Endothelin ETA receptors mediate the signaling and secretory actions of endothelins in pituitary gonadotrophs

Endocrinology. 1992 Jan;130(1):465-74. doi: 10.1210/endo.130.1.1309344.

Abstract

Specific receptors for endothelin (ET), localized by autoradiographic studies with [125I]ET in frozen sections of the rat pituitary gland, were abundant in the adenohypophysis, but not in the neurohypophysis. Specific binding of [125I]ET-1 and [125I]ET-3 was also demonstrable in 3-day-old primary cultures of anterior pituitary cells. The binding of [125I]ET-1 to its receptors was time and temperature dependent and was followed by rapid internalization of the receptor-ligand complex. Binding of [125I]ET-1 and [125I]ET-3 to pituitary tissues and cells was more effectively displaced by ET-1 and ET-2 than by ET-3. In cultured pituitary cells, ET-1 caused a rapid increase in polyphosphoinositide hydrolysis, and inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] production, with a prompt rise in the cytoplasmic calcium concentration ([Ca2+]i) and LH secretion. The Ins(1,4,5)P3 response to 100 nM ET-1 was transient, with a spike at 10 sec followed by an exponential decrease toward the low steady state level. Ins(1,3,4)P3 and inositol bisphosphate (InsP2) increased more slowly, reaching peak values 30-40 sec after stimulation. The kinetics of the [Ca2+]i response to ET-1 were similar to those of the Ins(1,4,5)P3 response and more rapid than those of the Ins(1,3,4)P3 and InsP2 responses. In perifused cells, ET-stimulated increases in LH release showed the same biphasic patterns as the Ins(1,4,5)P3 and [Ca2+]i responses. ET-1 was more potent than ET-3 in stimulating [Ca2+]i and LH responses, consistent with its higher affinity for the pituitary ET receptors. The initial activation of Ca2+ signaling and LH exocytosis by ETs was followed by prolonged refractoriness to both ET-1 and ET-3. The development of desensitization occurred more rapidly in ET-1- than ET-3-stimulated cells and correlated temporally with endocytosis of the receptor-ligand complex. These findings indicate that stimulation of gonadotropin release by ETs occurs via activation of ETA-type receptors, which are coupled to polyphosphoinositide hydrolysis and [Ca2+]i mobilization, and undergo rapid internalization and profound desensitization.

MeSH terms

  • Animals
  • Calcium / metabolism
  • Dose-Response Relationship, Drug
  • Endocytosis
  • Endothelins / metabolism
  • Endothelins / pharmacology*
  • Female
  • Inositol Phosphates / biosynthesis
  • Luteinizing Hormone / metabolism*
  • Pituitary Gland, Anterior / drug effects*
  • Pituitary Gland, Anterior / metabolism
  • Rats
  • Rats, Inbred Strains
  • Receptors, Cell Surface / physiology*
  • Receptors, Endothelin

Substances

  • Endothelins
  • Inositol Phosphates
  • Receptors, Cell Surface
  • Receptors, Endothelin
  • Luteinizing Hormone
  • Calcium