Kinin-induced prostaglandin synthesis by renal papillary collecting tubule cells in culture

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Abstract
Cells having morphological and histochemical properties of collecting tubules were isolated from rabbit renal papillae. Confluent monolayer cultures of these renal papillary collecting tubule (RPCT) cells formed hemicysts and adhered with morphological asymmetry to Millipore filters. Cultures of 1-day-old RPCT cells synthesized cAMP in response to arginine vasopressin (AVP) (half-maximal response at 10-10 M), oxytocin and parathyroid hormone (half-maximal responses at 5 .times. 10-9 M) but not to adrenergic agents. After 10 days of growth (4-fold increase in cell number), RPCT cells retained the same pattern of histochemical and hormonal responses as 1-day-old cells. Hormones were tested for their influence on the release of immunoreactive prostaglandins (iPG) by RPCT cells; the major product under both basal and stimulated conditions was iPGE2. At very low concentrations (.gtoreq. 10-10 M), bradykinin, lysyl-bradykinin and methionyl-lysyl-bradykinin caused 4- to 6-fold increases in the rate of iPGE2 formation within 3 min; smaller (< 2-fold) increases were observed with relatively high concentrations of epinephrine (10-5 M), norepinephrine (10-5 M), and angiotensin II (10-7 M), but only after longer incubations. Significantly, neither AVP (10-7 M) nor [deamino]AVP (10-7 M) caused PG release by RPCT cells. Apparently, kinins can act directly on the collecting tubule to elicit PGE2 formation; furthermore, this effect of kinins may be natriuretic, since PGE2 has been shown to inhibit Na+ resorption by the medullary collecting tubule and thick ascending limb.