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PubMed1986

Dynamics of thyrotropin-releasing hormone-induced thyrotropin and prolactin secretion by acutely dispersed rat adenohypophyseal cells. Evidence for 'all-or-none' secretion by heterogeneous secretory units, each with a specific response threshold.

We have examined the dynamics of thyrotropin-releasing hormone (TRH)-stimulated secretion of prolactin (PRL) and thyrotropin-stimulating hormone (TSH) using enzymatically dispersed rat adenohypophyseal cells suspended in a perfusion chamber with a volume of 0.2 ml to minimize mixing and dilution. One-min exposure to 3-300 nM TRH, the effective dose range, elicited immediate pulses of PRL and TSH secretion with dose-dependent amplitudes. At all TRH concentrations, following a brief burst of secretion lasting less than 1 min, release of both hormones declined precipitously. Increasing the duration of stimulation up to 30 min with half-maximal TRH concentrations did not alter the dynamics of the initial response and was ineffective in maintaining the initial amplitude of secretion. This phenomenon could not be attributed to exhaustion of readily releasable intracellular PRL and TSH, since an increment in TRH concentration elicited a second pulse of hormone secretion with temporal response characteristics identical to the first. The amplitude of the second pulse was dependent on both the initial concentration of TRH and the magnitude of the increment in TRH concentration. With a stepwise increase in TRH concentration during continuous perfusion, the sum of PRL or TSH secreted from all bursts of secretory activity approximated that achieved with a single exposure to the highest concentration of TRH employed. The high-amplitude secretory response to a given concentration of TRH was restored after an 8-min perfusion with medium alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Age-related differences in the spontaneous and thyrotropin-releasing hormone-stimulated release of prolactin and thyrotropin in ovariectomized rats.

Effect of estradiol on the spontaneous and thyrotropin-releasing hormone (TRH)-stimulated release of prolactin (PRL) and thyrotropin (TSH) in young and aged ovariectomized (Ovx) rats was investigated. Old (22-26 months) and young (3 months) female rats were Ovx 3 weeks before use. They were injected subcutaneously with estradiol benzoate (EB, 25 micrograms/kg) or sesame oil for 3 days and were catheterized via the right jugular vein. Twenty hours after the last administration of EB, rats were injected with TRH (10 micrograms/kg) through the catheter. Blood samples were collected before and 5, 10, 20, 40 and 60 min after TRH injection. On the day following blood sampling, all rats were decapitated. The anterior pituitary glands (APs) were excised, and incubated with or without TRH (10 ng/ml) at 37 degrees C for 30 min. The basal level of PRL concentration in plasma samples was 5-fold higher in old Ovx rats than in young Ovx rats. Five min after TRH injection, the increase in plasma PRL was greater in old animals than in young animals. Plasma PRL remained higher in old animals than in young animals at 10, 20, 40 and 60 min following TRH challenge. Administration of EB to old and to young Ovx rats produced increases in both basal and TRH-stimulated secretions of PRL, but did not affect the difference in plasma PRL patterns between old and young animals. The release of PRL from APs was increased significantly in all rats after a 30-min incubation with TRH. In Ovx rats injected with oil, the basal release of PRL in vitro was increased with age.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1989

Lidocaine inhibits dispersed anterior pituitary cell thyrotropin and prolactin secretion induced by thyrotropin-releasing hormone or high medium potassium.

Lidocaine at a concentration greater than or equal to 0.1 mM inhibited thyrotropin (TSH) and prolactin (PRL) secretion by perifused acutely dispersed rat adenohypophyseal cells stimulated by 10-100 microM thyrotropin-releasing hormone (TRH) or 30 mM K+. The concentration of lidocaine required for half-maximal inhibition of TSH and PRL secretion was approximately 1 and 0.5 mM, respectively. Maximal lidocaine inhibition of TRH-induced secretion was induced within 15 min and a normal response to these secretagogues returned within 20 min after removal of lidocaine from the perifusion medium. The inhibition of secretion by lidocaine may be caused by blocking depolarization of the cell membrane and depressing intracellular calcium mobilization and calcium influx across the plasma membrane.

Animals↗
PubMed1990

Release of thyrotropin and prolactin by a thyrotropin-releasing hormone (TRH) precursor, TRH-Gly: conversion to TRH is sufficient for in vivo effects.

