Plasma GH Responses Research Articles

Plasma GH Response to D- end L-Amphetamine in Monkeys

Plasma GH Response to D- end L-Amphetamine in Monkeys

Cortisol and GH responses to D- and L-amphetamine in monkeys.

Equimolar doses of D-amphetamine and L-amphetamine, and a water placebo were injected intravenously on different days into rhesus monkeys, and their plasma cortisol and GH responses were determined over a 3-hour period. D- and L-amphetamine (but not the placebo) equally suppressed plasma cortisol concentration and equally increased plasma GH concentration. Pretreatment of the monkeys with large doses of pimozide, a specific dopamine receptor blocker, did not appear to block the hormonal responses to either isomer of amphetamine. The results suggest that the hormonal responses to both D- and L-amphetamine were mediated by noradrenergic neurones stimulatory to GH and inhibitory to ACTH, and that D- and L-amphetamine exert equipotent noradrenergic effects in the neuroendocrine system.

Stimulation of rhesus monkey GH release: arginine vs plasma volume expansion.

Plasma GH and cortisol responses were examined in unanesthetized adult male rhesus monkeys infused with approximately 30 ml (8.3 ml/kg) of arginine monohydrochloride (Arg 0.5 g/kg), 0.9% saline (NS) or Dextran 75 and following 15 ml infusions of acid-saline (AS), or somatostatin (GHRIH 30 mug/kg). None of the infusions were accompanied by GH elevations. Rebound GH elevations occurred after each 30 ml infusion and after GHRIH but not after 15 ml AS. Although the amplitude of GH responses were not significantly different (p greater than 0.05), responses to Arg and dextran were significantly delayed as compared to responses following NS and GHRIH which did not differ from each other. Both of the latter responses occurred within 15 min of infusion completion. The delay following dextran was significantly longer than that following Arg (p less than 0.05). Since the volume of saline and the dosage of Arg were equivalent to those used in the standard intravenous Arg test, results suggest that effects of infusion volume upon GH secretion and upon GH responses to Arg warrant examination in the human. In addition, it is suggested that GH responses to NS and to dextran are mediated via an intravascular volume control mechanism and that GHRIH may be released upon activation of such a mechanism. GH elevations may represent rebound responses upon termination of GHRIH secretion.

Pituitary hormone response to brain stimulation in man.

Plasma cortisol, GH and LH responses to electrical stimulation of the orbital part of the frontal lobe and the cingulate area of the brain were studied in patients undergoing limbic leucotomy. In six out of 15 patients the plasma cortisol levels increased by 5-7--18-0 mug/100 ml after orbito-frontal stimulation whereas plasma GH values did not rise during this period. Plasma LH levels remained unchanged. No definite hormone responses could be attributed to stimulation of the cingulate area. It appears that the orbito-frontal area of the brain is concerned with augmenting the release of ACTH but not that of GH or LH.

Treatment of Cushing's disease with reserpine and pituitary irradiation.

Eighteen patients with Cushing's disease were treated with reserpine and pituitary irradiation. Complete remission was obtained in 9 out of 18 patients after reserpine treatment of 1-2 mg per day for a mean period of 20.4 months, and pituitary irradiation with a mean of 5,865 rads. In another 9 patients, reserpine 0.8-2 mg per day for a mean period of 22.5 months, and pituitary irradiation with a mean of 6,650 rads, were employed. Of these 9 patients, an additional subtotal adrenalectomy was carried out in 6 patients who are now in complete remission. Because of severe psychic symptoms resulted from the original disease in 2 of the remaining 3 patients, subtotal adrenalectomy was performed first and pituitary irradiation and reserpine treatment followed. Remission was eventually obtained in these 2 cases. One patient refused the operation, and thus had little clinical remission. All of the 17 cases in remission were followed up for periods of 6 months to 10 yr. During this time, only one case which had responded to reserpine and pituitary irradiation relapsed, but regained remission following resumption of therapy. Another died of cerebral glioblastoma 4 yr after remission of the disease. It was noteworthy that endocrinologic data including: plasma levels of ACTH and 11-OHCS, suppressibility by dexamethasone, responses of plasma GH to arginine and to insulin loads, and diurnal rhythm of plasma 11-OHCS were nearly normal in a considerable number of the cases in remission. Effectiveness of the combined therapy with reserpine and pituitary irradiation for treating Cushing's disease may support a working hypothesis that reserpine acts through some as yet unknown mechanism to correct a presumed central nervous disorder, while suitable pituitary irradiation probably corrects the pituitary dysfunction directly.

