Arterial muscle membrane abnormalities of hydralazine-treated spontaneously hypertensive rats
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Alkaline phosphatase activity and Ca2+ accumulation were examined in the plasma membrane enriched fractions isolated from mesenteric arteries of spontaneously hypertensive (SHR) and Kyoto-Wistar normotensive (WKY) rats after a long-term antihypertensive treatment with hydralazine. The membrane biochemical abnormalities of arterial smooth muscle such as enhanced alkaline phosphatase activity and reduced ATP-dependent Ca2+ transport previously observed in untreated SHR were persistently observed in hydralazine treated SHR with normalized systolic blood pressure. Our results suggest that the antihypertensive effects of hydralazine do not involve the reversal or modification of the altered Ca2+ handling by vascular muscle membrane in hypertension.
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