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Am J Physiol Heart Circ Physiol 281: H2233-H2240, 2001;
0363-6135/01 $5.00
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Vol. 281, Issue 5, H2233-H2240, November 2001

Ca2+ influx mediates enhanced alpha 2-adrenergic contraction in aortas from rats treated with NOS inhibitor

Harshini Mukundan and Nancy L. Kanagy

Vascular Physiology Group, Department of Cell Biology and Physiology, Health Sciences Center, University of New Mexico, Albuquerque, New Mexico 87131-5218

Previously, we reported that aortic segments from rats made hypertensive with the nitric oxide synthase inhibitor Nomega -nitro-L-arginine (L-NNA) exhibit enhanced contractile sensitivity to both alpha 2-adrenergic receptor (alpha 2-AR) stimulation and to KCl-induced depolarization. We hypothesized that increased contractile responses to these agents was due to a change in the common effector L-type voltage-dependent calcium channel (VDCC). In aortic segments from control and L-NNA-treated rats, contraction to the alpha 2-AR agonist UK-14304 stimulated Ca2+ influx but released intracellular Ca2+ only in control arteries. UK-14304-induced contraction was blocked by the VDCC antagonist nifedipine in both control and L-NNA aortas but contraction of aortas from L-NNA-treated rats was blocked by lower concentrations. Calcium imaging studies in fura 2-loaded freshly isolated aortic vascular smooth muscle cells also demonstrated UK-14304-stimulated Ca2+ influx sensitive to nifedipine only in cells from L-NNA-treated rats. We conclude that alpha 2-AR contraction in the rat aorta is mediated primarily by Ca2+ influx and that L-NNA-induced hypertension increases the dependence of this contraction on VDCCs.

Nomega -nitro-L-arginine; alpha 2-adrenergic receptor; UK-14304; vascular smooth muscle cells; L-type voltage-dependent calcium channels; nifedipine; hypertension


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