The pituitary ACTH, GH, LH, FSH, TSH and prolactin reserves in patients with Cushing's syndrome.

In order to know the pituitary reserves of ACTH, GH, LH, FSH, TSH and prolactin in patients with Cushing's syndrome, the responses of these hormones to hydrocortisone, lysine-8 vasopressin (LVP), insulin-induced hypoglycemia, luteinizing hormon-releasing hormone (LH-RH) and thyrotropin releasing hormone (TRH) were examined before and after treatment. Fourteen patients with Cushing's disease (adrenal hyperplasia), 3 patientswith adrenal adenoma and one patient with adrenal carcinoma were investigated. Before treatment, sufficient response of plasma ACTH to LVP was observed in patients with Cushing's disease, while no response was observed in 3 patients with adrenal adenoma. There was no significant difference in the responses of other pituitary hormones between the patients with Cushing's disease. and the patients with adrenal adenoma. The response of plasma GH to insulin-induced hypoglycemia was impaired in most these patients. The response of plasma TSH to TRH was impaired in 6 of 8 patients tested. The response of plasma LH and FSH to LH-RH were preserved in 6 and 5 of 8 patients, respectively. The response of plasma prolactin to TRH was normal in most patients tested. After treatment, the improvements of the impaired responses of GH, TSH, LH and FSH wereobserved. Therefore, the impaired reserve observed in these patients before treatment seemed to be due to the hypercortisolemia. If the difference of the suppressibility of these pituitary hormones by cortisol may be judged simply from our observation, the orderof the suppressibility is supposed to be ACTH, GH, TSH, LH and FSH, and then prolactin.

Evidence of GH deficiency in the Munich-Wistar rat.

The Munich-Wistar (MW) rat is typified by a renal abnormality in which some glomeruli are present on the kidney surface. Studies using these rats for micropuncture led to the chance observation that body growth was significantly retarded when compared to normal Wistar (W)rats. Plasma GH levels (as determined by radioimmunoassay) in nonstressed, decapitated rats were immeasurable (<1 ng/ml) in male MW rats (n= 10), compared to 33.5 ± 11.7 ng/ml in 10 controlanimals. In 10 female MW rats plasma GH levels were less than4 ng/ml; in 7 out of 10 animals values were less than 1 ng/ml. In contrast, normal female W rats had plasma GH levels of 22.1 ± 9.6 ng/ml. Pituitary GH concentration was significantly higher in both female (13.9 ± 1.9 vs 10.4 ± 1.0 μg/mg; p< .05) and male (22.1 ± 1.9 vs 15.7 ± 0.6 μg/mg; p <.01) MW rats. Plasma rolactin, TSH, T4 and corticosterone levels were normal. Plasma GH responses to hypothalamic e ectrical stimulation and to morphine administration were also normal in MW rats. It is pos...

Elevations in plasma growth hormone concentration after luteinizing hormone-releasing hormone (LRH) in patients with active acromegaly.

ABSTRACT Out of 16 patients with active acromegaly, 6 increased plasma GHafter LRH and 10 after TRH administration. These increases were unrelated to basal plasma GH levels and to plasma GH responses to insulin and arginine. Two patients who responded to LRH did not increase plasma GH after TRH. is suggested that these GH responses to non-specific releasing hormones may be due either to an alteration of the cellular membrane or to an extra-pituitary action, probably at a hypothalamic locus, of these peptides.

Plasma growth hormone response to thyrotropin-releasing hormone in patients with active acromegaly.

Out of 21 patients with active acromegaly, 12 increased plasma GH concentration after TRH injection (200 μg iv). No correlation was found between basal plasma GH levels, plasma GH response to hypoglycemia, arginine, oral glucose load and plasma GH response to TRH. The plasma GH peak often preceded that of TSH. One patient TSH unresponsive to TRH and 2 patients poorly responsive to TRH showed a rise in plasma GH. In 1 patient who increased both TSH and GH after TRH, the plasma TSH response was abolished by triiodothyronine administration, while that of plasma GH remained unchanged. Since it has been demonstrated that a releasing hormone acts activating the adenylcyclase system after binding to specific cellular receptors, it is suggested that in some functioning pituitary tumors the activity of TRH in promoting GH release may be attributed to an alteration of the cellular membrane. Another speculative possibility is that TRH acts at a hypothalamic rather than at a pituitary locus.

