ADH response to peripheral and central cortisol administration

Cornette-Finn, Kuuleialoha M.
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Cortisol affects water balance, but whether this effect is mediated through antidiuretic hormone (ADH) is unclear. This study examines the response of plasma ADH (pADH) in two groups of conscious dogs; one received cortisol centrally (ivt) in the third ventricle at 300 ng/min, the other peripherally (iv) at 4.16 µg/kg/min, in 4 states of water balance, i.e., dehydration, normal hydration, 5% NaCl iv infusion (0.05 ml/kg/min), and after a water load (40 ml/kg given iv over 30 min), as compared to control experiments without cortisol. Cortisol, either ivt or iv, had no affect on pADH or plasma osmolality (pOsm) during dehydration or normal hydration. Ivt cortisol infusion caused a progressive decline in plasma cortisol (pCort) while iv cortisol infusion increased pCort (control 2.0 µg%, ivt pCort 0.5 µg%, iv pCort 17 µg%, P<0.01). During the 5% NaCl iv infusion, pADH and pOsm increased similarly in both the control and ivt cortisol experiments from 1.0 to 1.9 µU/ml and 295 to 305 mOsm/kg H2O, respectively (P<0.01). The increase in pADH seen with 5% NaCl infusion was delayed in the iv cortisol experiment as compared to the iv control (75 min versus 45 min, P<0.01). This delay was also seen in pOsm; 45 min in iv cortisol versus 15 min in iv control (P<0.01), indicating that the elevated pCort apparently delays the development of increased pOsm and the subsequent increase in pADH. During a water load, the cumulative urine excreted was 99% of that ingested with iv cortisol (P<0.05), 82% in the control, and 70% with ivt cortisol; in all three cases similar decreases in pADH and pOsm occurred. The free water clearance (FWC) was augmented in the iv cortisol infusion and attenuated in the opposite situation of pCort insufficiency which was established during the ivt cortisol infusion. Thus, the present study demonstrates that cortisol has a peripheral effect in that elevated plasma cortisol 1) delays the rise in pOsm during hypertonic saline infusion 2) increases FWC during a water diuresis but 3) does not alter the pADH versus pOsm relationship, therefore 4) affects the ability to excrete a water load independent of ADH. These data are compatible with a mechanism in which excess cortisol enhances the Na+ "leak" pathway of the cells by increasing the membrane permeability to Na+, thereby increasing the osmolar content of the cells.
Bibliography: leaves 135-147.
xiv, 147 leaves, bound ill. 29 cm
Vasopressin, Hydrocortisone
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