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Supersensitivity of muscarinic receptors in rat isolated detrusor smooth muscle (DSM) after chronic nitric oxide inhibition
© Mónica et al; licensee BioMed Central Ltd. 2007
Published: 25 July 2007
It has been suggested that disturbance of the NO-cGMP pathway lead to impaired relaxation of the urethral outflow region, increased bladder afferent activity and overactive bladder, but the precise role of NO in regulating the detrusor smooth muscle (DSM) functions remains to be determined.
Our present work aimed to examine the functional and biochemical alterations of rat DSM after chronic NO blockade.
Male Wistar rats were treated orally with L-NAME (20 mg/rat/day) for 30 days. Age-matched control animals received tap water alone. Concentration-response curves to full agonist carbachol (CCh, 1 nM-30 μM) in the DSM were obtained. The values of potency (pEC50) and maximal responses (Emax) were calculated. The IP3 accumulation and the nitric oxide synthase (NOS) activity, as well as morphometric analyses were evaluated in the urinary bladder of control and L-NAME-treated rats.
Morphometric analyses in isolated rat detrusor and trigone smooth muscle in control and L-NAME-treated groups in 30 days. *p < 0.05.
1194 ± 73.09
1098 ± 67.72
705 ± 19.56
861 ± 21.85*
610 ± 37.18
658 ± 32.24
526 ± 24.29
677 ± 30.49*
547 ± 66.36
494 ± 56.15
176 ± 12.47
183 ± 17.11
Our findings show that long-term NO inhibition significantly increases the sensitivity of DSM for the muscarinic agonist carbachol via accumulation of IP3, suggesting that NO exerts a modulatory effect on the contractility mediated by muscarinic receptors.
Financial Support by FAPESP.
This article is published under license to BioMed Central Ltd.