This is a proposal for continuing studies of neurogenic hypertension in the rat induced by asinoaortic denervation, SAD. Major objectives are to delineate plasma and tissue indices that reflect the state of sympathetic nervous activity and to determine what processes develop in the course of time to alter these indices. Specific studies will: 1. test the hypothesis that degradative enzyme activity and catecholamine metabolites increase in tissues and blood in the course of SAD hypertension and, 2. estimate degree of participation of the renin-angiotensin system. Sensitive radio-enzymatic assays will be used to measure plasma and tissue catecholamines, their metabolites, normetanephrine and dihydroxymandelic acid, and the degradative enzymes, catechol-O-methyl transferase and monoamine oxidase. Plasma and tissue dopamine beta hydroxylase activity will be measured by spectrophotometric method. Longitudinal studies in the same rats of plasma renin concentration and catecholamines will be made at intervals up to 6 months: effects on pressure of inhibitors of the renin-angiotensin system will be studied. Additional aims are: 1. to identify neurotransmitter changes in specific brain cells of SAD rats using punch techniques and microradioenzymatic assays and, 2. to determine the course, distribution and specific location of nerve terminals from baroreceptor afferents in the nucleus tractus solitarius by histochemical methods. Continuing studies will include: 1. effects of dietary sodium and adrenalectomy on the course of neurogenic hypertension and associated plasma indices, 2. investigation of a centrally located baroreceptor reflex mechanism unmasked by SAD from the difference in a centrally located baroreceptor reflex mechanism unmasked by SAD from the difference in blood pressure responses to pressor agents before and after small doses of pentobarbital and, 3. comparative studies of plasma and tissue indices of female SHR and female SAD rats.