Abnormalities in hypothalamic and neurohypophysial vasopressin content are not a consequence of XXXX in the spontaneously @entity101 @entity35 .

@entity101 @entity3371 @entity1951 @entity3449 @entity854 @entity35 @entity1063 @entity6659 @entity2955
In order to determine if the decreased hypothalamic and increased posterior pituitary content of @entity1951 (VP) observed previously in spontaneously @entity101 @entity35 (SHR) were a secondary consequence of the @entity101 , the effect of preventing the development of @entity101 on VP content of the hypothalamoneurohypophyseal system was evaluated. Two methods for preventing the @entity101 were used: (1) chronic angiotensin-converting enzyme inhibition (oral @entity3371 , 100 mg/kg/day at 4-12 weeks of age); and (2) intraventricular @entity2955 ( @entity2955 , 200 micrograms at 4 and 5 weeks of age). Both of these treatments markedly attenuated the increase in systolic blood pressure in SHRs at 5-11 weeks of age. The @entity3371 -treated @entity35 had a significant elevation in serum @entity3449 activity at 12 weeks of age indicating the presence of chronic converting enzyme inhibition, and the @entity2955 -treatment resulted in a depletion of hypothalamic (86%) and brainstem (76%) @entity1063 content. @entity6659 content was reduced in untreated SHRs compared to normotensive @entity35 -Kyoto @entity35 (WKYs, P = 0.0015). It was not significantly altered in either strain by the @entity2955 treatment. @entity3371 caused a @entity6659 content in both SHRs and WKYs (P less than 0.01). Posterior pituitary VP content was elevated in untreated SHRs compared to WKYs (P less than 0.001), and remained elevated with @entity3371 and @entity2955 treatments. These data indicate that the abnormalities in VP content in the hypothalamus and posterior pituitary of SHRs are not a response to the @entity101 . Therefore, they may represent @entity854 in the SHR.(ABSTRACT TRUNCATED AT 250 WORDS)
