Salt Lowers Pituitary Stress Response

Peptides. 1990 Jan-Feb;11(1):59-63.
Long-term salt loading impairs pituitary responsiveness to ACTH secretagogues and stress in rats.
Dohanics J, Kovacs KJ, Folly G, Makara GB.
Male Wistar rats were allowed to drink tap water ad lib (W), 2% saline (S) or 2% saline containing dexamethasone (S+D, 1 mg/l) for 7 days. On the 8th day rats were subjected to a 3-min ether stress. Plasma ACTH, corticosterone and prolactin concentrations were determined before and after ether exposure. Prestress concentrations of plasma ACTH were low and did not vary among the three groups. In response to ether stress W rats exhibited twice as high plasma ACTH concentrations as did S rats. Rats of the S+D group exhibited a small but statistically significant ACTH response. Plasma corticosterone concentration in S rats was increased while in S+D rats was significantly decreased under resting conditions compared to that in W rats. Ether stress caused large increases in plasma corticosterone concentrations in W and S rats while a small but statistically significant increase was observed in S+D rats. Prolactin responses to ether were smaller in groups S and S+D than in group W. To test whether the decreased ACTH response to ether exposure was a result of a decreased sensitivity of corticotrope cells to corticotropin releasing factor (CRF)-41 or arginine vasopressin (AVP), adenohypophysial fragments from W, S and S+D rats were incubated in the presence of different doses of CRF-41 or AVP. Pituitary fragments obtained from W rats secreted larger amounts of ACTH than did pituitaries from S rats in response to either CRF-41 or AVP. CRF-41 caused only a slight increase and AVP caused no significant increase in ACTH release from pituitary fragments obtained from S+D rats. These results indicate that prolonged osmotic stimulation impairs ACTH and prolactin but not corticosterone responses to ether stress. We suggest that the decreased sensitivity of corticotropes to CRF-41 and AVP is a possible mechanism that could account for the deficient ACTH response to ether stress in S rats.