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Abstract This study provides new information about the relative importance of calcium mobilization and entry in the renal vascular response to adrenoceptor activation in afferent arterioles isolated from 7- to 8-wk-old Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Intracellular free calcium concentration (Ca 2+ i ) was measured in microdissected arterioles utilizing ratiometric photometry of fura 2 fluorescence. There was no significant strain difference in baseline Ca 2+ i . Norepinephrine (NE; 10 −6 and 10 −7 M) elicited immediate, sustained increases in Ca 2+ i . The general temporal pattern of response to 10 −6 M NE consisted of an initial peak and a maintained plateau phase. The response to NE was partially blocked by nifedipine (10 −6 M) or 8-( N,N -diethylamino) octyl-3,4,5-trimetoxybenzoate (TMB-8; 10 −5 M). A calcium-free external solution abolished the sustained Ca 2+ i plateau response to NE, with less influence on the peak response. In the absence of calcium entry, TMB-8 (10 −5 M) completely blocked the calcium response to NE in WKY but not SHR, suggesting strain differences in mobilization. A higher concentration of TMB-8 (10 −4 M), however, blocked all discernible mobilization in both strains. We conclude that there are differences in Ca 2+ handling in renal resistance vessels between young WKY and SHR with respect to mobilization stimulated by α-adrenoceptors. Afferent arterioles of young SHR appear to have a larger inositol-1,4,5-trisphosphate-sensitive pool or release from a site less accessible to TMB-8. spontaneously hypertensive rats Wistar-Kyoto rats norepinephrine hypertension 8-( N,N -diethylamino) octyl-3,4,5-trimetoxybenzoate nifedipine vascular smooth muscle inositol-1,4,5-trisphosphate-mediated mobilization L-type calcium channel renal circulation Footnotes Present address of M. Salomonsson: Dept. of Medical Physiology, Univ. of Copenhagen, Blegdamsvej 3, 2200 Copenhagen N, Denmark. Address for reprint requests and other correspondence: W. J. Arendshorst, Dept. of Cell and Molecular Physiology, CB #7545, School of Medicine, Rm. 152, Medical Sciences Research Bldg., Univ. of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7545 (E-mail: arends@med.unc.edu ). The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Copyright © 2001 the American Physiological Society
AJP - Renal Physiology – The American Physiological Society
Published: Aug 1, 2001
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