Key result
Deprivation of female sex hormones via ovariectomy modulated intracellular Ca2+ concentration and cell shortening in rat cardiac myocytes, effects reversed by the NHE1 inhibitor cariporide.
Deprivation of female sex hormones modulates intracellular Ca2+ in cardiac myocytes via increased NHE1 activity, contributing to sex differences in cardiac function during acidosis.
May inform sex-specific acidosis therapies; leaves open NHE1 inhibition effects in human cardiac myocytes.
Compared to sham-operated controls, myofilaments from hearts of ovariectomized (OVX) rats demonstrate an increase in Ca2+ sensitivity with no change in maximum tension (Wattanapermpool J and Reiser PJ. Am J Physiol 277: H467-H473, 1999). To test the significance of this modification in intact cells, we compared intracellular Ca2+ transients and shortening of ventricular myocytes isolated from sham and 10-wk OVX rats. There was a decrease in the peak Ca2+ transient with prolonged 50% decay time in OVX cardiac myocytes without changes in the resting intracellular Ca2+ concentration. Percent cell shortening was also depressed, and relaxation was prolonged in cardiac myocytes from OVX rats compared with shams. Ovariectomy induced a sensitization of the myofilaments to Ca2+. Hypercapnic acidosis suppressed the shortening of OVX myocytes to a lesser extent than that detected in shams. Moreover, a larger compensatory increase in %cell shortening was obtained in OVX myocytes during prolonged acidosis. The elevated compensation in cell shortening was related to a higher amount of increase in the amplitude of the Ca2+ transient in OVX myocytes. However, these differences in Ca2+ transients and %cell shortening were no longer evident in the presence of 1 microM cariporide, a specific inhibitor of Na+/H+ exchanger type 1 (NHE1). Our results indicate that deprivation of female sex hormones modulates the intracellular Ca2+ concentration in cardiac myocytes, possibly via an increased NHE1 activity, which may act in concert with Ca2+ hypersensitivity of myofilament activation as a determinant of sex differences in cardiac function.
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Bupha‐Intr et al. (2006) studied Female sex hormone deprivation. Ovariectomy (OVX) vs. Sham-operated controls was evaluated on Intracellular Ca2+ transients and percent cell shortening. Deprivation of female sex hormones via ovariectomy modulated intracellular Ca2+ concentration and cell shortening in rat cardiac myocytes, effects reversed by the NHE1 inhibitor cariporide.
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