Wayne Leebaw - Academia.edu (original) (raw)
Papers by Wayne Leebaw
The Journal of Clinical Endocrinology and Metabolism, Oct 1, 1977
The site, hypothalamic and/or pituitary, for dopaminergic inhibition of prolactin (PRL) secretion... more The site, hypothalamic and/or pituitary, for dopaminergic inhibition of prolactin (PRL) secretion is unknown. Consequently, the effect of central dopamine (DA) augmentation on stimulated PRL release was determined in 5 healthy men. Regular insulin (o.1 U/kg i.v.), a potent central stimulus for PRL secretion, and TRH, a direct hypophyseal stimulus, were given alone or one hour after the third and fourth doses, respectively, of L-dopa plus the peripheral decarboxylase inhibitor, carbidopa (Sinemet 20/200 or 25/250 every 6 hours). PRL increased from 26.6 +/- 5.8 to 48.8 +/- 5.2 ng/ml (p less than 0.01) 40 minutes after insulin administration. In contrast, during Sinemet therapy the hypoglycemia-mediated PRL release did not occur, and the PRL levels were significantly lower than after insulin alone from 40 through 180 minutes. Following TRH, neither the maximal PRL rise (69.3 +/- 3.2, TRH alone vs 48.7 +/- 19.8 ng/ml, TRH + Sinemet) nor the maximal increment (37.5 +/- 5.5 vs 29.9 +/- 20.3 ng/ml) was significantly affected by Sinemet. It is concluded that central DA augmentation abolishes central but not peripherally mediated PRL release.
The Journal of Clinical Endocrinology and Metabolism, Sep 1, 1978
Although the role of the neurotransmitter, dopamine (DA), in the regulation of PRL has been well ... more Although the role of the neurotransmitter, dopamine (DA), in the regulation of PRL has been well documented, controversy exists regarding its participation in the regulation of the other pituitary hormones. Consequently, we infused DA into six healthy male subjects (ages 19-32) and studied its effects on both basal pituitary hormone levels and augmented hormonal release induced by insulin hypoglycemia (ITT), TRH, and gonadotropin-releasing hormone (GnRH). DA alone produced a modest though significant increase in GH concentration from 2.2 +/- 0.5 to 11.9 +/- 3.7 ng/ml (P less than 0.05) by 60 min, but the peak incremental GH response to ITT was significantly inhibited by DA (43.5 +/- 5.0 vs. 16.3 +/- 3.3 ng/ml; P less than 0.01). PRL concentrations fell during the DA infusion (20.4 +/- 3.0 to 10.6 +/- 1.5 ng/ml; P less than 0.02) at 235 min, and the PRL responses to both ITT and TRH were completely abolished. Although the basal LH and FSH concentrations were unaffected by DA, the incremental LH response to GnRH was inhibited (45.5 +/- 10.6 to 24.4 +/- 5.4 mIU/ml; P less than 0.05), while the FSH response was unchanged. DA significantly reduced the basal TSH concentration from 3.9 +/- 0.2 to 2.5 +/- 0.2 micro U/ml (P less than 0.01) at 230 min and blunted the peak incremental TSH response to TRH (6.0 +/- 1.5 vs. 2.9 +/- 0.9 microU/ml; P less than 0.01). DA had no effect on basal cortisol levels, the cortisol response to ITT, basal plasma glucose, or the degree of hypoglycemia after ITT. Our data provide new evidence that DA has an inhibitory as well as a stimulatory role in the regulation of GH secretion in normal humans. It inhibits centrally as well as peripherally mediated PRL secretion and blunts the LH response to GnRH. In addition, DA lowers both basal and TRH-mediated TSH release, confirming the reports of other investigators.
The Journal of Clinical Endocrinology and Metabolism, Sep 1, 1977
Abstract Although it has been known for many years that insulin-induced hypoglycemia causes growt... more Abstract Although it has been known for many years that insulin-induced hypoglycemia causes growth hormone (GH) and cortisol secretion in man, its effects on prolactin (PRL) secretion have been variable. Consequently, we investigated the effects of alteration in ...
