Cardiovascular reflex modulation of plasma catecholamine concentrations in the anesthetized cat.

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Abstract
The purpose of this study was to examine the role of carotid sinus and cardiopulmonary mechanoreceptors in the reflex control of adrenal medullary catecholamine secretion. Afferent input from carotid sinus and cardiopulmonary mechanoreceptors was decreased by carotid occlusion or cervical vagal cold block, respectively. Increases in arterial pressure were significantly greater when either intervention was tested in the presence of the other, with the role of the carotid sinus baroreflex being dominant. Neither carotid occlusion nor vagal cold block resulted in a significant increase in plasma epinephrine or norepinephrine concentrations. However, carotid occlusion during vagal block caused a significant increase in plasma epinephrine (+87%) and norepinephrine concentrations (+128%). Likewise, vagal block during carotid occlusion increased plasma epinephrine (+82%) and norepinephrine concentrations (+73%). Similar experiments performed in a group of chemically sympathectomized animals (pre-treated with 50 mg/kg 6-hydroxydopamine) indicted that adrenal medullary norepinephrine as well as epinephrine release could be modulated by the carotid sinus and cardiopulmonary reflexes. Mean arterial blood pressure and heart rate were significantly lower in 6-hydroxydopamine-treated animals, compared with untreated controls. Although of lesser magnitude, responses to carotid occlusion and vagal block in 6-hydroxydopamine-treated animals were qualitatively similar to those in untreated animals. Plasma catecholamine concentrations did not increase from either manipulation. However, when the second manipulation was added to the first, significant increases occurred. We conclude from these data that both the carotid sinus and cardiopulmonary reflexes modulate the release of adrenal catecholamines. An interaction between the two reflexes exists whereby the influence of one reflex on catecholamine secretion is apparent only in the absence of the other input.