Effects of prostacyclin on short-circuit current and water flow in the toad urinary bladder

Abstract

The effects of prostaglandins of the E series on sodium and water transport have been studied extensively. PGE2 has been shown to inhibit the increase in osmotic water flow produced by vasopressin and to stimulate short-circuit current (SCC) in the toad bladder. On the other hand, the effects of prostacyclin (PGI2), an arachidonic acid product, on sodium and water transport have not been extensively evaluated. The present studies describe the effects of PGI2 on basal and vasopressin-stimulated osmotic water flow and on SCC in the urinary bladder of the toad. Studies were performed in the absence or presence of indomethacin. PGI2 in the absence of indomethacin had no effect on basal or vasopressin-stimulated osmotic water flow. When indomethacin was present, thereby eliminating intrinsic prostaglandin biosynthesis, PGI2 inhibited basal but not vasopressin-stimulated osmotic water flow. PGI2 increased SCC in the presence or absence of indomethacin. 6-keto PGF1 alpha, the stable metabolite of PGI2, had no effect on SCC. PGI2 stimulated cAMP production in isolated toad bladder epithelial cells. 2',5'-Dideoxyadenosine, an inhibitor of cAMP production, blocked the increase in SCC produced by PGI2, suggesting that the effects of this compound on SCC are mediated via cAMP.

Effects of prostacyclin on renal haemodynamics, renal tubular function and vasoactive hormones in healthy humans. A placebo‐controlled dose–response study

“…and Natov et al [7] included healthy control subjects. According to animal studies PGI 2 has a direct effect on The present study showed that prostacyclin infusion increased renal plasma flow, the plasma level of ANP, ANG II, and tubular water and sodium handling [1][2][3]. However, it is generally assumed that especially the prostaglandin E HR in healthy control subjects.…”

“…Some during PGI 2 infusion. Also, to our knowledge no information exists about the interaction between PGI 2 on the one hand affect the vascular bed, while others have their main effects on the renal tubular handling of sodium and water [1][2][3].The and renal haemodynamics, vasoactive and sodium and water regulating hormones on the other hand in healthy control prostaglandin analogue prostacyclin (PGI 2 ) has been shown to affect both renal and systemic haemodynamics in humans subjects. Therefore we have investigated the acute effect of [4][5][6][7], although the information is ambiguous regarding the effect on renal tubular handling of sodium and water.…”

Purinergic regulation of basal and arginine vasopressin-stimulated hydraulic conductivity in rabbit cortical collecting tubule

“…Our results also suggest the presence of a functional "P site" in the mammalian cortical collecting tubule. Thus, DDA, a known P site agonist (Londos & Wolff, 1977;Londos et al, 1980Londos et al, , 1983Daly, 1982;Pohlman, Yates, Needleman & Klahr, 1983), inhibited the Jv and Lp response to AVP. Inhibition of AVP-stimulated Jv and Lp was observed when DDA was given both prior to and following AVP exposure.…”