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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.

The effect of thyroid hormone on renin productiona and release by rat kidney slices was studied. Rat kidney slices were incubated in Warburg flasks containing Krebs-Ringer-Phosphate- Glucose- Dextran solution at 37 C for 5 hours. Renin content, renin released into the incubation media and oxygen consumption were measured. Kidney slices actively secreted renin. Kidney slices of hyperthyroid rats released more renin, and kidney slices of hypothyroid rats released less renin than normal kidneys (p less than 0.001). The addition of 1-thyroxine to the incubation medium increased significantly (p less than 0.001) renin release by kidney slices from normal and hypothyroid rats. Thyroid hormone affects renin release through a mechanism independent of the ouabain-sensitive sodium pump and protein synthesis, since ouabain and cycloheximide did not modify renin release or production. The results of this study suggest that thyroid hormone plays a role in renin release from the juxtaglomerular cells.

The vasoconstrictor responses induced by noradrenaline (NA), adrenaline (AD), serotonin (ST) and vasopressin (VP) on the anterior mesenteric artery of the rat and its branches, were maintained, although somewhat reduced when perfused with a Ca free solution that depletes extracellular Ca. The vasoconstrictor responses were abolished when Lanthanum, EDTA, Verapamil or Nifedipine were added to the Ca free solution. These drugs are known to displace plasmalemmal bound Ca that triggers vasoconstriction when the agonists attach to the receptors thus blocking the vasoconstrictor responses. When the mesenteric arteries were perfused with a Ca containing solution, to block the vasoconstriction induced by the agonists the concentration of La3+, EDTA, Verapamil and Nifedipine must be raised. Thus these drugs appear to compete with extracellular ionic Ca for the membranal sites involved in the activity of the agonists. K induced vasoconstriction was abolished when extracellular Ca was depleted by a Ca free solution and with lower concentrations of the anticalcic drug than those used to cancel the effect of the agonists. Ca appears to be attached to voltage operated channels less firmly than to receptor operated channels. NA, AD, ST and VP showed different sensitivity to the blocking effect of the various anticalcic drugs. This is probably explained by small differences in the structure of the Ca channels operated by the agonists.