Platelet Ca2+ Is Not Increased in Stroke-Prone Spontaneously Hypertensive Rats Comparative Study With Spontaneously Hypertensive Rats

Abstract We have reported that cytosolic Ca 2+ concentration ([Ca 2+ ] i ) is increased in platelets from spontaneously hypertensive rats (SHR) in both basal and thrombin-stimulated conditions. To determine whether the correlation between blood pressure and cellular Ca 2+ metabolism exists in stroke-prone SHR (SHRSP), we investigated Ca 2+ handling using fura 2 and aggregation response in platelets of 12- to 13-week-old male SHRSP, SHR, and Wistar-Kyoto rats (WKY). Systolic pressure was highest in SHRSP and lowest in WKY (213±8, 172±7, and 135±5 mm Hg, respectively). Basal [Ca 2+ ] i was significantly higher in SHR than WKY (45.9±4.5 versus 41.2±4.8 nmol/L, P 2+ ] i rise was greater in SHR and smaller in SHRSP than in WKY in the presence of extracellular Ca 2+ (530±50 and 408±52 versus 475±50 nmol/L, respectively; P 2+ ] i response to thrombin was greatest in SHRSP and least in WKY. Ionomycin (5 μmol/L)–stimulated [Ca 2+ ] i rise was similar in WKY, SHR, and SHRSP (731±97, 743±88, and 683±70 nmol/L, respectively). Thrombin-induced maximum platelet aggregation response was higher in SHR and lower in SHRSP than WKY (82±4% and 61±15% versus 73±6%, respectively; P 2+ ] i in SHRSP was similar to that in WKY, and thrombin-stimulated [Ca 2+ ] i was attenuated. These results suggest that platelet Ca 2+ handling differs between SHR substrains and that an increased [Ca 2+ ] i is not obligatory in genetically hypertensive rats.