Mechanisms by which ganglioplegics and atropine enhance cardiovascular responsiveness

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Abstract
At least four mechanisms contribute to the increased responsiveness to pressor drugs caused by ganglioplegic agents: 1) Elimination of parasympathetic reflexes alone was found to have a prominent effect on pressor responsiveness, especially to norepinephrine. 2) Elimination of sympathetic compensatory reflexes caused the expected increase in responsiveness. 3) Tetraethylammonium had a direct effect on blood vessels of the dog's perfused hind limb that resulted in sensitization to norepinephrine, though not to angiotensin; this direct effect of the ganglioplegic was similar to that produced by surgical denervation. 4) Tetraethylammonium caused enhancement of response to epinephrine but not to norepinephrine in pithed cats and this effect seems best explained by a blocking action of the ganglioplegic on adrenergic vasodilator receptors. Because of the participation of these different mechanisms, ganglioplegics and surgical denervation do not necessarily affect pressor responsiveness in the same manner. Additionally, the different mechanisms involved account for the various degrees of augmentation of response to different pressor drugs since the latter have their major actions on different portions of the cardiovascular system. Responsiveness may vary greatly during a single experiment and also from day to day; this variability is due in large part to the nervous system since it is abolished by cervical section of the spinal cord.