UNLABELLED: The aim of the present study was determinate the role of nitric oxide (NO) in the action of CCK on arterial blood pressure and function of isolated rat heart. Intravenous administration of NO synthase (NOS) inhibitor-NG-nitro-L-arginine methyl ester (L-NAME-100.0 micrograms/kg) increased arterial blood pressure and abolished the hypertensive effect of CCK (administered in the highest dose: 425.0 pmoles/kg i.v.). Donors NO: L-arginine (L-Arg-100.0 mg/kg i.v.) and sodium nitroprusside (SNP-10.0 micrograms/kg i.v.) decreased arterial blood pressure, the hypotensive effect evoked by SNP was greater than produced by L-Arg. CCK administered with L-Arg evoked hypotension (opposite to the hypertensive effect evoked by CCK). When we used CCK at the higher doses (212.5; 425 pmoles/kg i.v.) simultaneously with L-Arg the hypotensive effect was greater than the hypotensive action evoked by L-Arg alone. Administration of CCK with SNP produced the hypotension (similar as after used SNP and opposite to the hypertensive action of the peptide). CCK (21.25, 42.5, 106.25 pmoles/0.1 ml) increased the cardiac contraction amplitude, the peptide injected in lower doses decreased coronary outflow. CCK had no effect on heart rate. L-NAME (10(-5) M) decreased coronary outflow, tendent to evoke bradycardia (p > 0.05) and the compound did not change the cardiac contraction amplitude of isolated heart. L-NAME abolished the influence of CCK on the function of isolated heart. L-Arg (10(-2) M) did not affect function of isolated heart. L-Arg abolished and when we used with CCK in the highest dose reversed the positive inotropic effect of the peptide and tendent to abolish a lowered coronary outflow evoked by CCK. SNP (10(-4) M) decreased the cardiac contraction amplitude. SNP diminished the positive inotropic effect of CCK and did not change other parameters of isolated heart. CONCLUSION: NO does not play a role in cardiovascular action of CCK directly, however inhibitor of NO synthase and donors of NO change the influence of the peptide, mainly on the heart. We suggest that the effect is indirectly through catecholamines.
UNLABELLED: The aim of the present study was determinate the role of nitric oxide (NO) in the action of CCK on arterial blood pressure and function of isolated rat heart. Intravenous administration of NO synthase (NOS) inhibitor-NG-nitro-L-arginine methyl ester (L-NAME-100.0 micrograms/kg) increased arterial blood pressure and abolished the hypertensive effect of CCK (administered in the highest dose: 425.0 pmoles/kg i.v.). Donors NO: L-arginine (L-Arg-100.0 mg/kg i.v.) and sodium nitroprusside (SNP-10.0 micrograms/kg i.v.) decreased arterial blood pressure, the hypotensive effect evoked by SNP was greater than produced by L-Arg. CCK administered with L-Arg evoked hypotension (opposite to the hypertensive effect evoked by CCK). When we used CCK at the higher doses (212.5; 425 pmoles/kg i.v.) simultaneously with L-Arg the hypotensive effect was greater than the hypotensive action evoked by L-Arg alone. Administration of CCK with SNP produced the hypotension (similar as after used SNP and opposite to the hypertensive action of the peptide). CCK (21.25, 42.5, 106.25 pmoles/0.1 ml) increased the cardiac contraction amplitude, the peptide injected in lower doses decreased coronary outflow. CCK had no effect on heart rate. L-NAME (10(-5) M) decreased coronary outflow, tendent to evoke bradycardia (p > 0.05) and the compound did not change the cardiac contraction amplitude of isolated heart. L-NAME abolished the influence of CCK on the function of isolated heart. L-Arg (10(-2) M) did not affect function of isolated heart. L-Arg abolished and when we used with CCK in the highest dose reversed the positive inotropic effect of the peptide and tendent to abolish a lowered coronary outflow evoked by CCK. SNP (10(-4) M) decreased the cardiac contraction amplitude. SNP diminished the positive inotropic effect of CCK and did not change other parameters of isolated heart. CONCLUSION: NO does not play a role in cardiovascular action of CCK directly, however inhibitor of NO synthase and donors of NO change the influence of the peptide, mainly on the heart. We suggest that the effect is indirectly through catecholamines.