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J Cabezas-Cerrato

Publications and source records attributed to J Cabezas-Cerrato.

At least 73 records · Page 4Linked to original sources
PubMed1984

Depending on the stimulus, central serotoninergic activation by fenfluramine blocks or does not alter growth hormone secretion in man.

The role of serotonin (5-HT) in the hypothalamic regulation of human growth hormone (GH) was reassessed through the use of fenfluramine, which selectively releases 5-HT from presynaptic terminals. Oral administration of L-dopa plus propranolol induced a potent and sustained GH release in the subjects tested (26 +/- 6 ng/ml). The administration of fenfluramine (20 mg i.v. as bolus plus 20 mg/30 min i.v.) completely suppressed the L-dopa-induced GH secretion (2 +/- 09.5 ng/ml). On the other hand, when arginine (30 g/30 min i.v.) was used as a GH stimulant of medium intensity (12.7 +/- 2.8 ng/ml), fenfluramine at the same dose was not able to alter the pattern of pituitary secretion (11.5 +/- 4.2 ng/ml). Fenfluramine alone induced a slight nonsignificant decrease in GH values with a parallel and significant increase in prolactin (PRL) secretion in accordance with the proposed serotoninergic activity of the drug. Rat PRL secretion by pituitaries incubated in vitro was inhibited by dopamine. Fenfluramine added to the system did not counteract the dopaminergic reduction of PRL release, making unlikely the possibility of an antagonism at the dopaminergic receptor as mechanism of action of fenfluramine on PRL secretion. In conclusion, depending on the stimulus under study, serotoninergic activation by fenfluramine either inhibits or does not alter GH secretion in man. No proof of a serotoninergic stimulatory component on GH regulation has been detected in this study. Fenfluramine is a valuable tool in neuroendocrinological studies, dealing with serotoninergic mechanisms.

Adult↗
PubMed1984

Cholinergic mediation of growth hormone secretion elicited by arginine, clonidine, and physical exercise in man.

The role of acetylcholine in human GH secretion was studied with atropine, which selectively blocks cholinergic muscarinic receptors and crosses the blood-brain barrier. Paired tests were performed in 22 normal subjects divided into 4 groups. The stimuli employed were arginine (30 g/30 min, iv), clonidine (300 micrograms, orally), physical exercise for 20 min, and saline. In the second test, atropine (1 mg, im) was administered before GH stimulation. Arginine elicited a GH secretory peak of 16.6 +/- 5 ng/ml (mean +/- SEM), which was completely blocked when atropine was administered with arginine (0.9 +/- 0.1 ng/ml). Atropine did not, however, modify the PRL secretory response; peak levels after arginine and atropine plus arginine were 16.3 +/- 3.1 and 16.8 +/- 2.5 ng/ml, respectively. Clonidine elicited a GH secretory peak (11.8 +/- 2.7 ng/ml) which also was blocked by pretreatment with atropine (1.2 +/- 0.2 ng/ml). Neither clonidine nor clonidine plus atropine altered PRL secretion. GH levels also were sharply increased after physical exercise, with a peak level of 19.4 +/- 4.9 ng/ml. Atropine completely blocked exercise-induced GH secretion (2 +/- 0.9 ng/ml). Atropine alone did not modify GH or PRL values compared with saline administration. The potency of the atropine-induced suppression of GH secretion by three different stimuli, each with presumably different mechanisms of action, suggests that acetylcholine plays an important role in the regulation of GH secretion.

Acetylcholine↗
PubMed1981

Free fatty acid inhibition of exercise-induced growth hormone secretion.

In order to investigate the effect of plasma free fatty acids (FFA) elevations on growth hormone (GH) secretion in humans, paired physical exercise (ph.e.) tests were performed in nine untrained healthy volunteers of both sexes. Ph.e. tests were accomplished on a bicycle ergometer under a moderate work load (450 kpm/min x 40 min). On one of two test days, subjects were given 60 gr of a soy bean oil emulsion (Intralipid) 3 hr before, followed by two 50 mg heparin bolus injection, administered 10 min before and 15 min after the start of the exercise. Ph.e. in the control group induced a clear-cut elevation of GH levels which peaks at 40 min. On the other hand Intralipid plus heparin induced FFA elevation, completely block GH secretion elicited by exercise (p less than 0.05 at 20 and 40 min). There also seems to be a threshold level of FFA (3 mEq/l) above which GH suppression was complete. On the contrary, below this level GH blockade was rather inconsistent. FFA elevation has been able to block all the GH stimuli tested so far, and this data support a role of plasma FFA in GH regulation.

Adolescent↗
PubMed1981

[Effect of phentolamine, diphenhydramine and cyproheptadine on arginine-induced growth hormone secretion (author's transl)].

Arginine stimulation test was performed on 36 healthy volunteers from both sexes, in order to determine whether alpha-adrenergic histaminergic or serotoninergic mechanisms was involved in growth hormone (GH) secretion. Arginine alone (30 gr/30 min) induced a clearcut GH response significantly different versus basal values in two different control groups. This response was accompanied by a slight, statistically non-significant, decrease in glucose and FFA levels. The concomitant administration of the alpha-adrenergic blocker phentolamine (0.5 mg/min x 90 min) did not alter the GH secretory pattern elicited by arginine. The addition of the H-1 histaminergic blocker diphenhydramine (50 mg i.v. as bolus 15 min before and 50 mg infused with arginine) completely suppressed the arginine induced GH secretion. Diphenhydramine, was also able to reduce GH basal values. Almost identical results were obtained with cyproheptadine, a serotoninergic, histaminergic and cholinergic blocker agent (2 mg q.i.d.; per os x 2 days and 4 mg per os 120 min before arginine). This drug suppressed arginine induced GH secretion without altering basal GH values. Blood glucose or FFA levels were not altered by any pharmacological manipulation vs. the control arginine group. It is concluded that either histaminergic H-1 or both histaminergic and serotoninergic blockade inhibit GH secretion elicited by arginine. On the other hand an alpha-adrenergic pathway in the arginine action is ruled out.

Adult↗
PubMed1980

[Lack of action of phentolamine, fenfluramine and cyproheptadine on the growth hormone secretion induced by glucagon (author's transl)].

The role of alpha-adrenergic and serotoninergic systems in the glucagon induced growth hormone (GH) release, has been investigated in 25 normal volunteers of both sexes divided into four groups. Group I received only glucagon (Gn) 1 mg s.c.; Group II received after Gn an phentolamine infusion over 150 min at the rate of 0.5 mg/min; Group III 30 min after Gn received fenfluramine 20 mg as a bolus injection, followed by another 20 mg infused over 90 min period; and Group IV after two days of treatment with cyproheptadine (2 mg p.o., q i d) received the last dose of 4 mg, 120 min before Gn administration. Gn elicited a clear-cut GH release in the four groups irrespective of treatment. GH peaked at 150 min and this elevation was significantly different from the basal values. No significant differences were present among the groups regarding GH, glucose or free fatty acid levels. These results suggest that the alpha-adrenergic and serotoninergic systems are not involved in the Gn induced GH release.

Adolescent↗