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Results for “PITUITARY HORMONES”

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At least 883 records · Page 49Linked to original sources
PubMed1986

Effect of receptor blockers (methysergide, propranolol, phentolamine, yohimbine and prazosin) on desimipramine-induced pituitary hormone stimulation in humans--I. Growth hormone.

In this report the effects of various receptor blockers on desimipramine (DMI)-induced growth hormone (GH) secretion in healthy male subjects are presented. Each trial consisted of two administrations: one of DMI i.v. alone and one of DMI i.v. in combination with the respective receptor blocker: methysergide (serotonin (5-HT) receptor blocker), propranolol (beta receptor blocker), phentolamine (alpha-1/alpha-2 receptor blocker), yohimbine (alpha-2 greater than alpha-1 receptor blocker), and prazosin (alpha-1 receptor blocker). DMI-induced GH stimulation was not significantly different after DMI i.v. alone (n = 12) than after three days' pretreatment with 12 mg methysergide p.o. in another group of subjects (n = 12). Following combined administration of DMI and propranolol (15 mg i.v.), GH secretion was significantly increased by 25 mg DMI (p less than 0.05) and 50 mg DMI (incomplete block design, n = 18). GH secretion was significantly lower (p less than 0.01) after DMI in combination with 60 mg phentolamine i.v. compared to that after administration of DMI alone in the same group (n = 12). Following 10 mg yohimbine i.v. in combination with DMI (n = 6), the DMI-induced GH increase was also significantly less (p less than 0.05) than that after DMI alone. The DMI-induced GH increase following DMI plus 1 mg prazosin p.o. (n = 12) was comparable to that after DMI alone. The results indicate that the GH-stimulating effect of DMI is primarily related to the ability of DMI to inhibit noradrenaline (NA) reuptake. Should serotonergic receptors be involved in the DMI-induced GH secretion at all, they transmit a positive stimulus. The alpha-1 receptors are most likely not (or not essentially) involved, whereas alpha-2 receptors affect the DMI-induced secretion positively, and beta receptors have an inhibitory effect.

Adolescent↗
PubMed1997

Abnormal effect of cigarette smoking on pituitary hormone secretions in insulin-dependent diabetes mellitus.

OBJECTIVE: We observed the effect of smoking two cigarettes on GH, AVP and cortisol secretion in patients with diabetes and normal subjects. DESIGN AND PATIENTS: We tested 10 male smokers with insulin-dependent diabetes mellitus (IDDM) and 10 normal smokers. On a different occasion, normal and diabetic smokers were tested with an insulin (0.15 U/kg body weight) tolerance test (ITT). MEASUREMENTS: Hypoglycaemia-induced hormonal responses in smokers were compared with those observed in 10 diabetic and 10 normal non smokers. RESULTS: All subjects showed similar basal GH, cortisol and AVP levels. In the normal subjects, cigarette smoking induced a significant increase in circulating GH, AVP and cortisol levels, with mean peaks 3.3, 3 and 1.58 times higher than baseline, respectively. Smoking-induced hormonal responses were significantly higher in diabetics (mean peak was 5.2 times higher than baseline for GH, 4.0 for AVP and 1.83 for cortisol). Insulin induced a similar hypoglycaemic nadir in all subjects at 30 minutes, even though the diabetic subjects had a delayed recovery in blood glucose levels. GH and AVP responses to hypoglycaemia were significantly higher in diabetic (mean peaks 11.5 and 3.2 times higher than baseline, respectively) than in normal (mean peaks 7.3 and 1.9) non-smokers, whereas these groups showed similar cortisol responses (mean peak 2.3 times higher than baseline). Smoking did not change any hypoglycaemia-induced hormonal rise in the normal controls, whereas it significantly enhanced GH, AVP and cortisol levels (mean peaks 14.5, 4 and 3.8 times higher than baseline, respectively) in diabetics. CONCLUSIONS: In patients with IDDM, cigarette smoking not only elicits higher GH, AVP and cortisol responses than in normal subjects, but also enhances the counter-regulatory hormone responses to insulin-induced hypoglycaemia. These findings suggest interactions between nicotine inhaled with cigarette smoking and diabetes-induced neuroendocrine alterations.

Adult↗
PubMed1980

Opiate regulation of estradiol-2-hydroxylase in brains of male rats: mechanism for control of pituitary hormone secretion.

Treatment of male rats with a single high dose of morphine (10 mg/kg, subcutaneously) results in a dramatic suppression of brain estradiol-2-hydroxylase activity. The suppression is blocked by naloxone and is decreased upon the development of tolerance. The injection of naloxone (0.4 mg/kg) alone produces a significant increase in brain estradiol-2-hydroxylase activity over control levels. The effects of the opiate agonists and antagonists on the activity of this brain enzyme coincide in degree and direction with their effects on plasma lutropin (luteinizing hormone) concentrations. Because the 2-hydroxyestrogens were shown to induce pituitary lutropin release, the present results indicate that the action of opiates, endogenous or exogenous, on pituitary gonadotropin release can be mediated by brain catechol estrogens.

Animals↗
PubMed1975

Pituitary hormones in women with chronic renal failure: the effect of chronic intermittent haemo- and peritoneal dialysis.

Measurements of plasma prolactin (hPr), growth hormone (HGH), thyrotrophin (TSH), luteinizing (LH)--and follicle stimulating hormone (FSH) were performed in 20 women with chronic renal failure on regular dialysis. There was no significant difference in any of the hormone levels before and after the dialysis and no significant influence of the type of dialysis (haemodialysis and peritoneal dialysis) or the time of dialysis. Higher levels of plasma prolactin was found in the women on peritoneal dialysis than in the haemodialyzed women presumably due to the medical treatment. In the peritoneally dialyzed group four women had irregular menstruations and normal gonadotrophic levels, but elevated hPr and it is suggested that this finding is similar to that seen in the amenorrhoeagalactorrhoea syndrome, where hPr presumably in some way have antigonadotrophic actions at the gonadal level.

Adolescent↗
PubMed2006

[The role of some pituitary hormones in patients with non-insulin-dependent diabetes mellitus and diabetic retinopathy].

The level of somatotropin and thyreotropin hormones was measured in blood plasma of patients with non-insulin-dependent diabetes mellitus with and without diabetic retinopathy (DR). Fifty eight patients (26 males and 32 females) aged from 35 to 75 were examined. The patients were divided into two groups. First group included 29 patients (13 males and 16 females) with non-insulin-dependent diabetes mellitus without DR. Second group included the same number of patients with non-insulin-dependent diabetes mellitus complicated by DR. The concentration of somatotropin hormones was increased and thyreotropin was decreased in patients with non-insulin-dependent diabetes mellitus with DR. The results suggest that somatotropin and thyreotropin contributes to the development of diabetic retinopathy in humans.

Adult↗
PubMed1977

Estrogen action in vitro: regulation of thyroid stimulating and other pituitary hormones in cell cultures.

Primary cell cultures of ovine pituitaries can maintain production of thyroid stimulating hormone (TSH) for as long as 24 days. These cultures responded in a normal fashion to thyroxine by decreasing TSH secretion. Addition of thyrotropin releasing hormone increased TSH secretion. Physiologic levels of estradiol-17 beta (10(-11)-10(-9)M) produced a five-fold increase in secretion of TSH and a two-fold increase in intracellular TSH concentration in cell cultures. Common estrogens, but not common progestins, androgens and glucocorticoids affected TSH production. Markedly different effects of estrogen in the pituitary on follicle stimulating, luteinizing and thyroid stimulating hormones and prolactin are discussed in terms of current models of estrogen action.

Animals↗