Cellular mechanism of substance P in the regulation of corticosteroid secretion by newt adrenal gland.
In this work, we have studied the effects and the possible cellular mechanism of Substance P (SP) on corticosteroid secretion by the adrenal gland of the urodele crested newt, Triturus carnifex. Adrenals were in vitro superfused with SP, prostaglandin E2 (PGE2), nitric oxide (NO) donor, cyclic GMP (cGMP) analogue, and inhibitors of phospholipase A1, phospholipase A2 (PLA2), phospholipase C, adenylate cyclase (AC), cyclooxygenase (COX), NO synthase (NOS), and soluble guanylate cyclase (sGC). PGE2, corticosterone, and aldosterone release and NOS activity were determined. SP, PGE2, NO donor, and cGMP analogue increased corticosterone and aldosterone; SP and PGE2 increased NOS, and SP increased PGE2. PLA2, AC, COX, NOS, and sGC inhibitors counteracted SP and PGE2 effects, except for PLA2, which did not affect PGE2. These results suggest that SP exhibits a stimulatory role on the corticosteroidogenesis of T. carnifex adrenal gland. In particular SP enhances PLA2 activity, increasing PGE2; this prostaglandin affects AC, which, in turn, enhances NO, and the latter therefore affects sGC, with the consequent corticosteroidogenesis increase.
Gobbetti
A
A
Department of Molecular, Cellular, and Animal Biology, University of Camerino, Italy.
Zerani
M
M
D000305:Adrenal Cortex Hormones / Q000378:metabolism*; D000311:Adrenal Glands / Q000166:cytology / Q000378:metabolism*; D000450:Aldosterone / Q000378:metabolism; D000818:Animals; D003345:Corticosterone / Q000378:metabolism; D006152:Cyclic GMP / Q000031:analogs & derivatives / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D008958:Models, Molecular; D019001:Nitric Oxide Synthase / Q000378:metabolism; D013373:Substance P / Q000378:metabolism*; D014319:Triturus
D000305:Adrenal Cortex Hormones; D013373:Substance P; D000450:Aldosterone; D019001:Nitric Oxide Synthase; D006152:Cyclic GMP; D015232:Dinoprostone; D003345:Corticosterone