Am J Physiol Cell Physiol Journal of Applied Physiology
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Am J Physiol Cell Physiol 273: C1371-C1377, 1997;
0363-6143/97 $5.00
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Vol. 273, Issue 4, C1371-C1377, October 1997

beta -Adrenergic regulation of constitutive nitric oxide synthase in cardiac myocytes

Anthony J. Kanai1, Stephan Mesaros2, Mitchell S. Finkel3, Carmine V. Oddis3, Lori A. Birder4, and Tadeusz Malinski4

1 Department of Biomedical Engineering, Duke University, Durham, North Carolina 27708; 3 Division of Cardiology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213; 4 Department of Physiology, University of North Carolina-Chapel Hill School of Medicine, Chapel Hill, North Carolina 27599; and 2 Department of Chemistry, Oakland University, Rochester, Michigan 48309

Nitric oxide (NO) has been implicated in endogenous control of myocardial contractility. However, NO release has not yet been demonstrated in cardiac myocytes. Accordingly, endogenous NO production was measured with a porphyrinic microsensor positioned on the surface of individual neonatal or adult rat ventricular myocytes (n > 6 neonatal and adult cells per experiment). In beating neonatal myocytes, there was no detectable spontaneous NO release with each contraction. However, norepinephrine (NE; 0.25-1 µM) elicited transient NO release from beating neonatal (149 ± 11 to 767 ± 83 nM NO) and noncontracting adult (157 ± 13 to 791 ± 89 nM NO) cells. NO was released by adrenergic agonists with the following rank order of potency: isoproterenol (beta 1beta 2) > NE (alpha /beta 1) > dobutamine (beta 1) approx  epinephrine (alpha /beta 1beta 2) > tertbutylene (beta 2); NO was not released by phenylephrine (alpha ). NE-evoked NO release was reversibly blocked by NG-monomethyl-L-arginine, trifluoperazine, guanosine 5'-O-(2-thiodiphosphate), and nifedipine but was enhanced by 3-isobutyl-1-methylxanthine (0.5 mM = 14.5 ± 1.6%) and BAY K 8644 (10 µM = 11.9 ± 1%). NO was also released by A-23187 (10 µM = 884 ± 88 nM NO), guanosine 5'-O-(3-thiotriphosphate) (1 µM = 334 ± 56 nM NO), and dibutyryl adenosine 3',5'-cyclic monophosphate (10-100 µM = 35 ± 9 to 284 ± 49 nM NO) but not by ATP, bradykinin, carbachol, 8-bromoguanosine 3',5'-cyclic monophosphate, or shear stress. This first functional demonstration of a constitutive NO synthase in cardiac myocytes suggests its regulation by a beta -adrenergic signaling pathway and may provide a novel mechanism for the coronary artery vasodilatation and enhanced diastolic relaxation observed with adrenergic stimulation.

norepinephrine; beta -adrenergic agonists; nitric oxide-selective porphyrinic microsensor


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