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Responses of Cerebral Arterioles to Adenosine 5ʼ-Diphosphate, Serotonin, and the Thromboxane Analogue U-46619 During Chronic Hypertension
Journal article   Open access   Peer reviewed

Responses of Cerebral Arterioles to Adenosine 5ʼ-Diphosphate, Serotonin, and the Thromboxane Analogue U-46619 During Chronic Hypertension

WILLIAM MAYHAN, FRANK FARACI and DONALD HEISTAD
Hypertension (Dallas, Tex. 1979), Vol.12(6), pp.556-561
12/1988
DOI: 10.1161/01.HYP.12.6.556
PMID: 3203960
url
https://doi.org/10.1161/01.HYP.12.6.556View
Published (Version of record) Open Access

Abstract

The goal of this study was to determine whether responses of cerebral arterioles to products released by platelets are impaired in stroke-prone spontaneously hypertensive rats (SHRSP). The diameter of pial arterioles was measured during suffusion with adenosine 5′-diphosphate (ADP), serotonin, and the thromboxane analogue U-46619, using Intravltal microscopy in normotensive Wistar-Kyoto rats (WKY) and SHRSP (7–10 months old). Responses of cerebral arterioles to ADP and serotonin were profoundly unpaired in SHRSP. ADP (10 M) increased pial arteriolar diameter 17 ± 3% (mean ± SE) in WKY and only 4 ± 1% in SHRSP. Serotonin (10 M) increased pial arteriolar diameter 15 ± 2% in WKY and, in contrast, reduced the diameter 13 ± 1% in SHRSP. Nitroglycerin produced a similar dilatation of cerebral arterioles In WKY and SHRSP, suggesting that impairment of dilatation in SHRSP in response to ADP and serotonin was not related to nonspecific impairment of vasodilatatlon in SHRSP. The thromboxane analogue U-46619 produced a similar constriction of arterioles in WKY and SHRSP. We also examined the possibility that impaired dilator responses of cerebral arterioles in SHRSP in response to ADP and serotonin may be related to production of a cyclooxygenase vasoconstrictor substance. Indomethacin (10 mg/kg i.v.) partially restored dilator responses to ADP and serotonin in SHRSP, without altering responses in WKY. Thus, we speculate that vasoactive substances released by platelets may release a prostanoid constrictor substance from cerebral vessels of SHRSP and thereby predispose SHRSP to cerebral ischemia and, perhaps, stroke.

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