Toad

About: Toad is a research topic. Over the lifetime, 1624 publications have been published within this topic receiving 28732 citations.

Neurohypophyseal Hormone-Sensitive Adenyl Cyclase of Toad Urinary Bladder

Abstract: An adenyl cyclase preparation derived from epithelial cells of the urinary bladder of the toad, Bufo marinus, is described. This cyclase preparation is specifically stimulated by neurohypophyseal hormones and various synthetic analogs which evoke a hydroosmotic response in the intact bladder. The relative stimulatory effects of these compounds have been compared on the cyclase preparation and in the intact bladder. The peptide concentrations required for half-maximal stimulation (affinity) in the cell-free and intact systems were parallel; however the magnitude of stimulation produced by saturating concentrations of peptides did not correlate. Furthermore, it was found that peptide analogs which inhibit the hydroosmotic effect of [8-arginine]-vasopressin on the intact bladder also inhibit the stimulation of the toad bladder cyclase preparation by vasopressin. Prostaglandin E1, mercaptans, and disulfides, which inhibit the hormone-induced hydroosmotic response of the intact bladder, did not antagonize the stimulation of the toad bladder cyclase preparation by vasopressin.

Inhibition of vasopressin-stimulated water flow in toad bladder by phorbol myristate acetate, dioctanoylglycerol, and RHC-80267. Evidence for modulation of action of vasopressin by protein kinase C.

Abstract: The action of vasopressin (AVP) in transporting epithelia is mediated by cyclic AMP(cAMP), whereas its effects in hepatocytes are mediated by calcium and phosphoinositides Based on our recent observation that AVP stimulates phosphoinositide turnover in toad bladder, we examined the role of calcium-phospholipid-dependent kinase (protein kinase C) as a modulator of AVP's hydroosmotic effect Phorbol myristate acetate (PMA), which can substitute for diglyceride as an activator of protein kinase C, the diglyceride dioctanoylglycerol, and RHC-80267, a glyceride lipase inhibitor that should increase diglyceride levels, inhibited AVP-stimulated water flow, but not water flow stimulated by cAMP, suggesting inhibition of cyclic AMP production Both the dioctanoylglycerol and RHC-80267, but not PMA, also decreased water flow in response to 8-bromo cAMP indicating a potential inhibition at post-cAMP events as well PMA increased prostaglandin synthesis; however, inhibition of water flow persisted even when prostaglandin synthesis was completely blocked by incubation with naproxen Furthermore, water flow was not inhibited by incubation with the inactive diglyceride substitute phorbol didecanoate, supporting the specificity of the PMA inhibition Consistent with the site of action at adenylate cyclase suggested by the transport experiments, PMA and RHC-80237 decreased both cell cAMP content and the cyclic AMP-dependent kinase ratio (-cAMP/+cAMP), an index of intracellular cyclic AMP effect Assay for protein kinase C activity in toad bladder epithelial cell supernatant demonstrated that the toad bladder indeed contains a kinase stimulable by phospholipid, calcium, and PMA As an apparently independent effect, we found that addition of PMA, but not dioctanoylglycerol or RHC-80267, to the mucosal bath increased both water permeability and the frequency of granular cell luminal membrane aggregates in the absence of vasopressin, consistent with stimulation of fusion events at the luminal membrane Our data suggest that protein kinase C can modulate AVP-stimulated water flow in toad bladder by inhibiting cAMP generation, and perhaps post-cAMP steps as well, and support the hypothesis that AVP-stimulated turnover of membrane phosphoinositides antagonize the effects of AVP via changes in diglyceride, calcium, and protein kinase C

Effect of PGE1, indomethacin, and polyphloretin phosphate on toad bladder response to ADH

Abstract: and fo&hloretin phosphate on toad bladder response to ADH Am. 1974.-Exogenous PGEr inhibits the short-circuit current response, as well as the water permeability response of the toad bladder to vasopressin. Since PGEI does not inhibit either response to cyclic AMP, it is thought to act by inhibiting the effect of vasopressin on adenylate cyclase. Indomethacin, an inhibitor of prostaglandin synthesis, and polyphloretin phosphate, a prostaglandin antagonist, were used in an attempt to evaluate the rcle of enclogenous prostaglan-dins in the water permeability response to vasopressin. Both agents enhanced the response to vasopressin and to cyclic AMP. Although the enhancement may be related to decreased activity of endogenous prostaglandins and/or to inhibition of cyclic AMP breakdown by cyclic nucleotide phosphodiesterase, neither mechanism explains the effects of these agents in the presence of exoge-nous PGEl. Under these conditions, indomethacin had no effect on the response to vasopressin, but still enhanced the response to cyclic AMP; polyphloretin phosphate inhibited the response to vasoprecsin and had no effect on the response to cyclic AMP. cyclic *4MP; vasopressin; transport of sodium; permeability to water; cyclic nucleotide phosphodiesterase IT IS WELL ESTABLISHED that the sodium transport and the water permeability responses of the toad urinary bladder to vasopressin are mediated by the elevated concentration of intracellular cyclic AMP that results from stimulation of adenylate cyclase activity by the hormone (8, 18, 19). Indirect evidence gathered in many tissues indicates that prostaglandins affect adenylate cyclase activity (1 O), and in the toad bladder they inhibit the adenylate cyclase response to vasopressin (4, 13, 20). In view of this inhibi-tory effect, it has been suggested (7) that endogenous pros-taglandins act as modulators of the response to vasopressin. In this study, the effect of indomethacin, an inhibitor of prostaglandin synthesis (5, 25), and the efiect of polyphlore-tin phosphate, a prostaglandin antagonist (2, 3), were examined in order to elucidate the role of endogenous prostaglandins in the toad bladder response to vasopressin. The results, in part confirming those of others (6, 21), are such that the effects of these agents cannot be attributed solely to altered activity of endogenous prostaglandins. In addition, in contrast to an earlier report (13), it was found that PGEl inhibits the short-circuit current (SCC) response to vasopressin as well as the water permeability response to vasopressin. METHODS In each series of experiments, Rufo marinus of one geographic origin, either Colombia (The Pet Farm, Miami, Fla.) …