Influence of 5‐hydroxytryptamine and the effect of a new serotonin receptor antagonist (sarpogrelate) on detrusor smooth muscle of streptozotocin‐induced diabetes mellitus in the rat *

Kodama, Masahito; Takimoto, Yukie

doi:10.1046/j.1442-2042.2000.00180.x

Cited by 33 publications

(25 citation statements)

References 18 publications

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“…Sikorski et al [11] suggested that the diminished contraction responses of the diabetic rat aorta to 5-HT may have occurred as a result of reductions in 5-HT receptor-mediated responses of smooth muscle. On the other hand, increased contraction responses to 5-HT were reported in diabetic pig bladder smooth muscle [12] . In comparison to this, according to our results, we may speculate that there was no change in 5-HT receptor regulation of diabetic HCC, and that sensitivity of smooth muscle cells of corpus cavernosum to 5-HT was not altered due to diabetes in ED patients.…”

Section: Discussionmentioning

confidence: 99%

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Contractility of Diabetic Human Corpus Cavernosum Smooth Muscle in Response to Serotonin Mediated via Rho-Kinase

Murat

Soner²,

Demir

et al. 2009

Pharmacology

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Background/Aims: Serotonin (5-hydroxytryptamine, 5-HT)-induced contraction and the involvement of RhoA/Rho-kinase pathway in the 5-HT-induced contraction was investigated isometrically in vitro in both diabetic and nondiabetic human corpus cavernosum (HCC) tissues. Methods: HCC tissues were obtained from 12 patients. The response to 5-HT (10^–9 to 10^–5 mol/l) was studied in isolated HCC tissues in the absence and in the presence of a Rho-kinase inhibitor (Y-27632). Results: Preincubation with Y-27632 attenuated maximum contractions induced by 5-HT in tissues of both nondiabetics and diabetics. When diabetic and nondiabetic groups were compared, no significant difference was seen in 5-HT-induced contraction alone, but in the presence of Y-27632, 5-HT-induced contraction was significantly higher in the diabetic group. Conclusion: These results suggest that the Rho-kinase-mediated pathway plays an important role for 5-HT-induced contraction in diabetic corpus cavernosum tissues.

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Section: Discussionmentioning

confidence: 99%

“…Due to diabetes mellitus, alterations of 5-HT-induced contractions have been seen in several tissues, such as in rat bladder, and the rabbit carotid and renal artery [9,10] . Therefore, the aim of our study was to find answers to two questions: (1) Does 5-HT-induced contraction alter in diabetic HCC?…”

Section: Rho-kinase Enzyme-induced 5-ht Contractionmentioning

confidence: 99%

Contractility of Diabetic Human Corpus Cavernosum Smooth Muscle in Response to Serotonin Mediated via Rho-Kinase

Murat

Soner²,

Demir

et al. 2009

Pharmacology

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“…This response was inhibited by a selective 5-HT 2A antagonist. However, when this response was related to the muscle mass (which was increased in diabetic animals), no difference was found (Kodama and Takimoto, 2000).…”

Section: Peripheral Targetsmentioning

confidence: 91%

“…Contractions due to direct stimulation of 5-HT 2 receptors of smooth muscle cells of cat, rat (Cohen, 1990;Saxena et al, 1985;Kodama and Takimoto, 2000;, and human (Klarskov and Hørby-Petersen, 1986) bladders, have been reported. Activation of 5-HT 3 receptors causes contractions mediated by stimulation of the receptor located on excitatory neurons in the bladder PHARMACOLOGY OF THE LOWER URINARY TRACT of cats (Saxena et al, 1985), mice (Holt et al, 1986), guinea pigs (Messori et al, 1995), rabbits (Chen, 1990;Barras et al, 1996), pigs (Sellers et al, 2000), and humans (Corsi et al, 1991;Tonini et al, 1994).…”

Section: Peripheral Targetsmentioning

confidence: 99%

Pharmacology of the Lower Urinary Tract: Basis for Current and Future Treatments of Urinary Incontinence

