English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Angiotensin II, when given into the vertebral arteries, acts at the area postrema to augment central sympathetic vasomotor activity. The mechanism of action is unknown but recent evidence implicates an interaction with the opiate system. In dogs anesthetized with chloralose either alone or in combination with morphine, naloxone blunted the pressor response to vertebrally administered angiotensin II by 50%. Addition of morphine to dogs anesthetized with chloralose only doubled the pressor response to identical doses of angiotensin II. On the other hand, the magnitude of the pressor responses to intravenously infused angiotensin II were unaltered by either naloxone or morphine. Likewise, responses to norepinephrine given vertebrally and intravenously were not similarly affected. Therefore, naloxone-induced changes in vascular responsiveness were not responsible for the altered sensitivity of the area postrema to angiotensin II following blockade of endogenous opiates. The data suggest that there exists a previously unrecognized interaction of the endogenous opiate system in the medulla in mediating the pressor effects of angiotensin II at the level of the area postrema.

Central opiate system modulation of the area postrema pressor pathway.