Prostaglandin receptors and hormonal actions on water fluxes in cultured canine renal cells (MDCK line).

Abstract

SUMMARY1. An established cellular line (MDCK) derived from canine kidney showed specific binding for prostaglandin E2, both when the determination of specific binding was carried out in cells attached to a semipermeable support and when this binding was determined in suspended cells in a calcium-free medium.2. Specific binding for tritiated prostaglandin F2z was also observed, and it was inhibited by increasing concentrations of non-radioactive PGF. in a dose-related pattern. Cross-reactivity between PGE2 binding and PGF2 was present.3. Arginine-vasopressin induced an increase in the apical-to-basal water flux when applied to the basolateral surface. No change was observed when the hormone was in contact with the apical surface of the monolayer.4. Prostaglandin E2 also induced an increase in water flux, with a slower time course than that of arginine-vasopressin. The presence of PGE2 inhibited the increase in water flux induced by antidiuretic hormone.5. The results suggest that MDCK monolayers depict a physiological antagonism between ADH and prostaglandins which is similar to that observed in natural epithelia.

Chloride secretion stimulated by prostaglandin E1 and by forskolin in a canine renal epithelial cell line.

“…Madin-Darby canine kidney cells have previously been utilized as a convenient in vitro model system for the elucidation of some aspects of the cellular action of prostaglandins on renal epithelial cells (Martinez & Reyes, 1984;Aboolian et al 1989). Hassid (1983) in particular has demonstrated that exogenous PGE2 stimulates intracellular cyclic AMP accumulation in the presence of IBMX; in the present experiments, using MDCK cells of a defined phenotype (Rugg & Simmons, 1984b), this finding has been confirmed.…”

“…In the present studies an established cultured epithelium of high electrical resistance, derived from dog kidney (MDCK), has been used to investigate a possible cellular basis for prostaglandin action upon ion transport. Prostaglandin modulation of water fluxes (Martinez & Reyes, 1984) and of intracellular Ca21 (Aboolian, Molen & Nord, 1989) have previously been reported in this cell line. The MDCK epithelium is highly differentiated (Simmons, Brown & Rugg, 1984) and expresses antigens consistent with a tubular origin in the distal/collecting tubule (Herzlinger, Easton & Ojakian, 1982;Ojakian, Romain & Herz, 1987).…”

“…Prostaglandin modulation of water fluxes (Martinez & Reyes, 1984) and of intracellular Ca21 (Aboolian, Molen & Nord, 1989) have previously been reported in this cell line. The MDCK epithelium is highly differentiated (Simmons, Brown & Rugg, 1984) and expresses antigens consistent with a tubular origin in the distal/collecting tubule (Herzlinger, Easton & Ojakian, 1982;Ojakian, Romain & Herz, 1987).…”

Development of the Receptors to Prostaglandin E(2) in the Rat Kidney and Neonatal Renal Functions

“…They were kept in ice-cold Ringer (4 0 C) and gassed with 02/C02 (95 %/5 %) until the beginning of the experiment. The Ringer contained (mAf): NaCl 110; KC1 5; NaHCOs Tritiated PGE2 Uptake in the Presence of Indomethacin and PAH Incubation in the presence of indomethacin in tended to inhibit the synthesis of the endogenous PGs and thus avoid the interference of these PGs with the binding of 3H-PGE2 as has been shown in cultured renal cells [Martinez and Reyes, 1984]. Both PAH and indomethacin eliminated the uptake of radiolabelled PGE2 in renal cortical slices due to tubular secretion [Meléndez and Reyes, 1982], These two fac tors interferred with an adequate estimation of the binding sites to PGs in the kidney.…”