Metabolism-clinical and Experimental, Jul 1, 1978
... There was no significant difference among the maximal prolactin increments following insulin ... more ... There was no significant difference among the maximal prolactin increments following insulin (36.7 ± 7.9 ng/ml), TRH (46.4 ± 6.3 ng/ml), or chlorpromazine (63.4 ± 21.9 ng/ml). In patients with definite pituitary abnormalities, 28 of 38 had diminished PRL release after insulin. ...
Metabolism, 1978
... There was no significant difference among the maximal prolactin increments following insulin ... more ... There was no significant difference among the maximal prolactin increments following insulin (36.7 ± 7.9 ng/ml), TRH (46.4 ± 6.3 ng/ml), or chlorpromazine (63.4 ± 21.9 ng/ml). In patients with definite pituitary abnormalities, 28 of 38 had diminished PRL release after insulin. ...
The Journal of Clinical Endocrinology & Metabolism, 1977
Abstract Although it has been known for many years that insulin-induced hypoglycemia causes growt... more Abstract Although it has been known for many years that insulin-induced hypoglycemia causes growth hormone (GH) and cortisol secretion in man, its effects on prolactin (PRL) secretion have been variable. Consequently, we investigated the effects of alteration in ...
The Journal of Clinical Endocrinology & Metabolism, 1977
The site, hypothalamic and/or pituitary, for dopaminergic inhibition of prolactin (PRL) secretion... more The site, hypothalamic and/or pituitary, for dopaminergic inhibition of prolactin (PRL) secretion is unknown. Consequently, the effect of central dopamine (DA) augmentation on stimulated PRL release was determined in 5 healthy men. Regular insulin (o.1 U/kg i.v.), a potent central stimulus for PRL secretion, and TRH, a direct hypophyseal stimulus, were given alone or one hour after the third and fourth doses, respectively, of L-dopa plus the peripheral decarboxylase inhibitor, carbidopa (Sinemet 20/200 or 25/250 every 6 hours). PRL increased from 26.6 +/- 5.8 to 48.8 +/- 5.2 ng/ml (p less than 0.01) 40 minutes after insulin administration. In contrast, during Sinemet therapy the hypoglycemia-mediated PRL release did not occur, and the PRL levels were significantly lower than after insulin alone from 40 through 180 minutes. Following TRH, neither the maximal PRL rise (69.3 +/- 3.2, TRH alone vs 48.7 +/- 19.8 ng/ml, TRH + Sinemet) nor the maximal increment (37.5 +/- 5.5 vs 29.9 +/- 20.3 ng/ml) was significantly affected by Sinemet. It is concluded that central DA augmentation abolishes central but not peripherally mediated PRL release.
The Journal of Clinical Endocrinology & Metabolism, 1978
Although the role of the neurotransmitter, dopamine (DA), in the regulation of PRL has been well ... more Although the role of the neurotransmitter, dopamine (DA), in the regulation of PRL has been well documented, controversy exists regarding its participation in the regulation of the other pituitary hormones. Consequently, we infused DA into six healthy male subjects (ages 19-32) and studied its effects on both basal pituitary hormone levels and augmented hormonal release induced by insulin hypoglycemia (ITT), TRH, and gonadotropin-releasing hormone (GnRH). DA alone produced a modest though significant increase in GH concentration from 2.2 +/- 0.5 to 11.9 +/- 3.7 ng/ml (P less than 0.05) by 60 min, but the peak incremental GH response to ITT was significantly inhibited by DA (43.5 +/- 5.0 vs. 16.3 +/- 3.3 ng/ml; P less than 0.01). PRL concentrations fell during the DA infusion (20.4 +/- 3.0 to 10.6 +/- 1.5 ng/ml; P less than 0.02) at 235 min, and the PRL responses to both ITT and TRH were completely abolished. Although the basal LH and FSH concentrations were unaffected by DA, the incremental LH response to GnRH was inhibited (45.5 +/- 10.6 to 24.4 +/- 5.4 mIU/ml; P less than 0.05), while the FSH response was unchanged. DA significantly reduced the basal TSH concentration from 3.9 +/- 0.2 to 2.5 +/- 0.2 micro U/ml (P less than 0.01) at 230 min and blunted the peak incremental TSH response to TRH (6.0 +/- 1.5 vs. 2.9 +/- 0.9 microU/ml; P less than 0.01). DA had no effect on basal cortisol levels, the cortisol response to ITT, basal plasma glucose, or the degree of hypoglycemia after ITT. Our data provide new evidence that DA has an inhibitory as well as a stimulatory role in the regulation of GH secretion in normal humans. It inhibits centrally as well as peripherally mediated PRL secretion and blunts the LH response to GnRH. In addition, DA lowers both basal and TRH-mediated TSH release, confirming the reports of other investigators.
