Stimulation of Sodium Transport Across the Isolated Toad Bladder by 1α-Hydroxycorticosterone from an Elasmobranch

1969 ◽  
Vol 26 (7) ◽  
pp. 1823-1835 ◽  
Author(s):  
A. S. Grimm ◽  
M. J. O'Halloran ◽  
D. R. Idler
Keyword(s):  
Seasonal Variation ◽  
Sodium Transport ◽  
Toad Bladder ◽  
Elasmobranch Fish ◽  
Peripheral Blood Plasma ◽  
Raja Radiata ◽  
Mineralocorticoid Activity ◽  
Relative Potencies ◽  
Stimulation Of

The mineralocorticoid activity of 1α-hydroxycorticosterone, an interrenal steroid in elasmobranch fish, was determined by the in vitro toad bladder bioassay. It stimulated the transport of sodium across the toad bladder at concentrations of 10−6, 10−7, and 10−8 M. The elasmobranch steroid had approximately 80% of the activity of d-aldosterone; it was slightly less active than aldosterone and corticosterone at the lower concentrations. Protein binding alone does not seem to explain the relative potencies of the two steroids. The concentrations of 1α-hydroxycorticosterone required to stimulate sodium transport across the toad bladder are comparable with those reported in the peripheral blood plasma of Raja radiata and R. ocellata. A seasonal variation in the number of positive responses was observed.

Refractoriness of toad bladder to stimulation of sodium transport

1972 ◽  
Vol 223 (1) ◽  
pp. 104-109 ◽  
Author(s):  
SA Mendoza ◽  
F Murad ◽  
JS Handler ◽  
J Orloff
Keyword(s):  
Sodium Transport ◽  
Toad Bladder ◽  
Stimulation Of

The stimulation of sodium transport by aldosterone

1971 ◽  
Vol 262 (842) ◽  
pp. 323-332 ◽  
Keyword(s):  
Protein Synthesis ◽  
Active Transport ◽  
Sodium Transport ◽  
Apical Plasma Membrane ◽  
Transport Pathway ◽  
Receptor Sites ◽  
Rna And Protein Synthesis ◽  
Inhibitor Of Protein Synthesis ◽  
Stimulation Of

Aldosterone, the major sodium retaining hormone in man, will stimulate active transport of sodium across the urinary bladder of the toad, Bufo marinus in vitro , at physiological concentrations of the hormone.The in vitro action of aldosterone is mimicked by steroid hormones with known mineralocorticoid properties and it is competitively inhibited by other analogues, e.g. spironolactone and cortisone. Aldosterone is bound to physiological receptor sites within the transporting epithelial cells, chiefly within the nuclei, and is displaced from these binding sites specifically by structural analogues including other mineralocorticoids. Effects of aldosterone are dependent upon availability of metabolizable substrates to support the active transport of sodium. Although the stimulation of sodium transport by aldosterone can be specifically inhibited by actinomycin D, an inhibitor of RNA synthesis, and by puromycin, an inhibitor of protein synthesis, direct evidence of stimulation of new RNA and protein synthesis during the latent period with physiological concentrations of aldosterone is still lacking. It is possible, however, that the amounts of RNA and protein that are involved are too small to be detected by available techniques. Evidence is summarized which leads us to conclude that the increased sodium transport induced by aldosterone is the consequence of a reduced resistance of the apical plasma membrane of the transporting epithelia to the entry of sodium into the transport pathway.

Failure of 16,16-dimethyl PGE2 to prevent inhibitory effect of ethanol on sodium transport in canine gastric mucosa

1985 ◽  
Vol 248 (3) ◽  
pp. G299-G306
Author(s):  
T. A. Miller ◽  
J. M. Henagan ◽  
Y. J. Kuo ◽  
L. L. Shanbour
Keyword(s):  
Gastric Mucosa ◽  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Inhibitory Effect ◽  
Gastric Epithelium ◽  
Bathing Solution ◽  
Inhibitory Effects ◽  
Stimulation Of