The mechanism by which TRH-Gly (pGlu-His-Pro-Gly), a biosynthetic precursor of thyrotropin-releasing hormone (TRH, pGlu-His-Pro-NH2), stimulates pituitary thyrotropin (TSH) and prolactin release has been studied in urethane-anesthetized 2-month-old (250 g) male Sprague-Dawley rats and in vitro with GH3 cells, a rat anterior pituitary tumor cell line. We used specific radioimmunoassays to measure TRH-Gly and TRH levels in rat cortex, hypothalamus, medulla, eyes and whole blood as a function of the intracisternal (IC) dose of TRH and TRH-Gly administered 40 min prior to sacrifice. IC injection of 1.0 mg of TRH-Gly led to a significant (p less than 0.005) increase in the TRH levels in hypothalamus, medulla and blood. The relative potency of IC and intracardiac (IK) TRH and TRH-Gly release of rat TSH was compared by radioimmunoassay and further refined using estimates based on in vivo kinetics of TRH-Gly alpha-amidation. The binding of TRH-Gly to the plasma membrane receptors for TRH on GH3 cells was also investigated. In regard to TSH release, TRH-Gly given IC had only 0.042% of the potency of TRH given IC and was consistent with its rate of IC alpha-amidation. IK TRH-Gly had 0.16% of the potency of IK TRH of TSH release and was also consistent with its rate of intravascular conversion to TRH. The mean peak TSH response occurred at 20 min after IC TRH-Gly or IC TRH injection but the post-peak decline was slower for IC TRH-Gly.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Aspects of chronic oral treatment with thyrotropin-releasing hormone: the hypothalamic-pituitary-thyroid axis in rats. A study with a pharmacological dose of thyrotropin-releasing hormone.

The effects of 16 days of oral treatment with thyrotropin-releasing hormone (TRH, 1 mg/24 h) on serum levels of thyrotropin (TSH), thyroxine (T4) and triiodothyronine (T3) and the kinetics of TRH in the blood were studied in normal rats. A second group of animals served as controls. TRH was dissolved by sonification (10 mg/l) and was stable in tap water. TRH was measured by a radioimmunoassay procedure (normal range: 20-80 pmol/l, antiserum K2B9 1:120,000 final dilution). An increase in basal TSH (7,200 +/- 440 ng/l, mean +/- SD) was found after 2 days of treatment (11,420 +/- 810 ng/l), but a significant increase was observed after 5 days of treatment (12,530 +/- 640 ng/l, p less than 0.001). T4 serum concentrations remained in the normal range during the entire period of study, whereas T3 serum concentrations (0.76 +/- 0.1 micrograms/l) were increased to 1.22 +/- 0.2 micrograms/l on day 5 (p less than 0.001). A subsequent decline of TSH, T4 and T3 up to the end of the study was observed. TRHmax concentrations were registered on day 5 (790 +/- 24 pmol/l). The mean value of TRHmax was 723 +/- 34 pmol/l. To improve the stability of TRH in tap water, 1-ml samples of drinking water with dissolved TRH were measured. The mean TRH concentration in drinking water was 73 +/- 1.5% (SD). No significant correlations were found between the area under the curve of TSH (184,340 ng.l-1.24 h) and that of TRH (14,954 pmol.l-1.24 h).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Correlation among the changes in the levels of thyroid hormones, thyrotropin and thyrotropin-releasing hormone during the development of Xenopus laevis.

The influence of thyroid hormones on neurogenesis suggested that these hormones might affect the maturation and development of neural centers which ultimately regulate thyroid function. Changes in the levels of the thyroid hormones, thyrotropin and the thyrotropin-releasing hormone in 'brain' and 'thyroid' fractions were, therefore, correlated at several developmental stages. All hormones showed increases from their initial detection through metamorphosis. The thyroid hormones were observed earliest in both fractions. These data are consistent with the notion that thyroid hormones influence the maturation of the particular neural regions whose later function is the regulation of the hypophyseal-thyroid axis.

Animals↗
PubMed1986

Cardiopulmonary bypass: a low T4 and T3 syndrome with blunted thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH).

