These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Differential modulation by basilar and mesenteric endothelium of angiotensin-induced contraction in canine arteries.
    Author: Yen MH, Sheu YZ, Chiou WF, Wu CC.
    Journal: Eur J Pharmacol; 1990 May 16; 180(2-3):209-16. PubMed ID: 2114297.
    Abstract:
    The contraction of ring segments of canine mesenteric and basilar arteries in response to angiotensins II and III was investigated. Removal of the mesenteric endothelium resulted in markedly intensified contraction in response to angiotensin II but did not affect the contractile response to angiotensin III. This angiotensin II-induced contraction was augmented by indomethacin (10(-5) M) and by methylene blue (5 X 10(-6) M) in the intact rings. These findings suggest that mesenteric endothelium modulates the vasoconstriction induced by angiotensin II but not that induced by angiotensin III. They also indicate that the mesenteric endothelium may contain relaxing factors such as prostacyclin or endothelium-derived relaxing factor as mediators. In contrast with mesenteric endothelium, removal of the basilar endothelium produced a much reduced contraction in response to either angiotensin. Acetylcholine, which caused a dose-dependent contraction in the basilar artery, elicited only a low-grade response if the functional endothelium was absent. These results suggest that basilar endothelium may release a contracting factor. It is possible that the main modulator of the peripheral arteries is a relaxing factor but that of the cerebral arteries is a contracting factor.
    [Abstract] [Full Text] [Related] [New Search]