Essential Hypertension and Psychosomatic Research

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Abstract
Advances in psychosomatic research in essential hypertension are reviewed. These discoveries may have profound implications for psychosomatic research and theory. Basic physiological change in this disease was earlier considered an increase in peripheral resistance (PR). How social and psychological factors increased or sustained PR was not known. At the onset of some forms of essential hypertension the initial change seems to be in CO (cardiac output), not PR. PR rises as a physiological adaptation to the increased CO and the increased CO may be mediated by increased .beta.-adrenergic sympathetic drive on the heart, emanating from the brain. Different mechanisms may initiate essential hypertension in different forms of the disease. One mechanism may be a disturbance in the control of renin release. Brain stimulation, specifically of the medulla oblongata, increased, and stimulation of the anterior hypothalamus decreased, plasma renin activity [PRA]. At least 2 different mechanisms (other than increases in PR) were capable of raising blood pressure (BP) and were under direct CNS control. PRA was directly correlated with the level of angiotensin II activity, which, in addition to its peripheral effects (e.g., on the kidney, adrenal cortex and blood vessels), directly affected various areas of the brain in animals. It was a potent inducer of thirst and affected the lower brain stem to raise BP. Patients consumed 4 times as much salt per day in a free choice situation and drank more fluids per day, suggesting that raised angiotensin levels were influencing salt and fluid intake. A number of animal models showed various genetically determined disturbances in BP regulatory mechanisms. Behavioral studies should show whether elevated BP alters behavior.