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1 Administration of bradykinin caused dose-dependent vasoconstriction in rat isolated perfused mesenteric arteries precontracted with noradrenaline.2 The vasoconstrictor response was not mediated by BK1-bradykinin receptors.3 Inhibition of cyclo-oxygenase with indomethacin, aspirin or meclofenamate abolished the vasoconstrictor effect of bradykinin, showing that a member of the arachidonic acid cascade may be involved. 4 Inhibitors of thromboxane synthesis (imidazole and UK 38485) did not affect or only reduced the bradykinin-induced vasoconstriction. 5 The endoperoxide H2/thromboxane A2 receptor antagonist SQ 29548 significantly reduced the vasoconstrictor effect of bradykinin, but did not affect the vasoconstrictor response to noradrenaline, adrenaline, vasopressin, 5-hydroxytryptamine or prostaglandins. 6 The eicosanoid(s) that mediate bradykinin-induced vasoconstriction appear to be synthesized outside the arterial endothelium. 7 The data suggest that the vasoconstrictor effect of bradykinin in the rat isolated mesenteric artery is mediated by vasoconstrictor arachidonic acid metabolites including the cyclic endoperoxides and/or the thromboxanes.

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THE co-existence of arterial hypertension and renal lesions has been observed for a long time. This fact has induced many investigators to attempt the production of arterial hypertension by experimental modification of the kidney. The methods used have been numerous and varied, e.g. surgical removal of part of the kidney, ligature of the renal artery or some of its branches, reduction of the calibre of the renal vein, ligature of the ureter, multiple emboli of the kidney, irradiation of the kidney, toxic nephritis, renal compression, etc. References to the principal experiments of this nature can be found in the articles by Braun-Menendez [1932], Goldblatt [1937] and Fasciolo [1938b].In 1927, with Biasotti, experiments were done on partial removal of the kidney, and in 1933 with Braun-Menendez on partial occlusion of the renal vein in the dog, but hypertension so obtained was generally inconstant and transient, therefore the experiments were discontinued. Eventually satisfactory and constant results were obtained using the technique of Goldblatt, Lynch, Hanzal & Sumerville [1934], compressing the renal artery and reducing its calibre by means of an adjustable forceps, which caused renal ischaemia and permanent hypertension with 50-100 mm. Hg rise above the initial blood pressure. The arterial tension generally rose from an initial level of 130-140 to 180-250 mm. Hg; 185 animals thus treated were studied.

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