Centrally-induced vasopressor responses to sodium-potassium adenosine triphosphatase inhibitor, ouabain, may be mediated via angiotensin II in the anteroventral third ventricle in the brain.

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Abstract
Central cardiovascular effects of the sodium-potassium adenosine triphosphatase (Na+, K+-ATPase) inhibitor, ouabain, were investigated by injecting it intracerebroventricularly (ICV) using conscious Wistar rats. Ouabain, 0.1-10 micrograms injected ICV, produced dose-related pressor responses attaining peak elevations after about 5 min. To investigate the underlying mechanisms of these central pressor responses, angiotensin II blockers were injected ICV before the injections of ouabain. 1-Sar, 8-Ile angiotensin II (ang IIa), 50 micrograms, given 3 min before the ouabain, abolished the pressor responses to ouabain, 5 micrograms. Angiotensin I converting enzyme inhibitor (CEI, captopril), 100 micrograms, also significantly attenuated the pressor responses to ouabain. Since previous results with ICV injections of ouabain suggested that the pressor responses are mediated via a release of brain angiotension II, and the site of action of brain angiotensin II is believed to be the anteroventral third ventricle (AV3V) area of the brain, ICV injections of ouabain were repeated using rats whose AV3V areas had been destroyed electrically. The pressor responses were smaller in the AV3V lesioned rats than in sham-operated rats. The abdominal sympathetic nerve activity was recorded using three conscious, normotensive Wistar rats. ICV injections of ouabain, 5 micrograms, elicited pressor responses as described above and these were accompanied by a corresponding increase in the nerve firing, lasting for 5-7 min. These responses were again abolished by pretreatment with an angiotensin II antagonist. These results suggest that centrally administered ouabain elicits vasopressor responses which increase peripheral sympathetic nerve activity.(ABSTRACT TRUNCATED AT 250 WORDS)

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