Send to

Choose Destination
See comment in PubMed Commons below
Vascul Pharmacol. 2007 May;46(5):373-82. Epub 2007 Jan 27.

Differential contributions of alpha-1 and alpha-2 adrenoceptors to vasoconstriction in mesenteric arteries and veins of normal and hypertensive mice.

Author information

Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824, USA.


Mesenteric veins are more sensitive than arteries to the constrictor effects of sympathetic nerve stimulation and alpha-adrenergic receptor agonists. In the present study, we tested the hypothesis that alpha(2)-adrenergic receptors (alpha(2)-ARs) contribute to in vitro agonist-induced constriction in veins but not arteries and that alpha(2)-AR function is down-regulated in mesenteric arteries and veins in deoxycorticosterone acetate-salt (DOCA-salt) hypertension. Norepinephrine (NE) concentration-response curves were similar in SHAM and DOCA-salt arteries and veins indicating that adrenergic reactivity of mesenteric blood vessels is not altered in murine DOCA-salt hypertension in vitro. Veins were 30-fold more sensitive to NE than arteries. The alpha(1)-AR antagonist, prazosin (0.003-0.3 microM), produced concentration-dependent rightward shifts of the NE concentration-response curves in arteries but not veins. The alpha(2)-AR agonists, clonidine and UK-14,304, did not constrict arteries or veins in the absence or presence of indomethacin (10 microM) and nitro-L-arginine (NLA; 100 microM). The alpha(2)-AR antagonists, yohimbine (0.003-0.3 microM) and rauwolscine (0.1 microM) did not affect NE responses in SHAM or DOCA-salt arteries but antagonized NE responses in veins. These data indicate that there are different alpha-AR contractile mechanisms in murine mesenteric arteries and veins. Alpha(1)-ARs, but not alpha(2)-ARs, mediate direct contractile responses in arteries and veins while alpha(2)-ARs contribute indirectly to NE-induced constrictions in veins but not arteries in vitro. There may be direct protein-protein interactions between alpha(1)- and alpha(2)-ARs or between their signaling pathways in veins. This contribution of alpha(2)-ARs may account for the greater sensitivity of veins compared to arteries to the contractile effects of NE.

[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center