Abstract
Address: 1Department of Pharmacology, Faculty of Medical Sciences, University of Campinas, Campinas (SP), Brazil, 2Department of Pharmacology, Pontifical Catholic University of Campinas, Campinas (SP), Brazil, 3Department of Physical Education; Institute of Bioscience, Paulista State University, Rio Claro (SP), Brazil, 4Section of Experimental Endocrinology, Department of Pharmacology, UNIFESP (SP), Sao Paulo, Brazil, 5Pharmacology Laboratory, Butanta Institute (SP), Sao Paulo, Brazil, 6Departament of Clinical Pathology, University of Campinas, Campinas (SP), Brazil and 7Faculty of Medicine, Pontifical Catholic University of Campinas, Campinas (SP), Brazil
Highlights
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
Incubation of urinary bladder with CCh (10-9–10-3 M) concentration-dependently increased the total [3H]-inositol phosphates in rat urinary bladder that was markedly higher in L-NAME-treated rats compared with control animals (Figure 1B)
The measurement of the thickness of rat isolated bladder revealed that L-NAME treatment for 30 days caused no alterations in the thickness of submucosa and muscular layers of the DSM when compared with control animals
Summary
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
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