Thyroid hormone serum concentrations, the thyrotropin (TSH) and prolactin (PRL) response to thyrotropin-releasing hormone (TRH) were evaluated in patients undergoing cardiopulmonary bypass (CPB) conducted in hypothermia. During CPB a marked decrease of thyroxine (T4) and triiodothyronine (T3) concentration with a concomitant increase of reverse T3 (rT3) were observed similarly to other clinical states associated with the 'low T3 syndrome'. Furthermore, in the present study elevated FT4 and FT3 concentrations were observed. In a group of patients, TRH administered during CPB at 26 degrees C elicited a markedly blunted TSH response. In these patients, PRL concentration was elevated but did not significantly increase after TRH. The increased concentrations of FT4 and FT3 were probably due to the large doses of heparin administered to these patients. Thus, the blunted response of TSH to TRH might be the consequence of the elevation of FT4 and FT3 in serum, however, other factors might play a role since also the PRL response to TRH was blocked.

Adult↗
PubMed1978

Thyrotropin, prolactin and growth hormone response to synthetic thyrotropin-releasing hormone in newborn infants.

The effects of 50 microgram synthetic thyrotropin-releasing hormone (TRH) intravenously on thyrotropin (TSH), prolactin (PRL) and growth hormone (GH) levels were studied in 8 normal male newborns during the first hours of life. Mean plasma GH concentrations were similar to baseline values during the period of study; on the contrary, plasma PRL and TSH values increased in all infants after TRH administration. These data demonstrate a normal pituitary reserve of PRL and TSH in the early period of human life.

Growth Hormone↗
PubMed1972

Inhibition of thyrotropin response to thyrotropin-releasing hormone by small quantities of thyroid hormones.

Inhibition of thyrotropin (TSH) release by chronic treatment with small quantities of triiodothyronine (T(3)) and thyroxine (T(4)) was evaluated by determining the serum TSH response to thyrotropin-releasing hormone (TRH) in normal subjects and hypothyroid patients. Response to TRH was determined before treatment and after each dosage of a synthetic combination of T(3) + T(4) had been given for 3-4 wk. Treatment of eight normal subjects with 15 mug T(3) + 60 mug T(4) reduced the maximum increase in serum TSH above baseline (maximum DeltaTSH) by 76% in response to 400 mug TRH and by 87% in response to 25 mug TRH. The average serum T(3) level during a 24 hr period in normal subjects who had been taking 15 mug T(3) + 60 mug T(4) for 3-4 wk was 129+/-10 ng/100 ml (mean +/-SEM), well within the normal range, 70-150 ng/100 ml, although higher than the pretreatment level, 98+/-7 ng/100 ml. The average serum T(4) level was unchanged from the pretreatment level. Treatment of the same subjects with 30 mug T(3) + 120 mug T(4) reduced the maximum DeltaTSH further.Six patients with primary hypothyroidism were treated, sequentially, with 15 + 60, 22.5 + 90, and 30 mug T(3) + 120 mug T(4). For each patient there was one increase in dosage of 7.5 mug T(3) + 30 mug T(4) which abruptly converted a maximum DeltaTSH that was greater than, or at the upper limit of, normal to one that was subnormal. Concurrent with these six abrupt changes in TSH response, the mean serum T(3) level increased only from 105+/-5 to 129+/-9 ng/100 ml, and the mean serum T(4) level increased only from 4.9+/-0.8 to 6.3+/-0.5 mug/100 ml. These data demonstrate the extreme sensitivity of TRH-induced TSH release to inhibition by the chronic administration of quantities of T(3) + T(4) which do not raise serum T(3) and T(4) levels above the normal ranges.

Adult↗
PubMed1972

Human prolactin and thyrotropin concentrations in the serums of normal and hypopituitary children before and after the administration of synthetic thyrotropin-releasing hormone.

