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• W2012488407 abstract "1 The functional consequences of a lack of endothelial nitric oxide synthase (eNOS) on left ventricular force development and the anti-adrenergic effect of acetylcholine (ACh) were investigated in isolated hearts and cardiomyocytes from wild type (WT) and eNOS knockout (eNOS–/–) mice. 2 eNOS expression in cardiac myocytes accounted for 20 % of total cardiac eNOS (Western blot analysis). These results were confirmed by RT-PCR analysis. 3 In the unstimulated perfused heart, the left ventricular pressure (LVP) and maximal rate of left ventricular force development (dP/dtmax) of eNOS–/– hearts were not significantly different from those of WT hearts (LVP: 97 ± 11 mmHg WT vs. 111 ± 11 mmHg eNOS–/–; dP/dtmax: 3700 ± 712 mmHg s−1 WT vs. 4493 ± 320 mmHg s−1 eNOS–/–). 4 The dobutamine (10-300 nm)-induced increase in LVP was enhanced in eNOS–/– hearts. In contrast, L-type Ca2+ currents (ICa,L) in isolated cardiomyocytes of WT and eNOS–/– hearts showed no differences after β-adrenergic stimulation. Dibutyryl-cGMP (50 μm) reduced basal ICa,L in WT cells to 72 ± 12 % while eNOS–/–ICa,L was insensitive to the drug. The pre-stimulated ICa,L (30 nm isoproterenol) was attenuated by dibutyryl-cGMP in WT and eNOS–/– cells to the same extent. 5 The Ca2+ (1.5-4.5 mm)-induced increase in inotropy was not different between the two experimental groups and β-adrenergic receptor density was increased by 50 % in eNOS–/– hearts. 6 The contractile effects of dobutamine could be inhibited almost completely by ACh or adenosine. The extent of the anti-adrenergic effect of both compounds was identical in WT and eNOS–/– hearts. Measurement of ICa,L in isolated cardiac myocytes yielded similar results. 7 These data demonstrate that in the adult mouse (1) lack of eNOS is associated with increased cardiac contractile force in response to β-adrenergic stimulation and with elevated β-adrenergic receptor density, (2) the unaltered response of ICa,L in eNOS–/– cardiac myocytes to β-adrenergic stimulation suggests that endothelium-derived NO is important in mediating the whole-organ effects and (3) eNOS is unimportant for the anti-adrenergic effect of ACh and adenosine." @default.
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• W2012488407 date "2001-04-01" @default.
• W2012488407 modified "2023-10-16" @default.
• W2012488407 title "Inotropic response to β‐adrenergic receptor stimulation and anti‐adrenergic effect of ACh in endothelial NO synthase‐deficient mouse hearts" @default.
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• W2012488407 doi "https://doi.org/10.1111/j.1469-7793.2001.0195g.x" @default.
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