Vasopressin-induced changes in permeability of peritoneal mesothelium for urea "in vitro".

Abstract

Vasopressin (ADH) acts in humans mainly upon renal collecting tubules. By changing their water permeability it plays a key role in regulation of renal water excretion. Acting upon vascular smooth muscle cells, it causes vasoconstriction and raised arterial blood pressure. This hormone was also proven to cause constriction of cultured mesangial cels, it causes vasoconstriction and raised arterial blood pressure. This urea (Seldin, Giebisch 1985), to release the natriuretic hormone as well as to stimulate hepatic glycogenolysis (Abramov et al. 1987). The influence of vasopressin upon peritoneal transport of solutes was studied, too. ADH influenced the passage of phosphate and rubidium through the isolated rabbit mesentery (Berndt, Gosselin 1961) as well as sodium flux through isolated rabbit omentum (Shear et al. 1966). It caused the drop in urea dialysance in dogs subjected to peritoneal dialysis (Henderson et al. 1971). The subject of our study was the assessment of the action of the antidiuretic hormone under "in vitro" conditions upon the peritoneal transfer of urea, the solute present in human body fluids and removable by peritoneal dialysis.