Synthetic thyrotropin-releasing hormone (TRH) was administered to normal children and hypopituitary patients in a dose of 7 mug/kg i.v. over 30-60 sec. Serum thyrotropin (TSH) and prolactin (HPr) concentrations were measured by radioimmunoassay before and at 15-min intervals for 2 hr after TRH. In 20 normal children HPr rose from a mean baseline value of 7.0+/-1.2 (SEM) ng/ml to a mean peak value of 39.5+/-5 ng/ml. In 11 patients with growth hormone (GH) deficiency without TSH deficiency. HPr values rose from a mean baseline of 3.6+/-0.8 ng/ml to a mean peak value of 13.9+/-2.8, a significantly less peak response as compared with normal children (P < 0.005). The TSH responses to TRH, however, were statistically indistinguishable from those of normal children. In 10 patients with GH and TSH deficiency both the mean baseline HPr levels (25.0+/-5 ng/ml) and the mean peak HPr levels after TRH (68.5+/-10 ng/ml) were significantly higher (P < 0.005 and < 0.025) than those of normal children. Similar comparisons were also true for the peak TSH responses (P < 0.05). Two panhypopituitary patients released no TSH and only small amounts of HPr after TRH. After thyroid replacement therapy in eight of the patients with GH and TSH deficiency, the mean HPr baseline levels (7.6+/-1.0 ng/ml) and peak levels (23.3+/-4.6 ng/ml) after the same dose of TRH were significantly less than their pretreatment levels (P < 0.001 and < 0.01) and were within the range for normal children. Synthetic TRH stimulates the simultaneous release of TSH and HPr in normal children and most hypopituitary patients. When the concentrations of thyroxine (T4) and triiodothyronine (T3) are low, the levels of HPr before and after TRH are elevated. After thyroid replacement therapy, HPr levels decrease to normal. T4 and/or T3 may condition the production or effects of prolactin-inhibiting factor (PIF) activity. The TSH and HPr responses after TRH in hypopituitary patients will determine whether the primary defect resides in the pituitary or hypothalamus, but cannot delineate the hypothalamic defect as a deficiency of hypothalamic hormone production or neurohumoral transmission.

Adolescent↗
PubMed1973

Assessment of thyrotropin-releasing hormone and thyrotropin reserve in man.

Endogenous thyrotropin-releasing hormone (TRH) reserve and pituitary thyrotropin (TSH) reserve were assessed in four normal subjects, three patients post-cryohypophysectomy, one patient with a hypothalamic lesion secondary to trauma, and four patients with Sheehan's syndrome. TSH reserve was determined by the immunoassayable TSH response to 500 mug TRH given i.v. (TRH stimulation test). TRH reserve was assessed by the rebound response in thyroidal iodine release (TIR) following withdrawal of pharmacologic doses of prednisolone (glucocorticoid withdrawal test). When compared with normals, the post-cryohypophysectomy patients demonstrated parallel impairment of TRH stimulation and glucocorticoid withdrawal testing. The patient with the hypothalamic lesion and the four patients with Sheehan's syndrome all had normal TRH stimulation tests, indicating adequate TSH reserve capacity, yet had abnormal glucocorticoid withdrawal tests, indicative of impairment in endogenous TRH reserve or neurohumoral transport. Three of the patients (hypothalamic injury and two Sheehan's) with impaired TRH reserve were euthyroid. THE FOLLOWING CONCLUSIONS WERE REACHED: (a) A combination of the TRH stimulation test and glucocorticoid withdrawal test may allow for differentiation between pituitary and suprahypophyseal disorders. (b) Certain cases of Sheehan's syndrome appear to have impaired endogenous TRH reserve or transport. (c) Euthyroidism can be maintained in spite of diminished TRH reserve.

Adolescent↗
PubMed1973

Repetitive administration of thyrotropin-releasing hormone results in small elevations of serum thyroid hormones and in marked inhibition of thyrotropin response.

