Browsing by Author "MACHO, P"

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    EFFECT OF ENDOTHELIN ON TOTAL AND REGIONAL CORONARY RESISTANCE AND ON MYOCARDIAL-CONTRACTILITY
    (1991) DOMENECH, R; MACHO, P; GONZALEZ, R; HUIDOBROTORO, JP
    Endothelin is a 21-amino acid peptide produced by the endothelium and has a potent vasoconstrictor effect. Because of the importance of the endothelium on vasomotor regulation, we studied the effect of endothelin on total and regional coronary vascular resistance and on myocardial contractility in the intact heart of anesthetized dogs. Intracoronary administration of 2 to 80 pmol/kg of endothelin produced a dose-dependent increase in coronary resistance, ischaemic decrease in myocardial contractility and atrium-ventricular blockade. The increase in resistance was greater towards the outer layer of the left ventricular wall. When the coronaries were perfused at a constant rate and vasoconstriction was prevented with adenosine or nitroglycerine, endothelin did not produce inotropic changes. These results show that endothelin is a potent vasoconstrictor of the resistance coronary vessels, producing a redistribution of transmural blood flow and a decrease in myocardial contractility secondary to ischaemia.
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    NEUROPEPTIDE Y (NPY) - A CORONARY VASOCONSTRICTOR AND POTENTIATOR OF CATECHOLAMINE-INDUCED CORONARY CONSTRICTION
    (1989) MACHO, P; PEREZ, R; HUIDOBROTORO, JP; DOMENECH, RJ
    The vasoactive effect of neuropeptide Y (NPY) a peptide commonly found in perivascular nerves, including those of the heart, was assessed in the coronary circulation of the isolated perfused dog heart and in superfused segments of isolated canine coronary arteries. The intracoronary administration of 0.7-23.5 nmol NPY to hearts during beta adrenergic blockade produced a dose-dependent increase in coronary vascular resistance ranging from 0.10 to 0.49 mmHg.cntdot.min-1.cntdot.ml-1.cntdot.100 g-1 without changes in myocardial oxygen consumption. The potency of NPY as a coronary vasoconstrictor was about 250 times that of noradrenaline. Pretreating the coronary system of these hearts with NPY caused a marked potentiation of the vasocontractile effect of noradrenaline, displacing its dose-response curve to the left in a non-parallel fashion. The addition of 0.2-3.7 nmol NPY did not induce contraction in superfused helical segments of large coronary arteries but it potentiated the tension developed in response to 0.18 .mu.M adrenaline in a concentration-dependent manner. Pretreatment of these arteries with 3.7 nmol NPY caused a significant leftward displacement of the adrenaline contractile effect. These results show that NPY is a potent coronary vasoconstrictor and a potentiator of the contractile effect of catecholamines and support the hypothesis that NPY may participate in the regulation of coronary vascular resistance.