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Intercellular calcium signaling and nitric oxide feedback during constriction of rabbit renal afferent arterioles

¹Physiology and Pharmacology, University of Southern Denmark, Odense, Denmark; and ²Department of Pharmacology, University of Hong Kong, Faculty of Medicine Building, Hong Kong SAR, China

Submitted 24 October 2006 ; accepted in final form 1 December 2006

Vasoconstriction and increase in the intracellular calcium concentration ([Ca²⁺]_i) of vascular smooth muscle cells may cause an increase of endothelial cell [Ca²⁺]_i, which, in turn, augments nitric oxide (NO) production and inhibits smooth muscle cell contraction. This hypothesis was tested in microperfused rabbit renal afferent arterioles, using fluorescence imaging microscopy with the calcium-sensitive dye fura-2 and the NO-sensitive dye 4-amino-5-methylamino-2',7'-difluorescein. Both dyes were loaded into smooth muscle and endothelium. Depolarization with 100 mmol/l KCl led to a transient vasoconstriction which was converted into a sustained response by N-nitro-L-arginine methyl ester (L-NAME). Depolarization increased smooth muscle cell [Ca²⁺]_i from 162 ± 15 nmol/l to a peak of 555 ± 70 nmol/l (n = 7), and this response was inhibited by 80% by the L-type calcium channel blocker calciseptine. After a delay of 10 s, [Ca²⁺]_i increased in endothelial cells immediately adjacent to reactive smooth muscle cells, and this calcium wave spread in a nonregenerative fashion laterally into the endothelial cell layer with a velocity of 1.2 µm/s. Depolarization with 100 mmol/l KCl led to a significant increase in NO production ([NO]_i) which was inhibited by L-NAME (n = 5). Acetylcholine caused a rapid increase in endothelial [Ca²⁺]_i, which did not transfer to the smooth muscle cells. L-NAME treatment did not affect changes in smooth muscle [Ca²⁺]_i after depolarization, but it did increase the calcium sensitivity of the contractile apparatus. We conclude that depolarization increases smooth muscle [Ca²⁺]_i which is transferred to the endothelial cells and stimulates NO production which curtails vasoconstriction by reducing the calcium sensitivity of the contractile apparatus.

blood flow; smooth muscle cell contraction

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