Ca
            <sup>2+</sup>
            SENSITIZATION IN CONTRACTION OF HUMAN BLADDER SMOOTH MUSCLE

Takahashi, Ryuji; Nishimura, Junji; Hirano, Katsuya; Seki, Nobuhiko; Naito, Seiji; Kobayashi, Hideo

doi:10.1097/01.ju.0000130419.32165.6b

Cited by 76 publications

(76 citation statements)

References 18 publications

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“…This is in agreement with previous work wherein identification of these proteins has also been demonstrated [25,27,30,31,37,45]. In addition, recent reports demonstrate that ROKβ is partly responsible for the high degree of force maintenance in the detrusor smooth muscle in overactive bladders [30][31][32].…”

Section: Discussionsupporting

confidence: 93%

“…In human, rat, rabbit and guinea pig bladder, the Rho-kinase pathway represents an important regulator of smooth muscle activity and tone [25,[27][28][29][30][31][32]. The prototype Rho-kinase inhibitor Y-27632 has been shown to attenuate contractions of bladder smooth muscle evoked by CCh, through the decrease of Ca 2+ sensitivity of the contractile apparatus [27][28][29].…”

Section: Discussionmentioning

confidence: 99%

“…Rhokinase is activated by RhoA and inhibits myosin phosphatase through the phosphorylation of its myosin binding subunit, leading to an increase in Ca 2+ sensitivity. The RhoA/Rho-kinase Ca 2+ sensitization pathway is involved in the regulation of bladder smooth muscle contraction and tone in humans [25,26] and animals [27][28][29]. Inhibition of Rho-kinase attenuates bladder hyperactivity in rabbits with partial outlet obstruction [30], diabetic rabbits [31] and hypertensive rats [32].…”

Section: Introductionmentioning

confidence: 99%

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Comparative pharmacological analysis of Rho-kinase inhibitors and identification of molecular components of Ca2+ sensitization in the rat lower urinary tract

Teixeira

Jin

Priviero

et al. 2007

Biochemical Pharmacology

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We aimed to compare the expression and function of molecular components of the RhoA/Rho-kinase signaling pathway in the contractile responses of detrusor, trigonal and urethral smooth muscle, using selective Rho-kinase inhibitors. Contractility studies and molecular approaches were employed to demonstrate the expression patterns and functional activity of the RhoA/Rho-kinase signaling pathway in the lower urinary tract. Frequency-response curves (1-32 Hz) and concentration-response curves (CRC) to carbachol (CCh, 0.01-30 μM), phenylephrine (PE, 0.01-300 μM) and endothelin-1 (ET-1, 0.01-100 nM) were significantly attenuated (p<0.01) following incubation with the Rhokinase inhibitors H-1152 (0

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Comparative pharmacological analysis of Rho-kinase inhibitors and identification of molecular components of Ca2+ sensitization in the rat lower urinary tract

Teixeira

Jin

Priviero

et al. 2007

Biochemical Pharmacology

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“…It may cause dysuria and frequent urination. ROCK activation plays a role in carbachol (CCh)-induced bladder smooth muscle contraction [110,111]. There is evidence [112] that overexpression of ROCKβ, with respect to both mRNA and protein levels, and increased MLC phosphorylation are present in the diabetic detrusor smooth muscle.…”

