Hypertension, Vol 7, 262-267, Copyright © 1985 by American Heart Association
AF Sved, T Imaizumi, WT Talman and DJ Reis
Lesions of the nucleus tractus solitarius (NTS) were studied to determine
whether they elevate plasma vasopressin levels and, if so, whether these
elevated levels of vasopressin contribute to the hypertension caused by NTS
lesions. Bilateral electrolytic lesions of the NTS caused acute, severe
hypertension in rats anesthetized with chloralose and in conscious, freely
moving rats. After placement of the NTS lesions there was a greater than
tenfold elevation in plasma vasopressin levels. Administration of an
antagonist of the vasoconstrictor action of vasopressin markedly diminished
the hypertension in both conscious and anesthetized rats. Following
ganglionic blockade with chlorisondamine, NTS lesions still elicited
hypertension, and the magnitude of the hypertension was not different from
that observed in rats not treated with chlorisondamine. The hypertension
produced by lesions of the NTS in ganglionic-blocked rats was completely
abolished by administration of a vasopressin antagonist. These results
indicate that (1) NTS lesions elevate plasma vasopressin levels and (2)
elevated plasma vasopressin contributes to the hypertension produced by
such lesions.
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Vasopressin contributes to hypertension caused by nucleus tractus solitarius lesions
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