Role of endothelium and nitric oxide in the response of equine colonic arterial rings to vasoconstrictor agents.
OBJECTIVE
To determine the in vitro contractile responses of equine colonic arteries to angiotensin II, histamine, serotonin, norepinephrine, prostaglandin F2 alpha, vasopressin, and a thromboxane-B2-analogue.


METHODS
The tension generated in colonic arterial rings placed in organ baths with oxygenated Tyrode's solution at 37 degrees C after exposure to the previously mentioned chemical agents was measured using force-transducers interfaced with a polygraph.


METHODS
Large colon arterial rings collected from eight horses.


METHODS
The rings were allowed to equilibrate for 45 minutes after applying 2 g tension. Bath solution was replaced and tension reapplied at 15-minute intervals. Cumulative-concentration-responses were determined for concentrations ranging from 10(-8) M to 10(-4) M on three vessel groups namely endothelium intact, endothelium denuded, and L-NAME treated. The maximal response for each vessel was considered as 100%; responses to lower concentrations were calculated as a percentage of the maximum. The EC50 value was determined for each concentration-response relationship of each agent.


RESULTS
Vessels with denuded endothelium or those incubated with L-NAME had greater contractile responses. Angiotensin, histamine, serotonin, and norepinephrine produced greater maximal responses than the other agents. Endothelium denuded rings had lower EC50 values. Responses to norepinephrine and serotonin were affected less by denudation.


CONCLUSIONS
Endothelium plays an important role in modulating responses of colonic arterial rings to contractile agents. Endothelium-derived vasodilators, other than nitric oxide, may modulate contractile responses of equine colonic arteries.


CONCLUSIONS
Endothelial damage associated with colonic vovulus may be a major factor for sustained reduced perfusion after surgical correction.
Venugopalan
C S
CS
Department of Veterinary Physiology, Pharmacology & Toxicology, School of Veterinary Medicine, Louisiana State University, Baton Rouge, USA.
Moore
R M
RM
Holmes
E P
EP
Sedrish
S A
SA
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000502:physiology; D003106:Colon / Q000098:blood supply*; D015237:Dinoprost / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000502:physiology*; D006632:Histamine / Q000494:pharmacology; D006736:Horses / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009638:Norepinephrine / Q000494:pharmacology; D012701:Serotonin / Q000494:pharmacology; D013931:Thromboxanes / Q000494:pharmacology; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D014667:Vasopressins / Q000494:pharmacology
D013931:Thromboxanes; D014662:Vasoconstrictor Agents; D014667:Vasopressins; D000804:Angiotensin II; D009569:Nitric Oxide; D012701:Serotonin; D006632:Histamine; D015237:Dinoprost; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester; D009638:Norepinephrine