Section: Role Of Rho/rock Pathway In Diabetic Cystopathymentioning

confidence: 99%

Long‐term diabetic complications may be ameliorated by targeting Rho kinase

Zhou

2011

Diabetes Metabolism Res

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This review addresses the roles of Rho/Rho-kinase (ROCK) pathway in the pathogenesis of diabetes complications. Diabetes can cause many serious complications and can result in physical disability or even increased mortality. However, there are not many effective ways to treat these complications. The small guanosine-5'-triphosphate-binding protein Rho and its downstream target Rho-kinase mediate important cellular functions, such as cell morphology, motility, secretion, proliferation, and gene expression. Recently, the Rho/Rho-kinase pathway has attracted a great deal of attention in diabetes-related research. These studies have provided evidence that the activity and gene expression of Rho-kinase are upregulated in some tissues in animal models of type 1 or type 2 diabetes and in cell lines cultured with high concentrations of glucose. Inhibitors of Rho-kinase could prevent or ameliorate the pathological changes in diabetic complications. The inhibitory effects of statins on the Rho/Rho-kinase signalling pathway may also play a role in the prevention of diabetic complications. However, the precise molecular mechanism by which the Rho/Roh-kinase pathway participates in the development or progression of diabetic complications has not been extensively investigated. This article evaluates the relationship between Rho/Roh-kinase activation and diabetic complications, as well as the roles of Roh-kinase inhibitors and statins in the complications of diabetes, with the objective of providing a novel target for the treatment of long-term diabetic complications.

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“…One explanation is that one of the agonists also exerts a Ca 2þ -independent action on tension development. Ca 2þ -sensitisation has been demonstrated in other urinary tract muscles, for example, a G q -protein-activated Rho kinase (ROK) for muscarinic activation in human and rat tissue detrusor 51,52 and in urethra, 53 as well as a diacyl glycerolactivated protein kinase C (PKC) pathway in guinea-pig detrusor. 51 Both routes inhibit myosin phosphatase and therefore enhance myosin light chain phosphorylation and force production.…”

Section: Bladder Base and Trigonementioning

confidence: 99%

Clinical and experimental aspects of Adreno‐muscarinic synergy in the bladder base and prostate

Roosen

Blake-James

Wood

et al. 2009

Neurourology and Urodynamics

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Recent clinical trials have shown that combination therapy using an alpha-receptor antagonist and an antimuscarinic is more effective than either agent alone in improving quality of life and objective urodynamic variables in men with bladder outflow obstruction. There appear to be no negative effects on bladder function. The mode of action of this combination is unknown but presumed to be an antimuscarinic reduction in detrusor overactivity and the alpha-receptor antagonist reduced outflow tract resistance. We have shown with in vitro experiments that in smooth muscles influencing outflow tract resistance (prostate, trigone) there is a profound contractile synergy between adrenergic and muscarinic pathways. We propose the hypothesis that both arms of the combination therapy reduce contractile tone of the outflow tract and that their simultaneous attenuation has a disproportionately large effect on outflow tract resistance. Our data from trigone muscle suggest that adrenergic and muscarinic receptor activation increase the intracellular [Ca(2+)] but the adrenergic pathway also operates through Ca(2+)-sensitisation of the contractile apparatus, primarily through a PKC-dependent pathway.

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Ca ²⁺ SENSITIZATION IN CONTRACTION OF HUMAN BLADDER SMOOTH MUSCLE

Cited by 76 publications

References 18 publications

Comparative pharmacological analysis of Rho-kinase inhibitors and identification of molecular components of Ca2+ sensitization in the rat lower urinary tract

Comparative pharmacological analysis of Rho-kinase inhibitors and identification of molecular components of Ca2+ sensitization in the rat lower urinary tract

Long‐term diabetic complications may be ameliorated by targeting Rho kinase

Clinical and experimental aspects of Adreno‐muscarinic synergy in the bladder base and prostate

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Ca 2+ SENSITIZATION IN CONTRACTION OF HUMAN BLADDER SMOOTH MUSCLE

Cited by 76 publications

References 18 publications

Comparative pharmacological analysis of Rho-kinase inhibitors and identification of molecular components of Ca2+ sensitization in the rat lower urinary tract

Comparative pharmacological analysis of Rho-kinase inhibitors and identification of molecular components of Ca2+ sensitization in the rat lower urinary tract

Long‐term diabetic complications may be ameliorated by targeting Rho kinase

Clinical and experimental aspects of Adreno‐muscarinic synergy in the bladder base and prostate

Contact Info

Product

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Ca ²⁺ SENSITIZATION IN CONTRACTION OF HUMAN BLADDER SMOOTH MUSCLE