Author
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Saari, Jack |
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ALLEN, CORRIE - 5450-20-00 |
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Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only Publication Acceptance Date: 4/14/1996 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: The effect of copper (Cu) deficiency on coronary vasoactivity was examined in the isolated, perfused rat heart. Male weanling Sprague-Dawley rats were fed diets that were deficient (CuD, <1 mg Cu/kg diet) or adequate (CuA, 5 mg Cu/kg diet) in Cu for 4-5 wks. Following anesthesia, the rats' hearts were removed and perfused via the aorta with Krebs-bicarbonate buffer (37 deg C, gassed with 95% O2 - 5% CO2) at 5.5 ml/min/g. Baseline perfusion pressures were 21% lower in CuD than in CuA hearts. Acetylcholine (ACh), when infused into the heart at a concentration (30 uM) that causes endothelium-dependent vasodilation in other tissues, caused intense vasoconstriction that peaked and then slowly declined. Peak pressure in response to ACh was 20% lower in CuD than in CuA rat hearts, thus peak pressures were proportional to baseline pressures. Relative to the peak pressure difference, the rate of decline in response was lower in CuD than in CuA hearts. Administration of bradykinin (BK) at a time coinciding with the peak response to ACh resulted in an enhanced decline in response that did not differ between CuD and CuA hearts. We conclude, as have others, that vascular resistance per weight of tissue is reduced in Cu-deficient hearts. We hypothesize that reduction in the decline of ACh-induced pressure change with Cu deficiency may be caused by reduced nitric-oxide mediated dilation to ACh, consistent with effects in other Cu-deficient tissues. Because BK causes vasodilation via an endothelium-derived hyperpolarizing factor, our findings on BK-induced vasodilation suggest that endothelium-mediated hyperpolarization is not affected by Cu deficiency. |
