Stimulation of the kallikrein-kinin system by pregnancy may help restore renal vasodilator response to glycine in Dahl salt-sensitive rats.

To the Editor We would like to contribute to the discussion of possible mechanisms involved in the pregnancy-induced restoration of the renal vasodilator response to glycine in Dahl salt-sensitive rats reported by Whitescarver and Heesch in the December issue of Hypertension. We want to call attention to the role of renal kinins, postulated as mediators of amino acid-induced hyperperfusion and hyperfiltration by Jaffa and collaborators. They have demonstrated in rats that the effects of amino acid infusion on glomerular filtration rate, renal plasma flow, and renal vascular resistance are associated with an increased production of kinins. The changes in glomerular hemodynamics induced by the amino acid load could be blunted by bradykinin antagonists and by infusion of aprotinin, a tissue kallikrein inhibitor, which prevented the increase of urinary kinins.