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Spinal and peripheral mechanisms contributing to hyperactive voiding in spontaneously hypertensive rats

Spinal and peripheral mechanisms contributing to hyperactive voiding in spontaneously... Abstract The influence of noradrenergic mechanisms involved in micturition in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats was investigated using continuous cystometry in in vivo and in vitro studies on isolated bladder and urethral tissues. Compared with WKY rats, SHR had a significantly lower bladder capacity (SHR: 0.7 ± 0.05 ml; WKY rats: 1.3 ± 0.06 ml; P < 0.001), micturition volume (SHR: 0.4 ± 0.04 ml, WKY rats: 1.2 ± 0.05 ml; P < 0.001), and an increased amplitude of nonvoiding (unstable) bladder contractions. The effects of intrathecal and intra-arterial doxazosin on cystometric parameters were more pronounced in SHR than in WKY rats. There was a marked reduction in nonvoiding contractions after intrathecal (but not intra-arterial) doxazosin in SHR. Norepinephrine (0.1 μM–1 mM) failed to evoke contractions in bladder strips from WKY rats, in contrast to a weak contractile response in SHR. The response to electrical field stimulation was significantly less in bladder strips from SHR than from WKY rats. In WKY rats, norepinephrine produced concentration-dependent inhibition (87 ± 5%, n = 6) of nerve-evoked bladder contractions. Almost no inhibition (11 ± 8%, n = 6) was found in SHR. Alterations in bladder function of SHR appear to be associated with changes in the noradrenergic control of the micturition reflex, in addition to an increased smooth muscle and decreased neuronal responsiveness to norepinephrine. The marked reduction in nonvoiding contractions after intrathecal doxazosin suggests that the bladder hyperactivity in SHR has at least part of its origin in supraspinal and/or spinal structures. bladder urethra α-adrenoceptors sympathetic nervous system Footnotes Address for reprint requests: K. Persson, Dept. of Clinical Pharmacology, Lund Univ. Hospital, S-221 85 Lund, Sweden. 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. §1734 solely to indicate this fact. Copyright © 1998 the American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Regulatory, Integrative and Comparative Physiology The American Physiological Society

Spinal and peripheral mechanisms contributing to hyperactive voiding in spontaneously hypertensive rats

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Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
0363-6119
eISSN
1522-1490
Publisher site
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Abstract

Abstract The influence of noradrenergic mechanisms involved in micturition in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats was investigated using continuous cystometry in in vivo and in vitro studies on isolated bladder and urethral tissues. Compared with WKY rats, SHR had a significantly lower bladder capacity (SHR: 0.7 ± 0.05 ml; WKY rats: 1.3 ± 0.06 ml; P < 0.001), micturition volume (SHR: 0.4 ± 0.04 ml, WKY rats: 1.2 ± 0.05 ml; P < 0.001), and an increased amplitude of nonvoiding (unstable) bladder contractions. The effects of intrathecal and intra-arterial doxazosin on cystometric parameters were more pronounced in SHR than in WKY rats. There was a marked reduction in nonvoiding contractions after intrathecal (but not intra-arterial) doxazosin in SHR. Norepinephrine (0.1 μM–1 mM) failed to evoke contractions in bladder strips from WKY rats, in contrast to a weak contractile response in SHR. The response to electrical field stimulation was significantly less in bladder strips from SHR than from WKY rats. In WKY rats, norepinephrine produced concentration-dependent inhibition (87 ± 5%, n = 6) of nerve-evoked bladder contractions. Almost no inhibition (11 ± 8%, n = 6) was found in SHR. Alterations in bladder function of SHR appear to be associated with changes in the noradrenergic control of the micturition reflex, in addition to an increased smooth muscle and decreased neuronal responsiveness to norepinephrine. The marked reduction in nonvoiding contractions after intrathecal doxazosin suggests that the bladder hyperactivity in SHR has at least part of its origin in supraspinal and/or spinal structures. bladder urethra α-adrenoceptors sympathetic nervous system Footnotes Address for reprint requests: K. Persson, Dept. of Clinical Pharmacology, Lund Univ. Hospital, S-221 85 Lund, Sweden. 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. §1734 solely to indicate this fact. Copyright © 1998 the American Physiological Society

Journal

AJP - Regulatory, Integrative and Comparative PhysiologyThe American Physiological Society

Published: Oct 1, 1998

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