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Am J Physiol Renal Physiol 278: F138-F147, 2000;
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Vol. 278, Issue 1, F138-F147, January 2000

alpha 1-Adrenoceptor subtypes in rat renal resistance vessels: in vivo and in vitro studies

Max Salomonsson, Kristina Brännström, and William J. Arendshorst

Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7545

This study provides new information about the relative importance of different alpha 1-adrenoceptors during norepinephrine (NE) activation in rat renal resistance vessels. In Sprague-Dawley rats, we measured renal blood flow (RBF) using electromagnetic flowmetry in vivo and the intracellular free calcium concentration ([Ca2+]i) utilizing ratiometric photometry of fura 2 fluorescence in isolated afferent arterioles. Renal arterial bolus injection of NE produced a transient 46% decrease in RBF. In microdissected afferent arterioles, NE (1 µM) elicited an immediate square-shaped increase in [Ca2+]i, from 90 to 175 nM (P < 0.001). Chloroethylclonidine (CEC) (50 µM) had no chronic irreversible alkylating effect in vitro but exerted acute reversible blockade on norepinephrine (NE) responses both on [Ca2+]i in vitro and on RBF in vivo. The RBF response was attenuated by ~50% by the putative alpha 1A-adrenoceptor and alpha 1D-adrenoceptor antagonists 5-methylurapidil (5-MU), and 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione dihydrochloride (BMY-7378) (12.5 and 62.5 µg/h), respectively. The in vitro [Ca2+]i response to NE was blocked ~25% and 50% by 5-MU (100 nM and 1 µM). BMY-7378 (100 nM and 1 µM) attenuated the NE-induced response by ~40% and 100%. The degree of inhibition in vitro was similar to the in vivo experiments. In conclusion, 5-MU and BMY-7378 attenuated the NE-induced responses, although relatively high concentrations were required, suggesting involvement of both the alpha 1A-adrenoceptor and alpha 1D-adrenoceptor. Participation of the alpha 1B-adrenoceptor is less likely, as we found no evidence for CEC-induced alkylation.

norepinephrine; alpha 1A-adrenoceptor; alpha 1B-adrenoceptor; alpha 1D-adrenoceptor; renal circulation; afferent arteriole; calcium; vascular smooth muscle


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