Repetitive administration of thyrotropin-releasing hormone (TRH) to human subjects was used to produce small elevations of endogenous serum triiodothyronine (T(3)) and thyroxine (T(4)) levels and thereby to determine the effect of these small elevations on the serum thyrotropin (TSH) response to subsequent doses of TRH. Each subject received 13 consecutive doses of 25 mug TRH at 4-h intervals. Serum T(3), T(4), and TSH levels were measured before the 1st, 7th, and 13th doses ("basal levels") and for the 4 h after each of these doses. In 10 normal subjects, the mean TSH response fell from 14.6 muU/ml after the 1st TRH dose to 6.9 and 3.0 muU/ml after the 7th, and 13th doses. These falls in TSH response were accompanied by rises in the mean basal serum T(3) levels from 81 to 115 to 114 ng/100 ml (normal range, 70-150 ng/100 ml) and rises in the mean basal serum T(4) from 6.7 to 8.6 to 9.5 mug/100 ml (normal range, 5-11 mug/100 ml). These data suggest that TRH-induced TSH release is extremely sensitive to inhibition by small elevations, not above the normal ranges, of serum T(3) and T(4) of endogenous origin. In four patients with primary hypothyroidism, the mean TSH responses were 92, 137, and 92 muU/ml after the 1st, 7th, and 13th TRH doses. The corresponding mean basal serum T(3) and T(4) levels at the times of these doses were 34, 30, and 32 ng/100 ml and 1.9, 1.9, and 1.7 mug/100 ml. These data show that repetitive administration of TRH does not result in progressively lower TSH responses in the absence of corresponding increases in serum T(3) and T(4) level. The progressive fall in TSH response observed in the normal subjects, therefore, was apparently due to the corresponding small increases in serum T(3) and T(4) levels and not to progressive depletion of pituitary TSH. In two patients with presumed TRH deficiency, the TSH responses were blunted by repetitive TRH doses but only when the serum T(3) and T(4) levels increased to within the normal ranges. TRH deficiency was thus confirmed for the first time by producing euthyroidism by replacement of TRH.

Adult↗
PubMed1980

Variable thyrotropin response to thyrotropin-releasing hormone after small decreases in plasma free thyroid hormone concentrations in patients with nonthyroidal diseases.

Although a normal serum thyrotropin (TSH) concentration is generally considered to be the most important finding to support the clinical impression of euthyroidism in patients with nonthyroidal diseases and decreased serum triiodothyronine (T(3)), the regulation of TSH secretion in sick patients has not been studied previously. Accordingly, we studied the regulation of TSH secretion in 23 patients with nonthyroidal diseases; 15 of the patients had decreased serum T(3). TSH regulation was studied by measuring the TSH response to injected thyrotropin-releasing hormone (TRH) before and after effecting a small decrease in serum thyroxine (T(4)) and/or T(3) concentrations by iodide treatment, 262 mg daily for 10 d. Iodide treatment significantly decreased (> 10%) the free T(4) index (FT(4)-I) and/or free T(3) index (FT(3)-I) in all patients. FT(4)-I values were correlated (0.611, P < 0.001), with free T(4) concentration determined by equilibrium dialysis. Despite decreased FT(4)-I and/or FT(3)-I after iodide treatment in all patients, the TSH response to TRH after iodide treatment was augmented in only 8 of 15 patients who had decreased serum T(3) (group 1) and in only 5 of 8 patients who had a normal serum T(3). Mean base-line TSH concentration was increased significantly (P < 0.05) from 0.9+/-0.1 to 1.5+/-0.3 muU/ml in group 1 only. Comparison of the mean TSH response to TRH showed that there was no significant difference between groups 1 and 2. Moreover, no significant difference in thyroidal parameters was observed between patients who had augmented TSH response to TRH after iodides and those who had either similar or decreased TSH response irrespective of the initial serum T(3). These studies show that an augmented TSH response to TRH in response to a small reduction in serum T(4) and T(3) concentration occurred in only 57% of the entire group of patients with nonthyroidal diseases and that the presence or absence of a normal TSH response to this stimulus did not seem to be related to the base-line serum T(3) concentration. Because an increase in serum TSH in response to decreased serum T(4) and T(3) did not occur in about one-half of patients with nonthyroidal diseases, normal serum TSH may not be a reliable index of the euthyroid state in these patients.

Adult↗
PubMed1977

Pituitary thyrotropin response to thyrotropin-releasing hormone in affective illness: relationship to spinal fluid amine metabolites.

The authors studied pituitary thyrotropin, i.e., thyroid-stimulating hormone (TSH), response to thyrotropin-releasing hormone (TRH) in patients with primary affective disorder. There were no overall differences between either depressed or manic patients and normal controls; however, the TSH response was significantly lower in the unipolar depressed patients than in either bipolar depressed patients or normal subjects. Bipolar patients in the manic phase tended to have a lower response than bipolar depressed patients. In the unipolar group, the TSH response showed a significant negative correlation with the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the CSF. These neuroendocrine responses may constitute markers of specific monoamine dysfunction in subgroups of patients with affective illness.

Age Factors↗
PubMed1982

Serum thyrotropin response to thyrotropin-releasing hormone in psychiatric patients: a review.

