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We examined the role of bradykinin in the onset and/or the maintenance of blood pressure and renal blood flow in deoxycorticosterone acetate (DOCA)-salt hypertensive rats by using a competitive antagonist of bradykinin [Arg—Pro-Hyp-Gly—Thi–Ser–Dphe–Thi—Arg; Hyp, L-4-hydroxyproline; Thi, β-(2-theinyl-L-alanine)] The intravenous injection of the bradykinin antagonist (25, 50 and 100 µg) produced an increase in mean arterial pressure in all rats treated with tap water, 1% NaCI and DOCA + 1% NaCI. However, the magnitude of the increase in mean arterial pressure was significantly lower in the DOCA-hypertensive rats than in the two groups of rats drinking tap water and 1% NaCI after 4 and 6 weeks, but there was no significant difference after 2 weeks. The bradykinin antagonist induced a decrease in renal blood flow in all rats. However, the extent of the fall in renal blood flow was reduced in the DOCA-hypertensive rats compared with the control rats drinking tap water. These results suggest that endogenous bradykinin is depressed in the established phase of hypertension in DOCA-hypertensive rats. It is also suggested that endogenous bradykinin may counteract the elevation of vascular resistance in the early stages of this model.