Résumé
1 The involvement of cyclo‐oxygenase (COX) products and nitric oxide (NO) in contractile responses of resistance arteries to angiotensin II (AII) were investigated in small mesenteric arteries from spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) rats. 2 In endothelium intact vessels, AII induced concentration‐dependent responses without any significant difference between the two strains. However, removal of functional endothelium resulted in enhanced sensitivity to AII, the pD2 value increasing from 8.4 ± 0.2 to 8.9 ± 0.2 (P < 0.05) in WKY and from 8.2 ± 0.1 to 8.6 ± 0.1 (P < 0.05) in SHR (not significantly different between strains, n = 9–12). In addition, endothelium removal enhanced maximal contractions elicited by AII in SHR (1.4 ± 0.1 to 2.1 ± 0.2 mN mm−1, n = 5; P < 0.01) but not in WKY (1.0 ± 0.1 to 1.2 ± 0.1 mN mm−1, n = 5) vessels. 3 In the absence of functional endothelium, the COX inhibitor indomethacin (10−5 m) reduced contractile responses elicited by AII in SHR arteries, resulting in 33 ± 5% (n = 5) decrease in maximal contraction. However, it produced minimal if any, effect on responses of WKY vessels. In both strains, the TP receptor antagonist GR32191 B (3 × 10−6 m) did not modify contractions elicited by AII in these conditions. 4 In the presence of functional endothelium, indomethacin (10−5 m) almost abolished the responses to AII in both strains. GR32191 B (3 × 10−6 m) reduced the sensitivity of WKY arteries to AII (pD2 = 8.1 ± 0.1, P < 0.01) without any effect on maximal contraction. In SHR arteries, it markedly reduced maximal contraction (47 ± 3.5%). 5 In both strains, the NO synthase inhibitor NG‐nitro‐L‐arginine methy lester (L‐NAME; 10−4 m) had no effect in the absence of functional endothelium but it markedly reduced the inhibitory influence of endothelium on contractile responses to AII Furthermore, in arteries with endothelium, it reduced the effect of both indomethacin and GR32191 B to the same level as observed in vessels without functional endothelium. 6 The results suggest that enhanced contraction caused by COX products was counteracted by enhanced relaxation caused by endothelium‐derived NO in resistance mesenteric arteries of the SHR exposed to AII, compared to WKY arteries. The COX products involved in alterations of SHR responses comprised an endothelium‐derived prostaglandin activating TP receptors and another non‐endothelial unidentified vasoconstrictor compound which did not activate these receptors.