthase, did not affect the response in SHR. Also, SQ 29,548 reversed the arachidonic acid–induced constriction to dilation in SHR arterioles, whereas it did not affect the dilator response in WKY arterioles. Constrictions of arterioles of WKY and SHR to U46,619 (a PGH₂/TxA₂ receptor agonist) were not different. These results demonstrate that in cremasteric arterioles of hypertensive rats, shear stress elicits an enhanced release of PGH₂, resulting in a reduced shear stress–dependent dilation. Thus, augmented hemodynamic forces can alter the shear stress–induced synthesis of prostaglandins, which may contribute to the elevated vascular resistance in hypertension.

Key Words: hypertension, genetic • microcirculation • muscle, cremasteric • prostaglandins

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