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Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on August 24, 2004; DOI: 10.1124/jpet.104.075259

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Received for publication July 30, 2004.
Revised August 19, 2004.
Accepted for publication August 20, 2004.

Regional hemodynamic actions of selective CRF2 receptor ligands in conscious rats

Sheila Gardiner 1*, Julie March 1, Philip Kemp 1, Anthony Davenport 2, Katherine Wiley 2, Terence Bennett 1

1 University of Nottingham 2 University of Cambridge

* Address correspondence to: E-mail: sheila.gardiner{at}nottingham.ac.uk

Abstract

In conscious, male, Sprague-Dawley rats, we compared regional hemodynamic actions of the selective corticotropin-releasing factor type 2 (CRF2) receptor ligands, human and mouse urocortin 2 (hUCN2, mUCN2), with those of CRF. Bolus i.v. doses of 3 and 30 pmol kg-1 hUCN2, mUCN2, or CRF had no significant hemodynamic actions, but at doses of 300 and 3000 pmol kg-1, all 3 peptides caused dose-dependent tachycardia and hypotension, with rapid-onset, short duration, mesenteric vasodilatation, and slower-onset, more prolonged, hindquarters vasodilatation, but little or no change in renal vascular conductance. Pre-treatment with the non-selective CRF receptor antagonist, astressin, or the selective CRF2 receptor antagonist, antisauvagine 30, abolished all the cardiovascular actions of all 3 peptides. Indomethacin had no effect on responses to hUCN2, and there was no evidence for any involvement of NO in the vasodilator actions of hUCN2. There was no evidence that recruitment of angiotensin and endothelin-mediated vasoconstrictor mechanisms counteracted the vascular actions of hUCN2. The results indicate that the hemodynamic effects of i.v. hUCN2, mUCN2 and CRF depend on activation of CRF2 receptors and do not involve NO or prostanoids.


Key words: antisauvagine-30, astressin, corticotropin releasing factor, hemodynamics, human urocortin 2, mouse urocortin 2


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