Angiotensin II enhances noradrenaline release from sympathetic nerves of the rat prostate via a novel angiotensin receptor: implications for the pathophysiology of benign prostatic hyperplasia

Fabiani, M. E., Sourial, M., Thomas, W. G., Johnston, C. I. and Frauman, A. G. (2001) Angiotensin II enhances noradrenaline release from sympathetic nerves of the rat prostate via a novel angiotensin receptor: implications for the pathophysiology of benign prostatic hyperplasia. Journal of Endocrinology, 171 1: 97-108. doi:10.1677/joe.0.1710097


Author Fabiani, M. E.
Sourial, M.
Thomas, W. G.
Johnston, C. I.
Frauman, A. G.
Title Angiotensin II enhances noradrenaline release from sympathetic nerves of the rat prostate via a novel angiotensin receptor: implications for the pathophysiology of benign prostatic hyperplasia
Journal name Journal of Endocrinology   Check publisher's open access policy
ISSN 0022-0795
1479-6805
Publication date 2001-10-01
Year available 2001
Sub-type Article (original research)
DOI 10.1677/joe.0.1710097
Open Access Status Not yet assessed
Volume 171
Issue 1
Start page 97
End page 108
Total pages 12
Place of publication Bristol, United Kingdom
Publisher BioScientifica
Language eng
Abstract The renin-angiotensin system (RAS) is present in the human prostate and may be activated in benign prostatic hyperplasia (BPH), possibly contributing to the pathophysiology of this disorder by enhancing local sympathetic tone and cell growth. The functional role of the PAS in the prostate, however, is unknown. The present study was undertaken to determine whether angiotensin (Ang) II enhances sympathetic transmission in the prostate. The neuronal stores of the rat prostate were labelled with [H-3]noradrenaline (NA). Ang II and Ang I enhanced [H-3]NA release in a concentration-dependent manner. The Ang II receptor subtype 1 (AT(1) receptor) antagonist losartan and the AT(2) receptor antagonist PD123319 inhibited this facilitatory effect of Ang II and Ang I, whereas the other AT(2) receptor antagonist, CGP42112, was without effect. Bradykinin also increased [H-3]NA release, which was inhibited by the B-2 receptor antagonist Hoe140. The angiotensin-converting enzyme inhibitor captopril inhibited the effect of Ang I, but potentiated that of bradykinin. Interestingly, captopril alone produced an increase in [H-3]NA release which was inhibited by Hoe140. Losartan, but not PD123319 or CGP42112, inhibited [I-125]-Ang II binding in Chinese hamster ovary cells transfected with the AT(1a) or AT(1b) receptor. In contrast, in cells expressing the AT(2) receptor, PD123319 and CGP42112, but not losartan, inhibited [I-125] -Ang II binding. In conclusion, Ang II enhances the release of NA from sympathetic nerves of the rat prostate via a novel functional receptor distinct from the cloned AT(1a) AT(1b) or AT(2). These data provide direct evidence in support of a functional role for the local RAS in modulating sympathetic transmission in the prostate, which may have important implications for the pathophysiology of BPH.
Formatted abstract
The renin-angiotensin system (RAS) is present in the human prostate and may be activated in benign prostatic hyperplasia (BPH), possibly contributing to the pathophysiology of this disorder by enhancing local sympathetic tone and cell growth. The functional role of the RAS in the prostate, however, is unknown. The present study was undertaken to determine whether angiotensin (Ang) II enhances sympathetic transmission in the prostate. The neuronal stores of the rat prostate were labelled with [3H]noradrenaline (NA). Ang II and Ang I enhanced [3H]NA release in a concentration-dependent manner. The Ang II receptor subtype 1 (AT1 receptor) antagonist losartan and the AT2 receptor antagonist PD123319 inhibited this facilitatory effect of Ang II and Ang I, whereas the other AT2 receptor antagonist, CGP42112, was without effect. Bradykinin also increased [3H]NA release, which was inhibited by the B2 receptor antagonist Hoe140. The angiotensin-converting enzyme inhibitor captopril inhibited the effect of Ang I, but potentiated that of bradykinin. Interestingly, captopril alone produced an increase in [3H]NA release which was inhibited by Hoe140. Losartan, but not PD123319 or CGP42112, inhibited [125I]-Ang II binding in Chinese hamster ovary cells transfected with the AT1a or AT1b receptor. In contrast, in cells expressing the AT2 receptor, PD123319 and CGP42112, but not losartan, inhibited [125I]-Ang II binding. In conclusion, Ang II enhances the release of NA from sympathetic nerves of the rat prostate via a novel functional receptor distinct from the cloned AT1a, AT1b or AT2. These data provide direct evidence in support of a functional role for the local RAS in modulating sympathetic transmission in the prostate, which may have important implications for the pathophysiology of BPH.
Keyword Endocrinology & Metabolism
Endocrinology & Metabolism
ENDOCRINOLOGY & METABOLISM
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Biomedical Sciences Publications
 
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