Acta Endocrinologica, 1978
Lergotrile mesylate, an ergot derivative and dopamine agonist, decreases basal (single sample) pr... more Lergotrile mesylate, an ergot derivative and dopamine agonist, decreases basal (single sample) prolactin levels and blunts phenothiazine-mediated prolactin release. To more thoroughly evaluate the effect of this drug, we measured prolactin and growth hormone concentrations hourly over 24 h in 5 healthy women and during insulin (0.1 U/kg) induced hypoglycaemia (ITT) in 6 women before and during 2-day lergotrile treatment. Lergotrile (4.0 to 6.0 mg/day) significantly decreased the mean 24-hour prolactin concentration in 3 and abolished the nocturnal rise in 4. For the entire group, the mean nocturnal levels (2400–0700 hours) were 24.0 #x00B1;7.5 vs 14.4 ± 3.9 ng/ml during waking (0800–2300 hours) pre-lergotrile (P<0.05), while during therapy the concentrations were 8.9 ± 2.8 vs 8.0 ± 1.4 ng/ml (NS), respectively. The prolactin response to ITT was also significantly inhibited by lergotrile with the peak response reduced from 78.2 ± 35.1 ng/ml to 9.0 ± 3.6 ng/ml (P < 0.05). The me...
The Journal of Clinical Endocrinology and Metabolism, Oct 1, 1977
The site, hypothalamic and/or pituitary, for dopaminergic inhibition of prolactin (PRL) secretion... more The site, hypothalamic and/or pituitary, for dopaminergic inhibition of prolactin (PRL) secretion is unknown. Consequently, the effect of central dopamine (DA) augmentation on stimulated PRL release was determined in 5 healthy men. Regular insulin (o.1 U/kg i.v.), a potent central stimulus for PRL secretion, and TRH, a direct hypophyseal stimulus, were given alone or one hour after the third and fourth doses, respectively, of L-dopa plus the peripheral decarboxylase inhibitor, carbidopa (Sinemet 20/200 or 25/250 every 6 hours). PRL increased from 26.6 +/- 5.8 to 48.8 +/- 5.2 ng/ml (p less than 0.01) 40 minutes after insulin administration. In contrast, during Sinemet therapy the hypoglycemia-mediated PRL release did not occur, and the PRL levels were significantly lower than after insulin alone from 40 through 180 minutes. Following TRH, neither the maximal PRL rise (69.3 +/- 3.2, TRH alone vs 48.7 +/- 19.8 ng/ml, TRH + Sinemet) nor the maximal increment (37.5 +/- 5.5 vs 29.9 +/- 20.3 ng/ml) was significantly affected by Sinemet. It is concluded that central DA augmentation abolishes central but not peripherally mediated PRL release.