By use of an in vitro canine gastric mucosal preparation, we evaluated the effects of ethanol (2, 4, 6, and 8%, vol/vol) and indomethacin (2.2 X 10(-4)M), with and without 16,16-dimethyl PGE2 pretreatment, on net sodium transport (JNanet) (mucosal to serosal) across gastric epithelium. Although administration of 2 or 4% ethanol to the mucosal bathing solution had no appreciable inhibitory effects on sodium transport, 6 and 8% ethanol and indomethacin significantly inhibited JNanet when compared with untreated control mucosa. This effect was accompanied by inhibition of transmucosal potential difference (PD) and short-circuit current (Isc). In other mucosae exposed to dimethyl PGE2 (8 X 10(-6) M) in the serosal bathing solution, significant increases in JNanet, PD, and Isc were noted when compared with control mucosa. Addition of 6 or 8% ethanol to the mucosal solution of dimethyl PGE2-pretreated tissue resulted in significant decreases in PD, Isc, and JNanet below control values that were not significantly different from mucosa exposed to 6 and 8% ethanol without PG pretreatment. When indomethacin was added to the mucosal solution following dimethyl PGE2 pretreatment, only slight decreases in PD and Isc below control levels were observed, and the inhibitory effects on JNanet induced by indomethacin without such treatment were abolished. These findings suggest that stimulation of JNanet by prostaglandin may play a role in its ability to prevent indomethacin damage to gastric epithelium but does not appear to be of importance in mediating protection against ethanol damage.

Na-K activated adenosine triphosphatase and sodium transport in toad bladder

1964 ◽  
Vol 207 (5) ◽  
pp. 1005-1009 ◽  
Author(s):  
Sjoerd L. Bonting ◽  
Mel Rose Canady
Keyword(s):  
Cyclic Amp ◽  
Atpase Activity ◽  
Sodium Transport ◽  
Toad Bladder ◽  
Active Sodium ◽  
Direct Stimulation ◽  
Sodium Potassium ◽  
Dependent Atpase ◽  
Atpase System

The effect of several agents in vitro on sodium transport by the intact toad bladder and on sodium-potassium activated, magnesium-dependent ATPase (Na-K ATPase) activity has been examined in an attempt to elucidate the relationship between the agents, the Na-K ATPase system, and active sodium transport. Ouabain and erythrophleine inhibited sodium transport and Na-K ATPase activity, but had no effect on sodium-potassium independent, magnesium-dependent ATPase (Mg-ATPase) activity. Vasopressin, adenosine 3',5'-monophosphate (cyclic-AMP), and aldosterone had no effect on Na-K ATPase or Mg-ATPase activity. The results are compatible with the assumption that the Na-K ATPase system is closely related to the active sodium pump, and that ouabain and erythrophleine inhibit sodium transport by the bladder through inhibition of the Na-K ATPase system. The stimulatory effect on sodium transport of vasopressin, cyclic-AMP, and aldosterone is not due to direct stimulation of the Na-K ATPase system.

Mineralocorticoid activity of 19-nor-DOC and 19-OH-DOC in toad bladder

1981 ◽  
Vol 241 (5) ◽  
pp. E406-E409 ◽  
Author(s):  
R. D. Perrone ◽  
J. H. Schwartz ◽  
H. H. Bengele ◽  
S. L. Dale ◽  
J. C. Melby ◽  
...  
Keyword(s):  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Toad Bladder ◽  
Sodium Reabsorption ◽  
Sodium Retention ◽  
Onset Of Action ◽  
Mineralocorticoid Activity

