Mechanisms of relaxation by urocortin in renal arteries from male and female rats

British Journal of Pharmacology - Tập 140 Số 5 - Trang 1003-1007 - 2003
Elena Sanz1, Luis Monge1, Núria Fernández1, Belén Climent1, Godofredo Diéguez1, Ángel Luis Garcı́a-Villalón1
1Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, Madrid 28029, Spain.

Tóm tắt

Urocortin is a peptide recently identified, which is structurally related to the corticotropin‐releasing factor (CRF). To analyze the mechanisms that could be involved in its effect on renal arteries from male and female rats, the response to urocortin was studied in isolated segments, 2 mm long, of renal arteries from male and female rats. In renal artery segments precontracted with endothelin‐1 (1 nM), urocortin (1 pM–10 nM) produced concentration‐dependent relaxation, which was similar in the arteries from male and female rats. This relaxation was reduced by the antagonists of urocortin receptors astressin (1 μM) and α‐helical CRF(9–41) (1 μM) in arteries from both male and female rats. In renal arteries from female rats, the relaxation to urocortin was reduced by the inhibitor of adenyl cyclase SQ22536 (300 μM), by 8‐bromo‐cyclic‐ADP‐ribose (cADPR; 30 μM), an antagonist of the endogenous activator of sarcoplasmic Ca2+ channel cADPR and by ryanodine (1 μM), which produces depletion of sarcoplasmic Ca2+. In renal arteries from male rats, the relaxation to urocortin was increased by ryanodine, and was not modified by SQ22536 or 8‐bromo‐cADPR. These results suggest that the mechanisms involved in the relaxation to urocortin in renal arteries differ between female and male rats. In female rats, this relaxation may be mediated by the production of cyclic AMP (cAMP), synthesis of cADPR and release of sarcoplasmic Ca2+, whereas in male rats it is not mediated by cAMP. British Journal of Pharmacology (2003) 140, 1003–1007. doi:10.1038/sj.bjp.0705516

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British Journal of Pharmacology

Tập 140 Số 5

1003-1007

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