The Journal of Clinical Endocrinology and Metabolism, Sep 1, 1978
Although the role of the neurotransmitter, dopamine (DA), in the regulation of PRL has been well ... more Although the role of the neurotransmitter, dopamine (DA), in the regulation of PRL has been well documented, controversy exists regarding its participation in the regulation of the other pituitary hormones. Consequently, we infused DA into six healthy male subjects (ages 19-32) and studied its effects on both basal pituitary hormone levels and augmented hormonal release induced by insulin hypoglycemia (ITT), TRH, and gonadotropin-releasing hormone (GnRH). DA alone produced a modest though significant increase in GH concentration from 2.2 +/- 0.5 to 11.9 +/- 3.7 ng/ml (P less than 0.05) by 60 min, but the peak incremental GH response to ITT was significantly inhibited by DA (43.5 +/- 5.0 vs. 16.3 +/- 3.3 ng/ml; P less than 0.01). PRL concentrations fell during the DA infusion (20.4 +/- 3.0 to 10.6 +/- 1.5 ng/ml; P less than 0.02) at 235 min, and the PRL responses to both ITT and TRH were completely abolished. Although the basal LH and FSH concentrations were unaffected by DA, the incremental LH response to GnRH was inhibited (45.5 +/- 10.6 to 24.4 +/- 5.4 mIU/ml; P less than 0.05), while the FSH response was unchanged. DA significantly reduced the basal TSH concentration from 3.9 +/- 0.2 to 2.5 +/- 0.2 micro U/ml (P less than 0.01) at 230 min and blunted the peak incremental TSH response to TRH (6.0 +/- 1.5 vs. 2.9 +/- 0.9 microU/ml; P less than 0.01). DA had no effect on basal cortisol levels, the cortisol response to ITT, basal plasma glucose, or the degree of hypoglycemia after ITT. Our data provide new evidence that DA has an inhibitory as well as a stimulatory role in the regulation of GH secretion in normal humans. It inhibits centrally as well as peripherally mediated PRL secretion and blunts the LH response to GnRH. In addition, DA lowers both basal and TRH-mediated TSH release, confirming the reports of other investigators.
The Journal of Clinical Endocrinology and Metabolism, Sep 1, 1977
Abstract Although it has been known for many years that insulin-induced hypoglycemia causes growt... more Abstract Although it has been known for many years that insulin-induced hypoglycemia causes growth hormone (GH) and cortisol secretion in man, its effects on prolactin (PRL) secretion have been variable. Consequently, we investigated the effects of alteration in ...
Metabolism-clinical and Experimental, Jul 1, 1978
... There was no significant difference among the maximal prolactin increments following insulin ... more ... There was no significant difference among the maximal prolactin increments following insulin (36.7 ± 7.9 ng/ml), TRH (46.4 ± 6.3 ng/ml), or chlorpromazine (63.4 ± 21.9 ng/ml). In patients with definite pituitary abnormalities, 28 of 38 had diminished PRL release after insulin. ...
Metabolism, 1978
... There was no significant difference among the maximal prolactin increments following insulin ... more ... There was no significant difference among the maximal prolactin increments following insulin (36.7 ± 7.9 ng/ml), TRH (46.4 ± 6.3 ng/ml), or chlorpromazine (63.4 ± 21.9 ng/ml). In patients with definite pituitary abnormalities, 28 of 38 had diminished PRL release after insulin. ...
The Journal of Clinical Endocrinology & Metabolism, 1977
Abstract Although it has been known for many years that insulin-induced hypoglycemia causes growt... more Abstract Although it has been known for many years that insulin-induced hypoglycemia causes growth hormone (GH) and cortisol secretion in man, its effects on prolactin (PRL) secretion have been variable. Consequently, we investigated the effects of alteration in ...
The Journal of Clinical Endocrinology & Metabolism, 1977
The site, hypothalamic and/or pituitary, for dopaminergic inhibition of prolactin (PRL) secretion... more The site, hypothalamic and/or pituitary, for dopaminergic inhibition of prolactin (PRL) secretion is unknown. Consequently, the effect of central dopamine (DA) augmentation on stimulated PRL release was determined in 5 healthy men. Regular insulin (o.1 U/kg i.v.), a potent central stimulus for PRL secretion, and TRH, a direct hypophyseal stimulus, were given alone or one hour after the third and fourth doses, respectively, of L-dopa plus the peripheral decarboxylase inhibitor, carbidopa (Sinemet 20/200 or 25/250 every 6 hours). PRL increased from 26.6 +/- 5.8 to 48.8 +/- 5.2 ng/ml (p less than 0.01) 40 minutes after insulin administration. In contrast, during Sinemet therapy the hypoglycemia-mediated PRL release did not occur, and the PRL levels were significantly lower than after insulin alone from 40 through 180 minutes. Following TRH, neither the maximal PRL rise (69.3 +/- 3.2, TRH alone vs 48.7 +/- 19.8 ng/ml, TRH + Sinemet) nor the maximal increment (37.5 +/- 5.5 vs 29.9 +/- 20.3 ng/ml) was significantly affected by Sinemet. It is concluded that central DA augmentation abolishes central but not peripherally mediated PRL release.
