Protein kinase C and the sub-sensitivity and sub-reactivity of the diabetic rat prostate gland to noradrenaline

Ramasamy, Sharmaine; Hodgson, Wayne Clarence; Ventura, Sabatino

doi:10.1016/s0014-2999(01)01541-2

Cited by 1 publication

(2 citation statements)

References 29 publications

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“…Thus, contractions induced by exogenous noradrenaline (Teng et al ., 1994) and by endogenous agonist released by field stimulation (Guh et al ., 1995; 1996; Haynes & Hill, 1997) were sensitive to Ca 2+ entry blockers such as nifedipine. One study in rats found that the protein kinase C inhibitors calphostin C and bisindolylmaleimide I did not affect noradrenaline‐induced contraction (Ramasamy et al ., 2002).…”

Section: Prostatementioning

confidence: 99%

“…If this would be α‐adrenoceptor‐related, an enhanced responsiveness of the receptors would be expected in diabetes. However, a study in rats with streptozotocin‐induced diabetes reported the opposite, that is, a reduced potency and efficacy of noradrenaline to contract the prostate in vitro , and insulin treatment in vivo restored the maximum effects but not the agonist potency; the protein kinase C inhibitor calphostin C (but not bisindolylmaleimide I) restored the contractile effects of noradrenaline in diabetic rats (Ramasamy et al ., 2002). The authors interpreted these findings to indicate that an increased protein kinase C activity in prostates from diabetic rats may impair α 1 ‐adrenoceptor function; desensitization of α 1 ‐adrenoceptor function by protein kinase C activation is well documented (Yang et al ., 1998a).…”

Section: Prostatementioning

confidence: 99%

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α₁‐, α₂‐ and β‐adrenoceptors in the urinary bladder, urethra and prostate

Michel

Vrydag

2006

British J Pharmacology

409

320

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1 We have systematically reviewed the presence, functional responses and regulation of a 1 -, a 2 -and b-adrenoceptors in the bladder, urethra and prostate, with special emphasis on human tissues and receptor subtypes. 2 a 1 -Adrenoceptors are only poorly expressed and play a limited functional role in the detrusor. a 1 -Adrenoceptors, particularly their a 1A -subtype, show a more pronounced expression and promote contraction of the bladder neck, urethra and prostate to enhance bladder outlet resistance, particularly in elderly men with enlarged prostates. a 1 -Adrenoceptor agonists are important in the treatment of symptoms of benign prostatic hyperplasia, but their beneficial effects may involve receptors within and outside the prostate. 3 a 2 -Adrenoceptors, mainly their a 2A -subtype, are expressed in bladder, urethra and prostate. They mediate pre-junctional inhibition of neurotransmitter release and also a weak contractile effect in the urethra of some species, but not humans. Their overall post-junctional function in the lower urinary tract remains largely unclear. 4 b-Adrenoceptors mediate relaxation of smooth muscle in the bladder, urethra and prostate. The available tools have limited the unequivocal identification of receptor subtypes at the protein and functional levels, but it appears that the b 3 -and b 2 -subtypes are important in the human bladder and urethra, respectively. b 3 -Adrenoceptor agonists are promising drug candidates for the treatment of the overactive bladder. 5 We propose that the overall function of adrenoceptors in the lower urinary tract is to promote urinary continence. Further elucidation of the functional roles of their subtypes will help a better understanding of voiding dysfunction and its treatment.

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