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Effect of long-term endogenous testosterone deprivation on function of voltage-dependent potassium channels in rat aortic artery / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12)1986.
Article Dans Chinois | WPRIM | ID: wpr-531972
ABSTRACT

AIM:

To explore the effect of long-term (6 months) endogenous testosterone deprivation by orchidectomy on the function of voltage-dependent potassium channels of vascular smooth muscle cells in rats.

METHODS:

Wistar rats were raised for 6 months after castration. Isometric tension measurement of aortic rings,whole-cell patch-clamp technique and Western blotting analysis were employed to examine the functional and posttranscriptional alterations of voltage-dependent potassium channels.

RESULTS:

Voltage-dependent potassium channel blocker,4-aminopyridine,significantly decreased the constriction of aortic artery rings from male rats after 6-month castration. In castrated rats the amplitude of voltage-dependent potassium currents of aortic artery smooth muscle cells was significantly decreased compared with that in control rats. Meanwhile,the expression of Kv 1.5 channel protein,which plays an essential role in mediating vasomotor function,was also reduced. The functional and molecular alterations of voltage-dependent potassium channels were both restored when the rats were concomitant applied with physiological level of testosterone after castration.

CONCLUSION:

Long-term deprivation of endogenous testosterone in rats significantly attenuates the function of voltage-dependent potassium channels,and the decreases in expression of Kv1.5 channel protein accounts for this alteration. Long-term application of physiological concentration of testosterone,which recovered the impaired function of voltage-dependent channels,may be beneficial for male gender with hypotestosteronaemia.

Texte intégral: Disponible Indice: WPRIM (Pacifique occidental) langue: Chinois Texte intégral: Chinese Journal of Pathophysiology Année: 1986 Type: Article

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Texte intégral: Disponible Indice: WPRIM (Pacifique occidental) langue: Chinois Texte intégral: Chinese Journal of Pathophysiology Année: 1986 Type: Article