In 1972 it was reported that in some euthyroid depressed patients the serum thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) was deficient. Since then, 41 reports describing 917 depressed patients have confirmed this finding. Although it is useful to report differences between mean response values of patient populations, it is necessary to identify those individuals in whom the fault occurs so that sensitivity, specificity, state-trait distribution, and clinical correlates can be determined. Present data allow some tentative conclusions: 1) the fault usually reflects a defect in central regulation of the pituitary-thyroid axis, 2) in some patients the fault may be a trait marker, and 3) it may represent a biological bridge between some depressed patients and some patients with other mental disorders.

Alcoholism↗
PubMed1977

Suppression of prolactin and thyrotropin secretion in the rat by antiserum to thyrotropin-releasing hormone.

Administration of antiserum to synthetic thyrotropin-releasing hormone (TRH) to male and female rats cause a 50% and a 70% suppression in serum levels of prolactin and thyrotropin, respectively, as compared with controls injected with normal rabbit serum. The degree of suppression was similar in diestrous and proestrous female rats and in male rats. These findings support the view that, in addition to its original designation, TRH also has a physiological role in regulating release of pituitary prolactin.

Animals↗
PubMed1976

Thyrotropin-releasing hormone and thyroid hormone interactions on thyrotropin secretion in the rat: lack of inhibiting effects of small doses of triiodo-L-thyronine in the hypothyroid rat.

Rats were thyroidectomized (T) and injected once daily with thyroxine (T4) or triiodothyronine (T3) ip; circulating thyrotropin (TSH) levels and TSH response to 100 ng of thyrotropin releasing hormone (TRH) iv, were measured in different groups of rats at several intervals after the last dose of T4 or T3. It was found that T rats on 1.8 mug T4 or 0.4 mug T3/100 g BW/day, response to TRH decreased after the injection of the hormone, maximum suppressive effect being found about 7-8 h after T4, or 4 h after T3. The response increased as T4 or T3 levels reached a nadir, in agreement with present views on TRH, T4, and T3 interactions at the pituitary level. The degree of TSH response to TRH appears as a sensitive parameter of T4 or T3 activity in this experimental model. However, in T rats on 0.2 mug T3/100 g BW/day, TSH response to TRH did not decrease, but actually increased, after the daily injection of T3. These animals appeared to be in a state of continuous thyroid hormone deficiency. The same 0.2 mug T3 dose effectively suppresses the elevated basal TSH levels of these animals. It is also capable of decreasing TSH response to 100 ng TRH in animals under more "euthyroid" conditions. These results in the T rats on 0.2 mug T3 are not easily fitted into the relatively simple model frequently described to explain TRH-T3 interactions and TSH secretion.

Animals↗
PubMed1975

Augmentation of thyrotropin responses to thyrotropin-releasing hormone following small decreases in serum thyroid hormone concentrations.

To determine whether slight decreases in serum thyroid hormone concentrations resulted in augmentation of the thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH), TSH responses to TRH were determined before and after 13 days of iodide treatment in 20 normal subjects. Slight reductions in serum thyroxine (t4) and/or triiodothyronine (T3) concentrations and slight increases in basal serum TSH concentrations occurred in normal subjects treated with 50 or 250 mg iodide daily, though serum T4, T3 and TSH concentrations remained within their respective normal range. In contrast, TSH responses to TRH were significantly greater at the end of the iodide treatment period. In the subjects who received 50 mg iodide daily, mean basal serum TSH concentrations were 3.1 and 3.2 muU/ml before and 4.9 and 4.6 muU/ml after iodide. Post-TRH mean peak serum TSH concentrations were 14.2 muU/ml before and 27.4 muU/ml after iodide (P smaller than 0.01). A very similar augmentation of peak serum TSH was found in the subjects who received 250 mg iodide daily (before iodide, peak TSH 17.2 muU/ml; after iodide, peak TSH 28.7 muU/ml). No changes in serum T4, T3 or TSH concentrations or TSH responses to TRH followed iodide administration in 4 thyroxine-treated hypothyroid patients. These results indicate that slight reductions in serum T4 AND T3 concentrations result in increased pituitary sensitivity to TRH, just as small increases in serum T4 and T3 concentrations decrease sensitivity to TRH.

Adolescent↗