The Journal of Clinical Endocrinology & Metabolism, 1978
Although the role of the neurotransmitter, dopamine (DA), in the regulation of PRL has been well ... more Although the role of the neurotransmitter, dopamine (DA), in the regulation of PRL has been well documented, controversy exists regarding its participation in the regulation of the other pituitary hormones. Consequently, we infused DA into six healthy male subjects (ages 19-32) and studied its effects on both basal pituitary hormone levels and augmented hormonal release induced by insulin hypoglycemia (ITT), TRH, and gonadotropin-releasing hormone (GnRH). DA alone produced a modest though significant increase in GH concentration from 2.2 +/- 0.5 to 11.9 +/- 3.7 ng/ml (P less than 0.05) by 60 min, but the peak incremental GH response to ITT was significantly inhibited by DA (43.5 +/- 5.0 vs. 16.3 +/- 3.3 ng/ml; P less than 0.01). PRL concentrations fell during the DA infusion (20.4 +/- 3.0 to 10.6 +/- 1.5 ng/ml; P less than 0.02) at 235 min, and the PRL responses to both ITT and TRH were completely abolished. Although the basal LH and FSH concentrations were unaffected by DA, the incremental LH response to GnRH was inhibited (45.5 +/- 10.6 to 24.4 +/- 5.4 mIU/ml; P less than 0.05), while the FSH response was unchanged. DA significantly reduced the basal TSH concentration from 3.9 +/- 0.2 to 2.5 +/- 0.2 micro U/ml (P less than 0.01) at 230 min and blunted the peak incremental TSH response to TRH (6.0 +/- 1.5 vs. 2.9 +/- 0.9 microU/ml; P less than 0.01). DA had no effect on basal cortisol levels, the cortisol response to ITT, basal plasma glucose, or the degree of hypoglycemia after ITT. Our data provide new evidence that DA has an inhibitory as well as a stimulatory role in the regulation of GH secretion in normal humans. It inhibits centrally as well as peripherally mediated PRL secretion and blunts the LH response to GnRH. In addition, DA lowers both basal and TRH-mediated TSH release, confirming the reports of other investigators.
Acta Endocrinologica, 1978
Lergotrile mesylate, an ergot derivative and dopamine agonist, decreases basal (single sample) pr... more Lergotrile mesylate, an ergot derivative and dopamine agonist, decreases basal (single sample) prolactin levels and blunts phenothiazine-mediated prolactin release. To more thoroughly evaluate the effect of this drug, we measured prolactin and growth hormone concentrations hourly over 24 h in 5 healthy women and during insulin (0.1 U/kg) induced hypoglycaemia (ITT) in 6 women before and during 2-day lergotrile treatment. Lergotrile (4.0 to 6.0 mg/day) significantly decreased the mean 24-hour prolactin concentration in 3 and abolished the nocturnal rise in 4. For the entire group, the mean nocturnal levels (2400–0700 hours) were 24.0 #x00B1;7.5 vs 14.4 ± 3.9 ng/ml during waking (0800–2300 hours) pre-lergotrile (P<0.05), while during therapy the concentrations were 8.9 ± 2.8 vs 8.0 ± 1.4 ng/ml (NS), respectively. The prolactin response to ITT was also significantly inhibited by lergotrile with the peak response reduced from 78.2 ± 35.1 ng/ml to 9.0 ± 3.6 ng/ml (P < 0.05). The me...