Abstract
Abstract
The urinary bladder of Bufo marinus has been shown to excrete H+ and NH4 + and this excretion is increased by metabolic acidosis. The involvement of the adrenal gland and its steroid secretions in the adaptation for increased acid and ammonia excretion by the bladder was tested during the course of this study. Groups of toads were adrenalectomized and maintained in chronic NH4Cl-induced acidosis. Three other groups of toads were adrenalectomized and put in acidosis but repleted with 2.5 mg/day of either Cortisol (CT), dexamethasone (Dexa), or deoxycorticosterone acetate (DOCA). All control groups were sham-operated. The bladders were excised after 3 days and mounted between 2-ml Lucite chambers. Net H+ and NH4 + fluxes into the mucosal media were measured and reported in units of nanomoles per 100 mg bladder per minute. In control acidotic toads H+ excretion was 20.1 ± 2.0 and the adrenelectomized nonreplete group H+ excretion was 14.2 ± 1.87 (P < 0.04). For the same groups NH4 + excretion was 2.90 ± 0.26 for the controls and 1.38 ± 0.19 for the adrenalectomized (P < 0.001). The H+ excretion in CT-, Dexa-, and DOCA-repleted toads was not significantly different from the control group. NH4 + excretion, however, showed a 55% decrease (P < 0.001) in the CT group, and a 45% decrease (P < 0.05) in the Dexa group. The NH4 + excretion in the DOCA repleted group was significantly different from the control group. Therefore, we conclude that the adrenal gland plays a role in the adaptive increase of H+ and NH4 + excretion by the urinary bladder in acidosis through the secretion of steroid hormones. The increase in NH4 + excretion appears to be a mineralocorticoid-stimulated process. We were not able to determine in this study if the steroid hormones had an exacting regulatory role or one of a permissive role over H+ and NH4 + excretion in the toad urinary bladder.
Get full access to this article
View all access options for this article.