Effects of autonomic nervous system-related agents on the intravesical pressure of the bladder in situ in female rats and ageing
We investigated cystometrically the effects of several autonomic nervous system-related agents on the intravesical pressure (IVP) in adult (11 ?? 23 weeks old, 200 ?? 350 g) and aged (2 years old, 350 ?? 770 g) female rats. Acetylcholine induced a dose-dependent and transient increase of IVP, which...
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Veröffentlicht in: | Folia Pharmacologica Japonica 1990, Vol.96(3), pp.103-115 |
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Format: | Artikel |
Sprache: | jpn |
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Zusammenfassung: | We investigated cystometrically the effects of several autonomic nervous system-related agents on the intravesical pressure (IVP) in adult (11 ?? 23 weeks old, 200 ?? 350 g) and aged (2 years old, 350 ?? 770 g) female rats. Acetylcholine induced a dose-dependent and transient increase of IVP, which was competitively antagonized by pirenzepine weakly and by atropine strongly. These results suggest the predominancy of M-2 receptors. Adrenaline induced dual actions of decrease and increase of IVP at low and high doses, respectively. Adrenaline (at only high doses), noradrenaline and phenylephrine increased IVP but not clonidine, suggesting the predominancy of α-1 receptors. Isoproterenol, salbutamol and clenbuterol decreased IVP to same extent and the effect of isoproterenol was markedly antagonized by propranolol and slightly by atenolol, suggesting the predominancy of β-2 receptors. ATP increased IVP dosedependently but not adenosine, suggesting the predominancy of P-2 receptors. Serotonin and prostaglandin F2α also increased IVP. In aged rats, the maximal response to acetylcholine was lower than in adult rats and the decrease in IVP by low doses of adrenaline was not observed. These results suggest that the increase of IVP involves the participation of cholinergic M-2 receptors to a large extent and also serotonergic, adrenergic α-1 and purinergic P-2 receptors to some extent and that the responsiveness to acetylcholine is reduced by ageing. |
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ISSN: | 0015-5691 1347-8397 |
DOI: | 10.1254/fpj.96.3_103 |