Role of cardiac eNOS expression during pregnancy in the coupling of myocardial oxygen consumption to cardiac work.

We assessed whether pregnancy results in enhanced nitric oxide (NO)-mediated control of myocardial oxygen consumption. Rats were studied before (C), at 1 wk (1w) or 2 wk (2w) of pregnancy, and at 4 days after giving birth (-4d). Left ventricular endothelial NO synthase (eNOS) protein expression was determined by immunoblotting. Oxygen consumption of left ventricular tissue samples was measured in vitro in response to increasing doses of bradykinin with or without addition of the NOS inhibitor N-G-nitro-L-arginine methyl ester (L-NAME). Echocardiography indicated an increased cardiac output during pregnancy. Myocardial eNOS protein expression significantly increased by 46+/-9 and 39+/-8% at 1w and 2w, respectively, and returned to control levels at -4d. Bradykinin (10(-4) M) decreased cardiac oxygen consumption in a NO-dependent manner by 17+/-2% at C, by 21+/-2% at 1w, by 24+/-2% at 2w (P<0.05 vs. C and -4d), and by 18&PLUSMN;1% at -4d. Myocardial eNOS protein expression is transiently increased during pregnancy in rats, and this increase is associated with enhanced NO-dependent control of myocardial oxygen consumption at a time when cardiac output is increased.