Andersson

Wein²

2004

Pharmacol Rev

452

364

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“…pBOO, bladder wall thickness tended to increase (15), and similar alterations might occur, at least in part, in this rat model. In the present study, 5-HT induced bladder contraction, as described in reports on rats, cats, dogs, and humans (6,(10)(11)(12)26). The contractile responses to 5-HT was significantly enhanced by pBOO, and expression of mRNA encoding the 5-HT 2A and 5-HT 2B receptors was increased in the detrusor muscle layer following pBOO.…”

Section: Discussionmentioning

confidence: 61%

Increased expression of 5-HT2A and 5-HT2B receptors in detrusor muscle after partial bladder outlet obstruction in rats

et al. 2015

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Serotonin (5-hydroxytryptamine; 5-HT)-induced bladder contraction is enhanced after partial bladder outlet obstruction (pBOO) in rats. We investigated time-dependent changes in bladder contraction and expression of 5-HT 2A and 5-HT 2B receptor mRNA in bladder tissue to elucidate the mechanism of this enhancement. On day 3 and 7 after pBOO, contractile responses of isolated rat bladder strips to 5-HT were increased compared with that in sham-operated rats; on day 14, the response had decreased to the same level as that in sham rat bladders. In contrast, carbacholinduced contraction was not enhanced by pBOO at any time point. In sham rats, 5-HT 2A receptor mRNA was expressed in the urothelium, and 5-HT 2B receptor mRNA was expressed in the detrusor muscle layer. In pBOO rats, both receptor mRNAs were increased in the detrusor muscle and subserosal layers, but not in the urothelium. The increase of 5-HT 2A receptor mRNA was maintained from day 3 to day 14 after pBOO, and 5-HT 2B receptor mRNA was increased on day 7 after pBOO. These results suggested that pBOO induced up-regulation of the 5-HT 2A and 5-HT 2B receptors in the detrusor muscle and subserosal layers of the bladder, and such up-regulation may be related to the enhanced bladder contractile response to 5-HT.Partial bladder outlet obstruction (pBOO) secondary to benign prostate hyperplasia has been considered an important factor associated with lower urinary tract symptoms (LUTS). LUTS include voiding symptoms (e.g., weak urine stream and urinary retention) and storage symptoms (e.g., urinary frequency, urgency and nocturia) (1). Voiding symptom is attributed to increased urethral resistance due to static and dynamic prostatic obstruction. In contrast, the mechanism responsible for storage symptoms secondary to pBOO remains unknown. To clarify the mechanism, several changes in the bladder have been investigated with animal models of pBOO (13,14,17). In these animal models, urothelium, subserosal layer, and detrusor muscle layer of the bladder are thickened (2, 7, 24). These morphological alterations result in some functional changes, such as detrusor overactivity. These morphological and functional alterations reach different states at different time points after pBOO (2,16,19). Therefore, both morphological and functional changes must be evaluated at several time points to reveal the mechanisms responsible for the storage symptoms secondary to pBOO. One of the important functional changes in the bladder with pBOO is the contractile response associated with detrusor overactivity. Contractile responses to ATP and acetylcholine are changed by pBOO; however, descriptions of these changes are not consistent among reports (2,7,19,25). Therefore, the myogenic change caused by pBOO is not fully understood. Serotonin (5-hydroxytryptamine; 5-HT) is a mono-

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Influence of 5‐hydroxytryptamine and the effect of a new serotonin receptor antagonist (sarpogrelate) on detrusor smooth muscle of streptozotocin‐induced diabetes mellitus in the rat *

Cited by 33 publications

References 18 publications

Contractility of Diabetic Human Corpus Cavernosum Smooth Muscle in Response to Serotonin Mediated via Rho-Kinase

Contractility of Diabetic Human Corpus Cavernosum Smooth Muscle in Response to Serotonin Mediated via Rho-Kinase

Pharmacology of the Lower Urinary Tract: Basis for Current and Future Treatments of Urinary Incontinence

<b>Increased expression of 5-HT</b><b><sub>2A</sub></b><b> and 5-HT</b><b><sub>2B</sub></b><b> receptors in detrusor muscle after partial bladder outlet obstruction in </b><b>rats </b>

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