Cardiovascular sensitivity changes to eicosanoids in rats with experimentally induced diabetes mellitus

This paper attempts to provide a short review of the evidence for: 1. Increased platelet production of thromboxane A2 and reduced vascular production of prostacyclin in the human and also animal models of diabetes. 2. Reduced depressor responsiveness to arachidonic acid of anaesthetized alloxan- and...

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Published inClinical and experimental pharmacology & physiology Vol. 19; no. 1; p. 9
Main Authors Hodgson, W C, Sikorski, B W, King, R G
Format Journal Article
LanguageEnglish
Published Australia 01.01.1992
Subjects
Aldehyde Reductase - antagonists & inhibitors
Animals
Arachidonic Acids - metabolism
Arachidonic Acids - pharmacology
Blood Platelets - metabolism
Blood Pressure - drug effects
Diabetes Mellitus, Experimental - metabolism
Diabetes Mellitus, Experimental - physiopathology
Eicosanoids - pharmacology
Epoprostenol - metabolism
Rats
Thromboxane A2 - metabolism
Vasoconstriction - drug effects
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Summary:This paper attempts to provide a short review of the evidence for: 1. Increased platelet production of thromboxane A2 and reduced vascular production of prostacyclin in the human and also animal models of diabetes. 2. Reduced depressor responsiveness to arachidonic acid of anaesthetized alloxan- and streptozotocin-induced diabetic rats. 3. Enhanced constrictor responsiveness to arachidonic acid in blood-perfused hindquarters of alloxan-induced diabetic rats. 4. Potentiation by the thromboxane A2-mimetic, U46619, of constrictor responses to 5-hydroxytryptamine in Krebs'-perfused hindquarters and kidneys of both control and alloxan-induced diabetic rats. 5. Alterations during diabetes in production of, and responsiveness to, eicosanoids may contribute to the cardiovascular changes which occur in this disease.
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1992.tb00391.x