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AJP - Renal Physiology, Vol 271, Issue 5 1004-F1011, Copyright © 1996 by American Physiological Society
ARTICLES |
K. P. Yip and D. J. Marsh
Department of Physiology, Brown University, Providence, Rhode Island 02912, USA.
Using confocal fluorescence microscopy, we followed the time course of intracellular calcium concentration ([Ca2+]i) in vascular smooth muscle cells (VSMC) and endothelial cells (EC) of microperfused afferent arterioles isolated from rat juxtamedullary nephrons. Measurements were made while arterioles were exposed to pharmacological agonists or myogenic stimulation. Luminal addition of acetylcholine triggered an immediate increase of [Ca2+]i in EC and vasodilation. Addition of norepinephrine to the bath solution constricted the vessel and initiated periodic oscillations of [Ca2+]i in VSMC and synchronized vasomotion. Increase of perfusion pressure from 80 to 120 mmHg induced an immediate 9.6 +/- 2.9% (P < 0.05, n = 9) increase of [Ca2+]i in VSMC that was sustained. The arteriole dilated transiently when the perfusion pressure was increased, and persistent vasoconstriction to reduced diameter was observed after 35 s. When nitric oxide (NO) production in the perfused vessel was blocked with nitro-L-arginine methyl ester prior to the pressure step, similar profiles of change in VMSC [Ca2+]i were observed and persistent vasoconstriction began after 28 s. The same pressure step triggered an increase of [Ca2+]i in EC by 11.3 +/- 1.1% (P < 0.05, n = 5). These observations suggest that myogenic constriction of afferent arterioles was associated with an increase of [Ca2+]i in VSMC, and the constriction was delayed by endogenous NO production.
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