Open AccessTestosterone modulates cardiomyocyte Ca2+ handling and contractile function
Author(s) -
Claire L. Curl,
L. Delbridge,
Benedict J. Canny,
Igor R Wendt
Publication year - 2009
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.931460
Subject(s) - contractility , testosterone (patch) , medicine , endocrinology , myocyte , intracellular , chemistry , extracellular , testosterone replacement , androgen , hormone , biochemistry
The extent to which sex differences in cardiac function may beattributed to the direct myocardial influence of testosterone isunclear. In this study the effects of gonadal testosteronewithdrawal (GDX) and replacement (GDX+T) in rats, oncardiomyocyte shortening and intracellular Ca2+ handling wasinvestigated (0.5 Hz, 25 oC). At all extracellular [Ca2+] tested(0.5-2.0 mM), the Ca2+ transient amplitude was significantlyreduced (by ~ 50 %) in myocytes of GDX rats two weeks postgonadectomy. The time course of Ca2+ transient decay wassignificantly prolonged in GDX myocytes (tau, 455±80 ms)compared with intact (279±23 ms) and GDX+T (277±19 ms).Maximum shortening of GDX myocytes was markedly reduced(by more than 60 %) and relaxation significantly delayed (bymore than 35 %) compared with intact and GDX+T groups. Thustestosterone replacement completely reversed the cardiomyocytehypocontractility induced by gonadectomy. These results providedirect evidence for a role of testosterone in regulating functionalCa2+ handling and contractility in the heart.