Responses of the basilar artery to products released by platelets during chronic hypertension

The goal of this study was to determine whether responses of the basilar artery to products released by platelets are altered during chronic hypertension. The diameter of the basilar artery was measured using intravital microscopy in normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) (6-8 months old) in response to adenosine 5′-diphosphate (ADP), serotonin, and the thromboxane analogue, U-46619. Dilatation of the basilar artery in response to nitroglycerin was also examined in WKY and SHR. Topical application of ADP (10 and 100 μM) produced only minimal changes in diameter of the basilar artery in WKY (3 ± 1% and 1 ± 1%, respectively) and SHR (-0.5 ± 2% and -2 ± 3%, respectively) (P > 0.05 vs WKY). Nitroglycerin, however, produced potent vasolidation in WKY and SHR. Constriction of the basilar artery in response to serotonin was potentiated in SHR compared to WKY. Serotonin (0.1 and 1.0 μM) constricted the basilar artery by 11 ± 2% and 20 ± 2%, respectively, in WKY and by 29 ± 3% and 40 ± 3%, respectively, in SHR (P < 0.05 vs WKY) In contrast, the thromboxane analogue (U-46619) (0.1 and 1.0 μM) produced similar constriction of the basilar artery in WKY (13 ± 1% and 18 ± 2%, respectively) and in SHR (14 ± 3% and 21 ± 6%, respectively). Thus, augmented vasoconstriction during chronic hypertension was specific for serotonin. Next, we examined the role of the cyclooxygenase pathway in responses of the basilar artery to ADP and serotonin. Indomethacin (10 mg/kg i.v.) did not alter responses of the basilar artery to ADP and serotonin in WKY or SHR. Thus, these findings suggest that potent constrictor responses of the basilar artery in response to serotonin and thromboxane during chronic hypertension, with minimal vasolidation in response to ADP, may be important in the pathogenesis of transient cerebral ischemia, or perhaps stroke, during chronic hypertension.