Plasma GH responses to hypothalamic, hippocampal and amygdaloid electrical stimulation: effects of variation in stimulus parameters and treatment with -methyl-p-tyrosine ( -MT).

Plasma GH responses, as measured by radioimmunoassay, were determined in individual pentobarbital—anesthetized rats following electrical, stimulation of several neural sites. Significant increments in plasma GH levels occurred with stimulation of the ventromedial hypothalamic nucleus, the hippocampus and the basolateral amygdala. Electrical stimulation of the corticomedial amygdala inhibited GH release. Effective stimulation parameters varied from one site to another. Trains of stimuli (5 sec on, 10 sec off) delivered for 2 min via monopolar electrodes placed bilaterally in the ventromedial nucleus were effective in eliciting GH release. Total stimulation periods of 10 and 5 min were required to elicit responses from hippocampus and basolateral amygdala, respectively, using unilateral bipolar electrodes. Current intensities of 500–700 μA were effective in the ventromedial nucleus provided long pulse durations of 1–2 msec were employed. Long pulse durations (1–2 msec) were necessary for eliciting GH releas...

Studies on the mechanism of pentobarbital-induced GH release in the rat.

Plasma GH responses, as measured by radioimmunoassay, were assessed in individual rats with indwelling jugular cannulae following administration of pentobarbital sodium (Pb) (50 mg/kg i.p.) Plasma GH

Responses of plasma ACTH, GH, LH and 11-hydroxycorticosteroids to various stimuli in patients with Cushing's syndrome.

The responses of pituitary hormones to insulin-induced hypoglycemia, lysine-8-vasopressin infusion and arginine infusion were examined in patients with Cushing's syndrome. In patients with adrenal hyperplasia, basal levels of plasma ACTH were slightly elevated and responses were preserved to both insulin-induced hypoglycemia and lysine-8-vasopressin infusion, though the magnitude of response was variable. All of the patients had an increase of plasma 11-hydroxycorticosteroids following lysine-8-vasopressin. After insulin-induced hypoglycemia, 11-hydroxycorticosteroids increased in only half of the patients. In patients with adrenal adenomas, plasma 11-hydroxycorticosteroid concentrations did not increase after insulin-induced hypoglycemia but there was a rise observed after lysine-8-vasopressin infusion. However, in patients with adrenal adenomas plasma ACTH was not detectable at any time during all of the studies. There was usually no increase of plasma GH concentration in response to any of the stimuli....

Pituitary response to insulin-induced hypoglycemia in obese subjects before and after fasting.

ABSTRACT Adrenocortical activity and hypothalamic-pituitary function were studied in 13 obese patients by means of insulin-induced hypoglycemia before and after a 10-day fast. Prior to fasting, plasma ACTH and cortisol responses to insulin tolerance testing (O.1 U insulin/kg) were normal but GH responses were significantly less (p <0.001) than observed in non-obese normal subjects. After fasting, plasma GH responses were not significantly changed but plasma ACTH and cortisol increments were markedly diminished (p <0.01). No significant fall in plasma cortisol, urinary 17-ketogenic steroid or free 11-hydroxycorticoid excretion was observed during fasting but there was a significant decrease (40%) in urinary 17-ketosteroid excretion. Plasma GH rose transiently during the first 4 days of fasting. It is postulated that, during prolonged fasting, actute hypoglycemia ceases to be an effective stimulus to ACTH secretion because of changes in intracerebral metabolism whereby substrate other than glucose meets ene...

Plasma growth hormone and plasma 11-OHCS in corticosteroid treated patients.

Plasma growth hormone and 11-OHCS in response to insulin hypoglycemia were determined simultaneously in corticosteroid treated patients. Long-term daily administration of corticosteroids, more than 800 tablets and longer than 6 months, had a marked inhibitory effect on GH secretion. Lower doses or shorter term administration on daily basis resulted in less suppression. Intermittent administration with various schedules usually had a less inhibitory effect than daily administration. In intermittently administered patients, better responses were observed in a group tested on off-day than in a group tested on on-day of corticosteroids. A single administration of 1-8 mg of dexamethasone to normal subjects at a midnight before a test had a variable effect on GH secretion. Plasma GH responses to arginine infusion were also suppressed by long-term and high-dose administration of corticosteroids. The suppression of GH seemed to go parallel with that of pituitary-adrenal axis determined by plasma 11-OHCS in corticosteroid treated patients.