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The influence of β-adrenergic activation on noradrenergic α1 activation of rabbit afferent arterioles

The influence of β-adrenergic activation on noradrenergic α1 activation of rabbit afferent... The aim of the present investigation was to examine the effect of β-adrenergic stimulation on smooth muscle calcium concentration ([Ca2+]i) in resting conditions and after administration of norepinephrine (NE) to stimulate α-adrenoceptors in isolated rabbit afferent arterioles loaded with the calcium-sensitive fluorescent probe fura-2. [Ca2+]i was evaluated in the proximal and distal parts of the arterioles. NE (4×10–7 M) increased [Ca2+]i in both these regions. The α1-adrenoceptor antagonist prazosin (10–7 M) totally abolished the NE-induced increase in [Ca2+]i, while the α2-adrenoceptor antagonist yohimbine (5×10–7 M) had no influence on the response to NE. When β-adrenoceptors were stimulated, using isoproterenol (10–7 M), the NE-induced increase in [Ca2+]i was significantly lower in both regions. Activation of β-adrenoceptors with isoproterenol did not affect the [Ca2+]i increase in response to depolarization with K+. Since β-adrenoceptor stimulation raises the smooth muscle cell levels of cAMP, an adenylate cyclase stimulator, forskolin (10–5 M) was administered prior to NE application. This maneuver also blunted the increase in [Ca2+]i in both regions. We conclude that the calcium response to NE in the isolated rabbit afferent arteriole is mediated by an α1-adrenoceptor. β-Adrenoceptor stimulation and forskolin blunt the increase in [Ca2+]i induced by NE stimulation, indicating that cAMP counteracts the NE-induced activation of α1-adrenoceptors. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Pflügers Archiv European Journal of Physiologyl of Physiology Springer Journals

The influence of β-adrenergic activation on noradrenergic α1 activation of rabbit afferent arterioles

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References (36)

Publisher
Springer Journals
Copyright
Copyright © 2000 by Springer-Verlag
Subject
Biomedicine; Human Physiology
ISSN
0031-6768
eISSN
1432-2013
DOI
10.1007/s004240000382
Publisher site
See Article on Publisher Site

Abstract

The aim of the present investigation was to examine the effect of β-adrenergic stimulation on smooth muscle calcium concentration ([Ca2+]i) in resting conditions and after administration of norepinephrine (NE) to stimulate α-adrenoceptors in isolated rabbit afferent arterioles loaded with the calcium-sensitive fluorescent probe fura-2. [Ca2+]i was evaluated in the proximal and distal parts of the arterioles. NE (4×10–7 M) increased [Ca2+]i in both these regions. The α1-adrenoceptor antagonist prazosin (10–7 M) totally abolished the NE-induced increase in [Ca2+]i, while the α2-adrenoceptor antagonist yohimbine (5×10–7 M) had no influence on the response to NE. When β-adrenoceptors were stimulated, using isoproterenol (10–7 M), the NE-induced increase in [Ca2+]i was significantly lower in both regions. Activation of β-adrenoceptors with isoproterenol did not affect the [Ca2+]i increase in response to depolarization with K+. Since β-adrenoceptor stimulation raises the smooth muscle cell levels of cAMP, an adenylate cyclase stimulator, forskolin (10–5 M) was administered prior to NE application. This maneuver also blunted the increase in [Ca2+]i in both regions. We conclude that the calcium response to NE in the isolated rabbit afferent arteriole is mediated by an α1-adrenoceptor. β-Adrenoceptor stimulation and forskolin blunt the increase in [Ca2+]i induced by NE stimulation, indicating that cAMP counteracts the NE-induced activation of α1-adrenoceptors.

Journal

Pflügers Archiv European Journal of Physiologyl of Physiology – Springer Journals

Published: Sep 12, 2000

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