title: Lesions of the anteroventral third ventricle and development of stress-induce hypertension in the borderline hypertensive rat.
abstract: The anteroventral third ventricle (AV3V) region plays a critical role in the pathogenesis of many forms of experimental hypertension. The present study sought to determine whether the integrity of this area was necessary for the development of stress-induced hypertension in the borderline hypertensive rat (BHR). Male BHRs were assigned to three groups at 8 weeks of age: 1) AV3V lesion, 2) sham lesion, and 3) maturation control. BHRs with AV3V and sham lesions were exposed to 12 weeks of conflict stress (2 hr/day, 5 days/wk). At the end of the conflict protocol period, direct measurement of resting mean arterial pressure indicated that BHRs with sham lesions had significantly higher blood pressure (153 +/- 2.9 mm Hg) than rats with AV3V lesions (126 +/- 5.2 mm Hg) and maturation control rats (133 +/- 4.3 mm Hg). Although AV3V lesions prevented stress-induced hypertension in BHRs, these rats were still capable of transiently raising blood pressure. Specifically, the results also indicate that BHRs with AV3V lesions showed greater increase in blood pressure in response to an electric foot-shock paradigm. This study suggests a critical role for this forebrain region in the production of stress-induced hypertension in genetically predisposed animals.
authors.affiliation: Department of Psychology, University of Iowa, Iowa City 52242.
authors.forename: B J
authors.initials: BJ
authors.lastname: Sanders
authors.forename: S
authors.initials: S
authors.lastname: Knardahl
authors.forename: A K
authors.initials: AK
authors.lastname: Johnson
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002552:Cerebral Ventricles / Q000473:pathology / Q000502:physiology*; D004597:Electroshock; D006339:Heart Rate; D006973:Hypertension / Q000209:etiology* / Q000235:genetics / Q000503:physiopathology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains / Q000235:genetics; D013312:Stress, Physiological / Q000150:complications* / Q000209:etiology