Psychological stresses involving active coping have been shown to enhance sympathetic (SNS) activity on the heart and vasculature, increasing blood pressure (BP) temporarily; however, the role of stress in hypertension development is still unclear. The failure of the kidneys to maintain normal BP by excreting sufficient sodium and water may be either a primary or secondary cause of hypertension; sodium retention may contribute to hypertension in other ways as well. In dogs, our laboratory has found that stress reduces renal excretion of sodium and water, primarily by enhancing tubular reabsorption; this retention is abolished by systemic infusion of propranolol or by renal denervation. Recently, we demonstrated that mental stress evokes similar sodium and water retention in young men, but only in those with hypertensive parents and/or borderline hypertension who showed signs of high SNS response. This proposal is a continuation of these human studies, designed to reconfirm that stress-induced sodium retention is related to risk factors for human hypertension, and to determine: 1) whether this response in humans, like dogs, primarily involves increased reabsorption rather than decreased glomerular filtration; 2) whether stress-induced sodium and water retention is prevented by propranolol but not by timolo, a beta-antagonist lacking propranolol's central nervous system effects (including reduction of renal nerve activity); 3) whether retention is induced by natural stresses (college examinations); and 4) whether sodium retention and concurrent BP levels at rest and during stress increase when salt intake is high and decrease when salt intake is high and decrease when salt intake is low. Responses to questionnaires will be used to determine habitual exercise levels and personality patterns including Type A, suppressed hostility and John Henryism (which is based on preference for active coping despite difficulties); these measures may be related to SNS response to stress and thus to risk of hypertension.
