Thyrotropin-releasing hormone secretion

Prolactin is an essential hormone for normal production of breast milk following childbirth. It also plays a pivotal role in a variety of reproductive functions. Prolactin is regulated primarily by the hypothalamus-pituitary axis and secreted solely by the lactotroph cells of the anterior pituitary gland. Under normal conditions, secretion of prolactin is predominantly under inhibitory control by dopamine and acts on the D2 receptors located on the lactotroph cells. Increase of hypothalamic thyrotropin-releasing hormone (TRH) in primary hypothyroidism can stimulate the release of prolactin. 

Located in close proximity to the primary capillary plexus in the hypothalamus are specialized neurosecretory cells. In fact, the axons of these cells terminate on the capillaries. The neurosecretory cells synthesize two types of hormones releasing hormones and inhibiting hormones (see Table 10.2). Each of these hormones helps to regulate the release of a particular hormone from the adenohypophysis. For example, thyrotropin-releasing hormone produced by the neurosecretory cells of the hypothalamus stimulates secretion of thyrotropin from the thyrotrope cells of the adenohypophysis. The hypo-thalamic-releasing hormone is picked up by the primary capillary plexus travels through the hypothalamic-hypophyseal portal veins to the anterior pituitary leaves the blood by way of the secondary capillary plexus and exerts its effect on the appropriate cells of the adenohypophysis. The hypophyseal hormone, in this case, thyrotropin, is then picked up by the secondary capillary plexus, removed from the pituitary by the venous blood, and delivered to its target tissue. 

Thyroid hormone production is regulated by TSH secreted by the anterior pituitary, which in turn is under negative feedback control by the circulating level of free thyroid hormone and the positive influence of hypothalamic thyrotropin-releasing hormone. Thyroid hormone production is also regulated by extrathyroidal deiodination of T4 to T3, which can be affected by nutrition, nonthyroidal hormones, drugs, and illness. 

TSH-secreting pituitary adenomas are diagnosed by demonstrating lack of TSH response to thyrotropin-releasing hormone stimulation, inappropriate TSH levels, elevated TSH a-subunit levels, and radiologic imaging. 

Thyroliberin (thyrotropin-releasing hormone, TRH) is one of the neurohormones of the hypothalamus (see p. 330). It stimulates pituitary gland cells to secrete thyrotropin (TSH). TRH consists of three amino acids, which are modified in characteristic ways (see p. 353). 

The secretion of anterior pituitary hormones is controlled in part by hypothalamic regulatory factors that are stored in the hypothalamus and are released into the adenohypophyseal portal vasculature. Hypothalamic regulatory factors so far identified are peptides with the exception of dopamine. Secretion of anterior pituitary hormones is also controlled by factors produced more distally that circulate in the blood. Predominant control of hormone production may be relatively simple, as with thyroid-stimulating hormone (TSH), the production of which is primarily stimulated by thyrotropin-releasing hormone (TRH) and inhibited by thyroid hormones, or it may be complex, as with prolactin, the production of which is affected by many neurotransmitters and hormones. 

Secondary hypothyroidism, or pituitary hypothyroidism, is the consequence of impaired thyroid-stimulating hormone (TSH) secretion and is less common than primary hypothyroidism. It may result from any of the causes of hypopituitarism (e.g., pituitary tumor, postpartum pituitary necrosis, trauma). Patients with secondary hypothyroidism exhibit undetectable or inappropriately low serum TSH concentrations. In secondary hypothyroidism, a normal thyroid gland lacks the normal level of TSH stimulation necessary to synthesize and secrete thyroid hormones. Such patients usually also have impaired secretion of TSH in response to exogenous thyrotropin-releasing hormone (TRH) administration. 

Control of thyroid function via thyroid-pituitary feedback is also discussed in Chapter 37. Briefly, hypothalamic cells secrete thyrotropin-releasing hormone (TRH) (Figure 38-3). TRH is secreted into capillaries of the pituitary portal venous system, and in the pituitary gland, TRH stimulates the synthesis and release of thyrotropin (thyroid-stimulating hormoneTSH). TSH in turn stimulates an adenylyl cyclase-mediated mechanism in the thyroid cell to increase the synthesis and release of T4 and T3. These thyroid hormones act in a negative feedback fashion in the pituitary to block the action of TRH and in the hypothalamus to inhibit the synthesis and secretion of TRH. Other hormones or drugs may also affect the release of TRH or TSH. 

Thyrotropin-releasing hormone is one of several small peptide hormones secreted by the anterior lobe of the pituitary gland. These are the master" hormones that function to stimulate hormone secretion from other endocrine glands. Thyrotropin stimulates the functioning of the thyroid gland. 

Thyrotropin-releasing hormone, or protirelin, is a tripeptide hormone found in the paraventricular nuclei of the hypothalamus as well as in other parts of the brain. TRH is secreted into the portal venous system and stimulates the pituitary to produce thyroid-stimulating hormone (TSH, thyrotropin), which in turn stimulates the thyroid to produce thyroxine (T4) and triiodothyronine (T3). TRH stimulation of thyrotropin is blocked by thyroxine and potentiated by lack of thyroxine. 

Felt V, Nedvidkova J (1982) Growth hormone and changes in the secretion of thyrotropic hormone after thyrotropin-releasing hormone (TRH) ineffectiveness of dopaminergic stimulation. Endokrinologie 80 201-206. 

Ishibashi M, Yamaji T (1984) Direct effects of catecholamines, thyrotropin-releasing hormone, and somatostatin on growth hormone and prolactin secretion from adenomatous and nonadenomatous human pituitary cells in culture, J Clin Invest 75 66-78. 

Pan J-T, Wang PS (1989) Effect of transient dopamine antagonism on thyrotropin-releasing hormone-induced prolactin secretion in the serotonin-blocked, estrogen-treated ovariectomized rats. Neuroendocrinology 49 281-285. 

Wang PS, Huang S-W, Tung Y-F, Pu H-F, Tsai S-C, Lau C-P, Chien EJ, Chien C-H (1994) Interrelationship between thyroxine and estradiol on the secretion of thyrotropin-releasing hormone and dopamine into hypophysial portal blood in ovariectomized-thyroidectomized rats. Neuroendocrinology 59 202-207. 

The pituitary gland is involved in feedback regulation of thyroid activity High levels of T4 in the bloodstream result in inhibition of TSH secretion. Low levels of T4 result in an increase in TSH secretion. These effects are dependent on the conversion of T4 to T3 within the pituitary, fhe activity of the pituitary is controlled by thyrotropin-releasing hormone (TRH), a hormone synthesized in the hypothalamus. TRH is a tripeptide with the structure pyroglutamate-histidine-proline-NH . Note the C-terminal amide group, which is required for the activity of many peptide hormones. TRH stimulates the synthesis and secretion of TSH. Apparently TRH is involved in regulating the sensitivity of the pituitary to the inhibitory feedback control mechanism mentioned earlier. 

Three possible causes of hypothyroidism are the decreased secretion of thyrotropin-releasing hormone (TRH) by the hypothalamus gland, decreased secretion of thyroid-stimulating hormone (TSH) by the pituitary gland, and decreased secretion of thyroid hormones by the thyroid gland. 

Harvey, S. Benzodiazepine antagonism of thyrotropin-releasing hormone receptors biphasic actions on growth hormone secretion in domestic fowl. J. Endocrinol. 137 35-42, 1993. 

Thyrotropin Releasing Hormone (TRH) 3 (362) PVN/Jtjrv, PeriVN Stimulates TSH secretion, also stimulates PRL release GQa-PLq3-Ca2+-PKC... 

---