Vascular Responses to Sodium Arachidonate in Experimental Hypertension

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Abstract
Vascular responsiveness to sodium arachidonate (C 20:4) was characterized in 4 models of hypertension [deoxycorticosterone acetate (DOCA) hypertensive rats, 2 kidney-one clip (2K-1C) renal hypertensive rats, spontaneously hypertensive rats (SHR) and psychosocial hypertensive mice]. Isolated arterial strips (aorta, mesenteric artery, tail artery) were equilibrated under optimal resting tension in physiological salt solution for measurement of isometric force generation. Dose-response curves to arachidonate (10-10 to 10-4 g/ml) in arteries from DOCA and 2K-1C hypertensive rats were shifted to the left compared to those in arteries from control rats. In arteries from SHR and psychosocial hypertensive mice, the dose-response relationships were unchanged compared to normotensive values. Arteries from DOCA hypertensive and 2K-1C hypertensive rats developed greater maximal contractile responses to arachidonate than controls; maximal responses in arteries from SHR and psychosocial hypertensive mice were unchanged compared to normotensive values. Contractions to arachidonate were inhibited by indomethacin (0.5 and 5 .mu.g/ml) and by aspirin (5 and 50 .mu.g/ml). The fatty acid, oleate (C 18:1), had no effect on the contractile state of the arteries, whereas prostaglandin F2.alpha. caused contraction. Altered responsiveness to exogenous arachidonate in arteries from DOCA and 2K-1C hypertensive rats, but not in arteries from SHR and psychosocial hypertensive mice.