Effects of hormonal and electrical stimulation of sodium transport on metabolism of toad urinary bladder.
The carbon dioxide produced by toad urinary bladders bathed on their mucosal surfaces by sodium Ringer solution and on their serosal surfaces by modified Leibovitz tissue culture medium was analysed by multiple regression on both sodium transport and time. The fractions contributed by metabolism related to transport and by basal metabolism were assessed, and the extent to which these might vary with time was determined. This analytical method, which improves the accuracy with which suprabasal metabolism is estimated, was used to examine the effects on metabolism of vasopressin, aldosterone, and mucosa-positive voltage-clamping. Vasopressin (0.05 u./ml), which on average increased sodium transport 2.9 times and concurrently increased the rate of carbon dioxide production in these transporting tissues, also altered the carbon dioxide production of non-transporting, amiloride-treated control hemibladders. For each hemibladder the ratio of sodium transported to suprabasal carbon dioxide produced after vasopressin was compared with that observed before vasopressin. Differences between the ratios were much reduced when the carbon dioxide productions of the paired transporting hemibladders were corrected for the effects of vasopressin on basal carbon dioxide production. With such analysis, it was confirmed that vasopressin did not alter the stoichiometry of sodium transport. A 30 mV, mucosa-positive voltage clamp, applied near the peak of the response to vasopressin, further increased both sodium transport and carbon dioxide production. No alterations of the ratio of sodium to suprabasal carbon dioxide were seen under these conditions where the maximal rate of active sodium transport in this tissue must have been approached. Active sodium transport was more than doubled some 4 h after adding aldosterone (10(-7) M). However, the related increase in suprabasal carbon dioxide production was greater than threefold. Therefore, whereas the stimulation resulting from vasopressin and voltage clamping had no effect on the ratio of sodium transported to suprabasal carbon dioxide produced, this ratio was reduced significantly by aldosterone. When the sodium transport of aldosterone-treated bladders was increased further by voltage clamping, the ratio of sodium transported to suprabasal carbon dioxide production remained at the reduced value. Sodium transport was increased by approximately 35% more when aldosterone-treated hemibladders were voltage clamped after vasopressin, the control paired hemibladders being exposed to vasopressin and voltage clamping alone.(ABSTRACT TRUNCATED AT 400 WORDS)
D000450:Aldosterone / Q000494:pharmacology*; D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology; D001693:Biological Transport, Active / Q000187:drug effects; D002025:Bufonidae; D066298:In Vitro Techniques; D008564:Membrane Potentials; D009092:Mucous Membrane / Q000187:drug effects / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*; D013268:Stimulation, Chemical; D001743:Urinary Bladder / Q000187:drug effects / Q000378:metabolism*; D014667:Vasopressins / Q000494:pharmacology*
D014667:Vasopressins; D001127:Arginine Vasopressin; D000450:Aldosterone; D012964:Sodium