Adrenal enucleation is followed by a period of increased sodium reabsorption thought to be due to excess mineralocorticoid activity. However, it has not been demonstrated that increased production of any known mineralocorticoid accounts for this antinatriuresis. Recently, 19-hydroxydeoxycorticosterone (19-OH-DOC) was found in incubates of regenerating adrenal capsules 3-4 days postenucleation and 19-nordeoxycorticosterone (19-nor-DOC) was identified in the urine of rats with regenerating adrenals. Because it was possible that these hormones might play a role in the sodium retention after adrenal enucleation, we compared the mineralocorticoid activity of these steroids to aldosterone using the toad bladder. Using short-circuit current as a measure of sodium transport, we found that 19-OH-DOC (10(-8) M) had no significant effect on sodium transport. However, 19-nor-DOC (10(-8) M) increased sodium transport to a degree not different from aldosterone (10(-8) M). Furthermore, the onset of action, duration of activity, and inhibition of effect of 19-nor-DOC by spironolactone were not different from that of aldosterone. We conclude that 19-nor-DOC exhibits a significant effect on sodium transport and thus has the potential to play a role in the sodium retention following adrenal enucleation. Under the conditions of these studies, 19-OH-DOC exhibited no effect on sodium transport.

IDENTIFICATION OF FOUR TYPES OF STEROID BY THEIR INTERACTION WITH MINERALOCORTICOID RECEPTORS IN THE TOAD BLADDER

1970 ◽  
Vol 48 (4) ◽  
pp. 563-574 ◽  
Author(s):  
K. G. M. M. ALBERTI ◽  
G. W. G. SHARP
Keyword(s):  
Sodium Transport ◽  
Specific Binding ◽  
Biological Response ◽  
Toad Bladder ◽  
Receptor Interaction ◽  
Mineralocorticoid Receptors ◽  
Multiple Points ◽  
Specific Binding Sites ◽  
Receptor Sites

SUMMARY The effects of various steroids on sodium transport across the toad bladder were examined in vitro. Cortisone, alone, had no effect on sodium transport but was an antagonist of aldosterone. Cortisone was shown to bind to the two non-specific binding sites for steroids in the nucleus of the toad bladder epithelial cells when present at a concentration of 10−7m. At higher concentrations it interacted with the mineralocorticoid receptors and displaced aldosterone from these sites. Cortexolone had a weak stimulating effect on sodium transport and also antagonized the effect of aldosterone. Cortexolone, when present in excess, displaced aldosterone from its receptor sites. Four types of steroid could be differentiated by their interaction with the mineralocorticoid receptor sites and the subsequent biological response: (a) steroids that bind to the receptors and produce the full biological effect on sodium transport; (b) steroids that do not bind and therefore are incapable of producing a response; (c) steroids that bind to the receptor sites, have no effect alone but inhibit the action of aldosterone; (d) steroids that bind to the receptor sites, produce a partial response on sodium transport and subsequently antagonize the action of aldosterone. Multiple points of attachment are postulated for the steroid—receptor interaction.

INHIBITION BY MANGANESE OF THE ACTION OF ANTIDIURETIC HORMONE ON ADENYL CYCLASE IN TOAD BLADDER

1971 ◽  
Vol 50 (2) ◽  
pp. 231-235 ◽  
Author(s):  
S. HYNIE ◽  
G. W. G. SHARP
Keyword(s):  
Epithelial Cells ◽  
Water Flow ◽  
Arginine Vasopressin ◽  
Sodium Transport ◽  
Adenyl Cyclase ◽  
Toad Bladder ◽  
Inhibitory Effects ◽  
Marked Contrast ◽  
Hormonal Activation ◽  
Stimulation Of

SUMMARY In view of the report that Mn2+ stimulates sodium transport in the toad bladder but inhibits the effect of vasopressin on both water flow and sodium transport, the effects of this ion on adenyl cyclase from mucosal epithelial cells of toad bladder were investigated. Mn2+ was found to inhibit activation of adenyl cyclase by arginine vasopressin in the presence of Mg2+ and had no effect on activation of the enzyme by sodium fluoride. This is in marked contrast to the effects of Mn2+ on hormonal activation of adenyl cyclase from other tissues in which no inhibitory effects are seen and in which Mn2+ can replace Mg2+ in the reaction mixture. It is concluded that stimulation of sodium transport by Mn2+ is unlikely to be explainable by adenyl cyclase activation and that Mn2+ is not useful in the differentiation of the two forms of adenyl cyclase which are thought to be required for mediation of water flow and sodium transport stimulation by vasopressin.

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