In vitro effects of crude extracts of Parkia biglobosa (Mimosaceae), Stereospermum kunthianum (Bignoniaceae) and Biophytum petersianum (Oxalidaceae) on corticosteroid secretion in rat.

Previous studies conducted in guinea pig, rat and rabbit have revealed that crude extracts from Parkia biglobosa, Stereospermum kunthianum and Biophytum petersianum exert hypotensive and/or hypoglycemic activities. Since corticosteroids are involved in the control of arterial blood pressure and glycemia, we have investigated the possible effects of these plant extracts on rat adrenal tissue in vitro. Short-term administration of crude semi-ethanolic extracts of P. biglobosa and S. kunthianum to perifused rat adrenal tissue did not induce any significant changes in corticosteroid output. Conversely, the B. petersianum extract caused a dose-dependent increase in corticosterone and aldosterone secretion. Repeated infusions or prolonged administration of B. petersianum extract did not produce any apparent attenuation of the steroid response. Altogether, these data indicate that a semi-ethanolic extract of B. petersianum dose-dependently stimulates corticosterone and aldosterone secretion in rat without any desensitization phenomenon.

Vasopressin-responsive adrenocortical tumor in a mild Cushing's syndrome: in vivo and in vitro studies.

We report a case of a Cushing's syndrome caused by an autonomously secreting unilateral adrenocortical tumor, characterized by a clinically and biologically mild hypercortisolemic state and an unusual response pattern to vasopressin. Laboratory tests showed normal early morning plasma cortisol and 24-h urinary cortisol excretion, but lack of nycthemeral variations and suppressed plasma ACTH. Urinary cortisol excretion was not suppressed by either the low dose or the high dose dexamethasone test. Injection of lysine vasopressin, (10 IU, im) induced a marked increase in plasma cortisol, without an elevation of plasma ACTH. Computed tomography scan revealed an adrenocortical mass of the left gland with a contralateral atrophic gland. Removal of the tumor led to complete remission of Cushing's symptoms. In vitro studies were then performed to investigate the effect of arginine vasopressin (AVP) on calcium mobilization in cultured tumor cells using a microfluorimetric technique. Application of AVP in the vicinity of the cells induced a rapid and marked increase in the intracellular calcium concentration. Preincubation of the cells with the V1 vasopressin receptor antagonist [d(CH2)5,Tyr(OMe)2]AVP totally suppressed the AVP-induced stimulation of intracellular calcium concentration. Reverse transcription followed by polymerase chain reaction of tumor ribonucleic acid with specific oligonucleotides amplified high levels of V1 receptor signal compared with normal adrenocortical ribonucleic acid. Specific oligonucleotides for the V2 or V3 receptors amplified only a faint signal. This is the first report describing a mild case of Cushing's syndrome caused by an AVP-sensitive cortisol-producing adenoma. The direct effect of AVP on cultured tumor cells was mediated through the V1 type of vasopressin receptor, similar to that previously characterized in normal human fasciculata cells, suggesting that the tumor expressed an eutopic V1 AVP receptor and exhibited overresponsiveness to AVP.