Several factors interact to maintain precise control of electrolyte transport in the mammalian cortical collecting duct. We have studied the effects of deoxycorticosterone, arginine vasopressin, and bradykinin on net transepithelial sodium and potassium transport in isolated, perfused rat cortical collecting ducts. Chronic administration of deoxycorticosterone to rats increased both sodium absorption and potassium secretion above very low basal levels. Consequently, deoxycorticosterone-treated rats were used for all remaining studies. Arginine vasopressin (10-10 M in the bath) caused a sustained fourfold increase in net sodium absorption and a sustained threefold increase in net potassium secretion. Bradykinin (10-9 M in the bath) caused a reversible 40-50% inhibition of net sodium absorption without affecting net potassium transport or the transepithelial potential difference. In the perfusate, up to 10-6 M bradykinin had no effect. We conclude: (a) As in rabbits, chronic deoxycorticosterone administration to rats increases sodium absorption and potassium secretion in cortical collecting ducts perfused in vitro. (b) Arginine vasopressin causes a reversible increase in net potassium secretion and net sodium absorption. (c) Bradykinin in the peritubular bathing solution reversibly inhibits net sodium absorption, possibly by affecting an electroneutral sodium transport pathway.

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(epsilon)-((gamma)-Glutamyl)lysine has been isolated from enzymatic hydrolyzates of cross-linked human fibrin. This compound was not detected in "non-cross-linked" fibrin prepared with ethylenediaminetetraacetic acid, which inhibits factor XIII; intermediate amounts were observed when the fibrin was prepared with glycine ethyl ester, which inhibits factor XIII competitively. These and ancillary experiments furnish conclusive evidence that epsilon-(gamma-glutamyl)lysine cross-links form in human fibrin during polymerization catalyzed by factor XIII.

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