Abstract |
1. Arachidonic acid (AA, 0.125-1.0 mg/kg) injected via the aorta into the autoperfused hindquarters caused dose-dependent increases in perfusion pressure. This effect was reduced after intravenous administration of the thromboxane receptor antagonist AH23848 (5 mg/kg) or indomethacin (5 mg/kg). 2. Responses to AA (0.125-1.0 mg/kg) were reduced markedly in the Krebs-perfused hindquarters when compared with those occurring in the blood-perfused preparation. 3. Doses of guanethidine (1 mg/kg) and pentacynium (1 mg/kg) blocking pressor responses to intravenous administration of the ganglion stimulants McN-A-343 and DMPP, respectively, did not affect responses to AA. 4. Constrictor responses to AA (0.5-1.0 mg/kg) in blood-perfused hindquarters were increased in 14 day alloxan-diabetic rats but those to the thromboxane A2-mimetic U46619 (0.5-8.0 micrograms/kg, i.a.) were reduced when compared with non-diabetic controls. 5. In 14 day alloxan-diabetic rats vasoconstrictor responses to noradrenaline and methoxamine were potentiated but those to 5-hydroxytryptamine were reduced compared with non-diabetic animals. 6. It is concluded that AA causes constriction in the blood-perfused hindquarters by release of a product of cyclo-oxygenase acting on thromboxane A2-receptors. A constituent of blood, perhaps the platelet, appears necessary for this effect. Conversion of AA to the constrictor metabolite is augmented during experimentally induced diabetes.
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Authors | A L Boura, W C Hodgson, R G King |
Journal | Clinical and experimental pharmacology & physiology
(Clin Exp Pharmacol Physiol)
Vol. 14
Issue 5
Pg. 481-7
(May 1987)
ISSN: 0305-1870 [Print] Australia |
PMID | 3677485
(Publication Type: Journal Article)
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Chemical References |
- Arachidonic Acids
- Alloxan
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Topics |
- Alloxan
- Animals
- Arachidonic Acids
(pharmacology)
- Diabetes Mellitus, Experimental
(physiopathology)
- Hindlimb
(drug effects)
- Perfusion
- Pressure
- Rats
- Vasoconstriction
(drug effects)
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