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It was recently reported that factor H, a regulatory component of the alternative complement pathway, is stored with von Willebrand factor (VWF) in the Weibel-Palade bodies of endothelial cells. If this were to be the case, it would have therapeutic importance for patients with the atypical hemolytic-uremic syndrome that can be caused either by a heterozygous defect in the factor H gene or by the presence of an autoantibody against factor H. The in vivo Weibel-Palade body secretagogue, des-amino-D-arginine vasopressin (DDAVP), would be expected to increase transiently the circulating factor H levels, in addition to increasing the circulating levels of VWF.

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Kallikrein release from the kidney: in vitro effects of AVP and DDAVP in three species.

Arch Int Pharmacodyn Ther

August 1988

Department of Renal and Metabolic Medicine, St. Mary's Hospital, Portsmouth, U.K.

Kallikrein released during superfusion of rat, monkey and human kidney cortical slices was mainly in the inactive form. Arginine vasopressin and the nonpressor synthetic analogue des-amino-D-arginine vasopressin increased the release of inactive kallikrein to a similar extent in all species. No detectable change in active kallikrein release occurred.

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Bradykinin, angiotensin II, arginine vasopressin (AVP) or des-amino-D-arginine vasopressin (DDAVP) were administered by intravenous infusion to 10 healthy men. The concentration of 6-oxo-prostaglandin F1 alpha (6-oxo-PGF1 alpha), the stable hydrolysis product of prostacyclin (PGI2), was measured in plasma using gas chromatography/negative ion chemical ionisation mass spectrometry. Dose-related increases in plasma concentrations of 6-oxo-PGF1 alpha occurred during administration of bradykinin (100-3200 ng kg-1 min-1).

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