| Abstract: | In a population of wild baboons living in East Africa, we have observed endocrine differences among individuals as a function of dominance rank. Among these differences, we previously observed indirect evidence for dominant males being more. responsive to sympathetic catecholamines than were subordinate males. The present report tests this explicitly. Male baboons of known rank were anesthetized, and sympathetic and parasympathetic activity was pharmacologically inhibited. In experiment I, males were challenged with epinephrine; over a wide dose range, dominant males had the largest and fastest rises in systolic pressure, the greatest peak systolic pressure, and the most rapid recovery from the epinephrine challenge. Similar rank-related differences in heart rate response to epinephrine also occurred. Experiment II showed that this phenomenon probably reflects rank-related differences at both the heart and vasculature. As evidence, the same rank differences in systolic blood pressure responsiveness occurred when males were challenged with the alpha receptor agonist phenylephrine (which predominantly constricts systemic veins and arterioles), while the same rank differences in heart rate responses occurred following stimulation with the beta receptor agonist isoproterenol (which selectively works at the heart). These data were obtained from animals stressed by anesthetization, known to cause considerable glucocorticoid secretion in this population. Such steroids are well known for their capacity to augment catecholamine action. In experiment III, we blocked endogenous glucocorticoid secretion with the steroidogenesis inhibitor metyrapone, and repeated the epinephrine challenge. Under these conditions, the rank differences in epinephrine responsiveness were eliminated. Thus, dominant males are not so much preferentially sensitive to catecholamine action, as much as to the potentiating effects of glucocorticoids upon such action. In agreement, we have observed previously that dominant males are also more sensitive to glucocorticoid negative feedback regulation. © Wiley-Liss, Inc. |
