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The overall goal of this research project deals with establishing whether hypertension, prolonged in nature and bearing hemodynamic, humoral and end-organ changes reminiscent of those described for either untreated human or experimental hypertension of genetic origin, can be produced in dogs by disrupting the anatomical integrity of vasodepressor pathways in the lower brain stem. To accomplish this aim we propose to interrupt the axonal flow of information in afferent fibers from the carotid sinus, aortic depressor and vagus nerves at a level in the tractus solitarii where these fibers first began to disperse into the nucleus of the tractus solitarii (nTS). This structure is known to contain the first relay station of the baroreceptor reflex. Current studies employing axonal transport of horseradish peroxidase (HRP) applied to the cervical vagus, carotid sinus and aortic depressor nerves have provided us with landmarks to carry out this procedure in mongrel dogs and also revealed that the electrolytic lesions can be placed bilaterally at a site where the procedure will no damage vagal efferent pathways. In conscious dogs instrumented beforehand with arterial and venous catheters and an electromagnetic flowmeter(s) to measure circulatory variables for several or 24 hours each day we will determine the short- (less than 7 days) and long-term (about 10 weeks) effects of bilateral nTS lesions to: 1) characterize the magnitude, persistence and hemodynamic features of the evolving hypertension; 2) establish with a variety of physiological and pharmacological procedures the relative roles of sympathetic and neuro-hormonal (i.e.; angiotensin II and vasopressin) mechanisms as co-participants in the hypertensive process; and 3) alternatively, uncover whether either technical (incomplete denervation) or peripheral and/or central adaptive processes are engaged in previous unsuccessful efforts to produce a model of neurogenic hypertension that is initiated by a primary imbalance of central nervous system function. In separate experiments, the procedure of central deafferentation will be used as a tool to characterize further the contribution of neurogenic factors to the pathogenesis of experimental renal hypertension (two kidney one clip). The data to be obtained in the proposed experiments will provide answers to two important questions: 1) How does the brain regulate arterial pressure? and 2) Can the brain mediate a sustained elevation in blood pressure?

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