Acute Effect of Propranolol on the Growth Hormone (GH) Response to GH-Releasing Hormone in Patients with Hyperthyroidism

Giustinal, A; Mg, Buffoli; Ferrari, C; Gazzoli, N.; Pizzocolo, G; Tassi, Carla; Wb, Wehrenberg

doi:10.1055/s-2007-1003740

Cited by 6 publications

(5 citation statements)

References 7 publications

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“…The mechanism by which the elevation in the serum concentration of thy roid hormones inhibits GH secretion remains to be explained. Recently, we have shown that in hyperthyroid patients pretreatment with the P-blocker propranolol en hances the GH response to GHRH (1-29)NH, [25], On the basis of these results it has been hypothesized that GH inhibition in hyperthyroid patients is mediated, at least in part, as in patients treated with glucocorticoids [26], by an increase in the hypothalamic secretion of somatostatin. However, it cannot be excluded that hyperthyroxinemia may inhibit GH secretion directly at the pituitary level.…”

Section: Discussionmentioning

confidence: 95%

Acute Effects of Clonidine and Growth-Hormone-Releasing Hormone on Growth Hormone Secretion in Patients with Hyperthyroidism

et al. 1991

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Patients with hyperthyroidism have reduced growth hormone (GH) responses to pharmacological stimuli and reduced spontaneous nocturnal GH secretion. The stimulatory effect of clonidine on GH secretion has been suggested to depend on an enhancement of hypothalamic GH-releasing hormone (GHRH) release. The aim of our study was to evaluate the effects of clonidine and GHRH on GH secretion in patients with hyperthyroidism. Eight hyperthyroid females with recent diagnosis of Graves’ disease (age range 20–55 years, body mass index range 19.2–26.2 kg/m²) and 6 healthy female volunteers (age range 22–35 years, body mass index range 19–25 kg/m²) underwent two experimental trials at no less than 7-day intervals: (a) an intravenous infusion of clonidine 150 µg in 10 ml of saline, or (b) a bolus intravenous injection of human GHRH (1–29)NH₂, 100 µg in 1 ml of saline. Hyperthyroid patients showed blunted GH peaks after clonidine (7.1 ± 1.7 µg/l) as compared to normal subjects receiving clonidine (28.5 ± 4.9 µg/l, p < 0.05). GH peaks after GHRH were also significantly lower in hyperthyroid subjects (8.0 ± 1.7 µg/l) as compared to normal subjects receiving GHRH (27.5 ± 4.4 µg/l, p < 0.05). No significant differences in the GH values either after clonidine or GHRH were observed in the two groups of subjects examined. Our data demonstrate that the GH responses to clonidine as well as to GHRH in patients with hyperthyroidism are inhibited in a similar fashion with respect to normal subjects. That clonidine is not able to reverse the blunted GH secretion in hyperthyroidism suggests that hyperthyroxinemia may either cause an increase in somatostatin release by the hypothalamus or block GH secretion acting directly at the pituitary level.

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Section: Discussionmentioning

confidence: 95%

Acute Effects of Clonidine and Growth-Hormone-Releasing Hormone on Growth Hormone Secretion in Patients with Hyperthyroidism

et al. 1991

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“…In our study, however, we did not find any differences in the GH response to GHRH before and after pblocker treatment. Previous reports have shown that both acute and chronic ,&blocker administration causes only small elevations in G H levels in response to hypoglycaemia or GHRH in hyperthyroid patients, with a lack of normalization of the altered response (Yeung, 1973;Nilsson et al, 1980;Giustina et al, 1991). An increase in the G H response to GHRH in hyperthyroidism was also observed after arginine infusion, which also inhibits hypothalamic somatostatin release, but the GH response was not normalized (Giustina et al, 1992).…”

Section: Dlscusslonmentioning

confidence: 97%

Low circulating IGF‐I levels in hyperthyroidism are associated with decreased GH response to GH‐releasing hormone

Ramos-Dias

Yateman

Camacho‐Hübner

et al. 1995

Clinical Endocrinology

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“…under chronic glucocorticoid treatment [28], Our data confirm that hyperthyroid patients have blunted GH responses to GHRH [9], The mechanism by which the elevation in the serum concentration of thyroid hormones inhibits GH secretion remains to be explained. We have shown that, in hyperthyroid patients, pretreat ment with the P-blocker propranolol enhances the GH response to GHRH ( 1-29)NH: [29], On the basis of these results, it has been hypothesized that GH inhibition in hyperthyroid patients is mediated, at least in part, as in patients treated with glucocorticoids [30], by an increase in the hypothalamic secretion of somatostatin.…”

Section: Discussionmentioning

confidence: 83%

Effect of Arginine on the GHRH-Stimulated GH Secretion in Patients with Hyperthyroidism

Giustina

Schettino²,

Bussi³

et al. 1992

Horm Res

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Patients with hyperthyroidism have reduced GH responses to pharmacological stimuli and reduced spontaneous nocturnal GH secretion. The stimulatory effect of arginine on GH secretion has been suggested to depend on a decrease in hypothalamic somatostatin tone. The aim of our study was to evaluate the effects of arginine on the GH-releasing hormone (GHRH)-stimulated GH secretion in patients with hyperthyroidism. Six hyperthyroid patients with recent diagnosis of Graves’ disease [mean age ± SEM, 39.2 ± 1.4 years; body mass index (BMI) 22 ± 0.4 kg/m²] and 6 healthy nonobese volunteers (4 males, 2 females; mean age ± SEM, 35 ± 3.5 years) underwent two experimental trials at no less than 7-day intervals: GHRH (100 µg, i.v.)-induced GH secretion was evaluated after 30 min i.v. infusion of saline (100 ml) or arginine (30 g) in 100 ml of saline. Hyperthyroid patients showed blunted GH peaks after GHRH (13.2 ± 2.9 µg/l) as compared with normal subjects (23.8 ± 3.9 µg/l, p < 0.05). GH peaks after GHRH were only slightly enhanced by arginine in hyperthyroid subjects (17.6 ± 2.9 µg/l), whereas, in normal subjects, the enhancement was clear cut (36.6 ± 4.4 µg/l; p < 0.05). GH values after arginine + GHRH were still lower in hyperthyroid patients with respect to normal subjects. Our data demonstrate that arginine enhances but does not normalize the GH response to GHRH in patients with hyperthyroidism when compared with normal subjects. We hypothesize that hyperthyroxinemia may decrease GH secretion, both increasing somatostatin tone and acting directly at the pituitary level.

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Acute Effect of Propranolol on the Growth Hormone (GH) Response to GH-Releasing Hormone in Patients with Hyperthyroidism

Cited by 6 publications

References 7 publications

Acute Effects of Clonidine and Growth-Hormone-Releasing Hormone on Growth Hormone Secretion in Patients with Hyperthyroidism

Acute Effects of Clonidine and Growth-Hormone-Releasing Hormone on Growth Hormone Secretion in Patients with Hyperthyroidism

Low circulating IGF‐I levels in hyperthyroidism are associated with decreased GH response to GH‐releasing hormone

Effect of Arginine on the GHRH-Stimulated GH Secretion in Patients with Hyperthyroidism

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