HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Effect of a specific and a nonspecific vasodilator on regional blood flows in experimental heart failure.

Abstract
Urotensin I, a vasoactive peptide isolated from fish urophyses, has previously been demonstrated to cause specific mesenteric dilation in the dog. This mechanism of action should limit its maximal cardiovascular actions: no additional cardiovascular effects should ensure once maximal mesenteric vasodilation is achieved. Provided that the mesenteric vasodilatation does not result in decreased flow to other organs, the agent may, therefore, offer a theoretical advantage as an afterload reducing agent. In pentobarbital anesthetized dogs which were in heart failure as a result of chronic aortico -- left atrial shunt, the effects of urotensin I on cardiovascular hemodynamics were compared with the effects of a nonspecific vasodilator, sodium nitroprusside. At equidepressor doses (approximately 15% decrease in mean arterial pressure; sodium nitroprusside, 2 micrograms . kg-1 . min-1 i.v.; urotensin I, 10 mU . kg-1 . min-1 i.v.), both agents produced comparable falls in total peripheral resistance, left ventricular end diastolic pressure, and pulmonary capillary wedge pressure. Forward cardiac output was increased by both substances, although the increases were not statistically significant. Shunt flow, estimated by echocardiography, was reduced by both. In spite of the marked similarity in hemodynamic effects in this model, the two agents affected regional blood flows differently. Sodium nitroprusside did not significantly alter regional flows measured by radioactive microspheres, although calculated splanchnic, skin, and myocardial vascular resistances were reduced. In contrast, urotensin I, as in the normal dog, greatly increased mesenteric blood flow; this redistribution of cardiac output did not, however, result in underperfusion of other vital organs. These data suggest that urotensin I may be a useful agent in the reduction of afterload in heart failure, particularly since the unique mechanism of action appears to minimize the potential for adverse effects due to excessive dosage.
AuthorsK L MacCannell, G D Giraud, K Lederis, P L Hamilton, G Groves
JournalCanadian journal of physiology and pharmacology (Can J Physiol Pharmacol) Vol. 60 Issue 2 Pg. 174-83 (Feb 1982) ISSN: 0008-4212 [Print] Canada
PMID7083066 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Urotensins
  • Vasodilator Agents
  • Nitroprusside
  • urotensin I
Topics
  • Animals
  • Cardiac Output (drug effects)
  • Coronary Circulation (drug effects)
  • Disease Models, Animal
  • Dogs
  • Female
  • Heart Failure (physiopathology)
  • Hemodynamics (drug effects)
  • Male
  • Nitroprusside (pharmacology)
  • Regional Blood Flow (drug effects)
  • Urotensins (pharmacology)
  • Vasodilator Agents (pharmacology)

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: