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1 Physiology and Pharmacology, University of Southern Denmark, Odense, Denmark
2 Dept. of Pharmacology, University of Hong Kong, Faculty of Medicine, Hong Kong, Hong Kong
3 Physiology and Pharmacology, University of Southern Denmark, Odense C, Denmark
4 Physiology and Pharmacology, University of Southern Denmark, Winslowparken 21, Odense C, DK-5000, Denmark
* To whom correspondence should be addressed. E-mail: oskott{at}health.sdu.dk.
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 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 nitric oxide-sensitive dye 4-amino-5-methylamino-2',7'-difluorescein (DAF-FM). 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 non-regenerative 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 depolarisation, 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, stimulates NO-production which curtails vasoconstriction by reducing the calcium sensitivity of the contractile apparatus.
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