The proposed studies have been designed to (1) investigate the role of enhanced behavioral and cardiovascular responsiveness to sensory stimuli in hypertension, (2) determine, whether local brain angiotensin II (AII) and/or vasopressin (VP) participate in the central control of the behavioral and cardiovascular response patterns that are elicited by sensory stimuli, and (3) explore, whether a startle paradigm can be used to investigate the effects of defined sensory stimuli on the vasomotion of microvessels in the hamster skin. An acoustic and tactile startle paradigm will be used to determine the exact nature of the enhanced behavioral and cardiovascular responses to define sensory stimuli in spontenaouesly hypertensive rats (SHR) vs. their normotensive Wistar-Kyto (WKY) control strain. Special attention will be paid to the rate of habituation of the responses that may occur in both strains. Subsequently measures of the most prominent characteristics of the enhanced startle response in SHR, as defined in these experiments, will be subjected to a genetic consegregation analysis in crossbred segregating populations in order to establish a cause-and-effect relationsahip to genetic hypertension. The relationship between hyperresponsivity to startling sensory stimuli and primary hypertension in SHR will be further investigated by testing a non-genetic rat model of hypertension (2 kidney-1 clip renal hypertension), as well as young pre-hypertensive SHR and animals in the developing phase of hypertension. The possible involvement of central neuropeptides (AII, VP) in the mediation of normal and exaggerated behavioral and ardiovascular responses to startling sensory stimuli will be studied by chronic intracerebroventricular infusions of the peptides and their specific receptor antagonists in different models of hypertensive and normotensive rats. Hyperreactivity to emotionally disturbing stimuli has been postulated to be a causal factor in the pathogenesis of primary hypertension in animals and man. The results of the proposed studies will provide further inside in the relationship between phasic hyperreactivitity to sensory stimuli and the development of hypertension, and may help to establish a definite cause-and-effect relationship. Futhermore, the studies will yield important information as to the possible role for local brain AII and VP in the mediation of centrally integrated behavioral and cardiovascular response patterns. The application of the startle pardigm to studies on vasomotion in microvessels of conscious hamsters could open major new possibilities for future research.
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