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Norepinephrine-induced calcium signaling pathways in afferent arterioles of genetically hypertensive rats

Norepinephrine-induced calcium signaling pathways in afferent arterioles of genetically... 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 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Renal Physiology The American Physiological Society

Norepinephrine-induced calcium signaling pathways in afferent arterioles of genetically hypertensive rats

AJP - Renal Physiology , Volume 281 (2): F264 – Aug 1, 2001

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Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
0363-6127
eISSN
1522-1466
Publisher site
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Abstract

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

Journal

AJP - Renal PhysiologyThe American Physiological Society

Published: Aug 1, 2001

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