Role of calcium influx and intracellular calcium stores in angiotensin II-mediated calcium hyper-responsiveness in smooth muscle from spontaneously hypertensive rats
Abstract
To investigate post-receptor mechanisms that underlie enhanced angiotensin II (Ang II)-stimulated cytosolic free Ca2+ concentration ([Ca2+]i) responses in vascular smooth muscle cells from small arteries of SHR. To determine whether Ca2+ influx is altered in SHR, effects of Ca2+ channel antagonists (nitrendipine and diltiazem) and depletion of extracellular Ca2+ on Ang II-stimulated [Ca2+]i responses in primary cultured unpassaged vascular smooth muscle cells from mesenteric arteries of spontaneously hypertensive rats (SHR), Wistar and Wistar-Kyoto (WKY) rats aged 17 weeks were studied. To assess whether Ca2+ stores contribute to increases in Ang II-stimulated Ca2+ mobilization and [Ca2+]i in SHR, cells were exposed to thapsigargin, a selective reticular Ca2+-ATPase inhibitor. [Ca2+]i was measured by fura-2 methodology. Basal and 1 nmol/l Ang II-stimulated [Ca2+]i were significantly greater in SHR cells (123 +/- 7.1 nmol/l basal; 268 +/- 7.0 nmol/l stimulated) than they were in those from WKY rats (88 +/- 4.8 nmol/l basal; 221 +/- 8.6 nmol/l stimulated) and Wistar rats (85 +/- 3.0 nmol/l basal; 216 +/- 8.3 nmol/l stimulated). In Ca2+-free medium, basal and Ang II-induced [Ca2+]i were reduced in all groups, but Ang II-stimulated...Continue Reading
References
Calcium currents are altered in the vascular muscle cell membrane of spontaneously hypertensive rats
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