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INOSITOL PHOSPHOLIPID TURNOVER AND INTRACELLULAR Ca 2+ RESPONSES TO THYROTROPHIN‐RELEASING HORMONE, GONADOTROPHIN‐RELEASING HORMONE AND ARGININE VASOPRESSIN IN PITUITARY CORTICOTROPH AND SOMATOTROPH ADENOMAS
Author(s) -
LEVY A.,
LIGHTMAN S. L.,
HOYLAND J.,
MASON W. T.
Publication year - 1990
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1990.tb00467.x
Subject(s) - endocrinology , medicine , corticotropic cell , vasopressin , somatotropic cell , inositol , growth hormone–releasing hormone , biology , phospholipid , anterior pituitary , pituitary gland , hormone , receptor , biochemistry , growth hormone , membrane
SUMMARY We have studied the inositol phospholipid turnover response to thyrotrophin‐releasing hormone (TRH) gonadotrophin‐releasing hormone (GnRH) and arginine vasopressin (AVP) in five corticotroph and six somatotroph pituitary adenomas. GnRH (100 nM) increased inositol phospholipid turnover in five of five somatotroph adenomas tested by an average of 36.4 |Mp 9.4% (mean |Mp SE). In a fifth, which was too small to allow inositol phospholipid turnover to be assessed, GnRH produced a rapid increase in mean intracellular calcium ion concentration. Only one of five corticotroph adenomas responded to GnRH with an increase in inositol phospholipid turnover of 19%. In contrast, all the somatotroph and corticotroph adenomas tested (four of four and five of five respectively) increased inositol phospholipid turnover in response to AVP (100 nM), by an average of 61 |Mp 11.8% and 415 |Mp 186% respectively. The finding of an inositol phospholipid or intracellular Ca 2+ response to thyrotrophin‐releasing hormone (TRH) (100 nM) in three of five somatotroph adenomas (Ca 2+ increasing from 50 to 175 nM in one and inositol phospholipid turnover increasing by 172 |Mp 1.9% and 49 |Mp 5.2% in two) and to GnRH in all five somatotroph adenomas concurs with the common clinical finding of paradoxi‐cal growth hormone responses to these releasing factors in patients with acromegaly. The lack of such a response in three of the four corticotroph adenomas suggests that the appearance of GnRH and TRH receptors on adenomatous pituitary cells is not common to all cells.