Submitted to: Circulation Research
Publication Type: Peer reviewed journal
Publication Acceptance Date: 10/5/2002
Publication Date: 2/1/2003
Citation: Gomez, R., Levander, O.A., Sterin-Borda 2003. Diminished beta-adrenoceptor-inotropic cardiac response in selenium-deficient mice relates with cardiac inducible nitric oxide synthase (inos) expression. Circulation Research. Interpretive Summary: Poor nutritional status of the essential trace element selenium has been associated with diseases of human heart muscle (cardiomyopathies) and with diseases of arteries of the heart (cardiovascular disease). Here we report an impaired ability of heart muscle to contract forcefully in mice fed a selenium-deficient diet. This decreased contractility in the heart muscle of the selenium-deficient mice correlates with an increased production of nitric oxide, a compound known to interfere with normal heart contraction if present in excessive amounts. These results demonstrate the need for an adequate level of selenium in the diet and suggest that selenium may play a key role in proper heart function.
Technical Abstract: Atria taken from mice fed a selenium-deficient diet (Se-) for 4 weeks have a diminished beta-adrenoceptor-inotropic cardiac response to isoproterenol (ISO) or norepinephrine (NE) compared with atria from mice fed the same diet supplemented with 0.2 ppm Se as sodium selenite (Se+). In Se- mouse atria, the dose response curves of ISO and E were shifted to the right and the potency of the beta-adrenoceptor agonists was decreased. This diminished response could be reversed by feeding the Se+ diet for 1 week or by pretreatment with nitric oxide snthase (NOS) inhibitors. Elevated serum concentrations of nitrite/nitrate as well as a 3-fold increase in atrial NOS activity were seen in the Se- vs Se+ mice. Elevated nitric oxide (NO) levels my account for some of the pathophysiological effects of selenium deficiency on the heart.