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Role of vacular smooth muscle IP3‐dependent Ca2+ release in arterial hypertension

It was recently reported that high blood pressure upregulates L‐type Ca2+ (CaL) channels in vascular smooth muscle cells (VSMC), and this event may contribute to the anomalous vascular tone that is a hallmark finding in hypertension. However, rises in cytoplasmic calcium (Ca2+cyt) levels and vasconstriction of VSMC are mediated not only by voltage‐gated Ca2+ influx through CaL channels but also by Ca2+ release from intracellular stores. Because IP3‐dependent Ca2+ release is the primary mode for the mobilization of Ca2+ stores in VSMC, we were interested in determining whether the expression or function of the vascular IP3 receptor is altered in hypertension. Initial Western blots indicated that IP3 receptor expression was increased in both the small mesenteric and renal arteries of spontaneously hypertensive rats and hypertensive aortic‐banded rats compared to arteries from age‐matched normotensive rats. In addition, vascular segments obtained from the arteries of hypertensive rats were more sensitive than control arteries to the induction of the PLC‐IP3 signal transduction cascade, as evidenced by accentuated contractions to the PLC activator m‐3M3FBS (50–200μM). These findings support the concept that the increased abundance of IP3 receptor protein in small arteries of hypertensive rats results in more functionally significant IP3 receptors, which may contribute to the development of the abnormal arterial tone during hypertension. Additional studies are being performed to dissect the signal transduction cascade leading to vascular IP3 receptor upregulation in hypertension.