Baroreflex and vagal mechanisms modulating left ventricular contractile responses to sympathomimetic amines in conscious dogs.
- 1 February 1979
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation Research
- Vol. 44 (2) , 195-207
- https://doi.org/10.1161/01.res.44.2.195
Abstract
The steady state effects of i.v. norepinephrine (NE), 0.2 .mu.g/kg per min, isoproterenol, 0.02 .mu.g/kg per min, and dopamine, 10 .mu.g/kg per min, on measurements of arterial and left ventricular (LV) pressures, dP/dt, LV diameter and velocity of shortening were compared before and after muscarinic blockade with atropine sulfate or methyl atropine bromide (0.1 mg/kg). In intact conscious dogs, NE increased mean arterial pressure by 24 .+-. 2 mm Hg and LV dP/dt by 1140 .+-. 90 mm Hg/s, but did not change LV velocity significantly and decreased heart rate by 13 .+-. 3 beats/min. After muscarinic blockade, NE caused significantly greater (P < 0.01) increases in mean arterial pressure of 49 .+-. 6 mm Hg, LV dP/dt of 3290 .+-. 240 mm Hg/s, LV velocity of 24 .+-. 6 mm/s and heart rate of 7 .+-. 3 beats/min. A similar augmentation of the contractile response to infusions of isoproterenol and dopamine was observed following muscarinic blockade. These responses were not dependent on arterial baroreceptors or on an intact sympathetic nervous system. After vagotomy and arterial baroreceptor denervation (ABD), NE increased LV dP/dt by 2970 .+-. 170 mm Hg/s and LV velocity by 20 .+-. 4 mm/s, i.e., by amounts similar to those found after muscarinic blockade for intact dogs and dogs with ABD. In dogs with ABD and vagotomy, the contractile responses to NE were not augmented further by muscarinic blockade. The parasympathetic nervous system can exert a powerful inhibitory influence on the inotropic responses to infused sympathomimetic amines, since after muscarinic blockade, the inotropic responses to NE, isoproterenol and dopamine increase 2-fold. The mechanism is independent of the arterial baroreceptor reflex and the sympathetic nervous system. It apparently involves an inhibitory action of vagally released acetylcholine on the .beta.-adrenergic inotropic response to sympathomimetic amines.This publication has 30 references indexed in Scilit:
- Cardiovascular Control Mechanisms in the Conscious StateNew England Journal of Medicine, 1975
- Effects of intracoronary infusions of acetylcholine and nicotine on the dog heart in vivoBritish Journal of Pharmacology, 1973
- Extent of Regulation of the Heart's Contractile State in the Conscious Dog by Alteration in the Frequency of ContractionJournal of Clinical Investigation, 1973
- Role of Muscarinic Cholinergic Receptors in Regulation of Guanosine 3′:5′-Cyclic Monophosphate Content in Mammalian Brain, Heart Muscle, and Intestinal Smooth MuscleProceedings of the National Academy of Sciences, 1972
- Elevation of Guanosine 3′,5′-Cyclic Phosphate in Rat Heart after Perfusion with AcetylcholineProceedings of the National Academy of Sciences, 1970
- A muscarinic inhibition of the noradrenaline release evoked by postganglionic sympathetic nerve stimulationNaunyn-Schmiedebergs Archiv für experimentelle Pathologie und Pharmakologie, 1969
- Alterations in myocardial contractility during stimulation of the cardiac nervesAmerican Journal of Physiology-Legacy Content, 1968
- A MUSCARINIC MECHANISM INHIBITING THE RELEASE OF NORADRENALINE FROM PERIPHERAL ADRENERGIC NERVE FIBRES BY NICOTINIC AGENTSBritish Journal of Pharmacology, 1968
- Electrical events in cardiac adrenergic nerves and noradrenaline release from the heart induced by acetylcholine and KClNaunyn-Schmiedebergs Archiv für experimentelle Pathologie und Pharmakologie, 1968
- Negative Inotropic Effect of the Vagus Nerves upon the Canine VentricleScience, 1964