PMID: 2508481Oct 1, 1989Paper

Mechanism of angiotensin II stimulation of Na-K-Cl cotransport of vascular smooth muscle cells

The American Journal of Physiology
N E Owen, K M Ridge

Abstract

Previous studies from this laboratory have demonstrated that Na-K-Cl cotransport of vascular smooth muscle cells is inhibited by hormones that increase intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels (e.g., catecholamines) and is stimulated by hormones that increase intracellular guanosine 3',5'-cyclic monophosphate (cGMP) levels (e.g., atrial natriuretic peptides). Others have suggested that calcium may also modulate Na-K-Cl cotransport of vascular smooth muscle cells. The goal of the present study was to characterize the mechanism of angiotensin II stimulation of Na-K-Cl cotransport of early passage cultured vascular smooth muscle cells. We found that when vascular smooth muscle cells were treated with angiotensin II or a calcium ionophore, Na-K-Cl cotransport was markedly enhanced above basal levels. We found that when calcium influx was blocked with the calcium chelator EDTA or with three different chemical types of calcium-channel blockers, the stimulatory effects of angiotensin II on Na-K-Cl cotransport were markedly inhibited. Furthermore, when intracellular calcium mobilization was blocked with high concentrations of the calcium chelator quin2 or with the intracellular calcium antagonist 8-(diethyl-amin...Continue Reading

Citations

Aug 5, 2004·Pflügers Archiv : European journal of physiology·Yana J AnfinogenovaSergei N Orlov
Oct 18, 2002·American Journal of Physiology. Heart and Circulatory Physiology·Jamie W MeyerGary E Shull
Apr 13, 2012·Hypertension Research : Official Journal of the Japanese Society of Hypertension·Hyun-Min ChoIn Kyeom Kim
Jan 5, 2000·Physiological Reviews·J M Russell
Jan 15, 2002·American Journal of Physiology. Renal Physiology·Gergely KovácsP Darwin Bell
Apr 22, 2010·Biochemical and Biophysical Research Communications·Hae-Ahm LeeIn Kyeom Kim

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