Thyroid-Releasing Hormone secretion

Less common etiologies include central nervous system lesions that physically compress the pituitary stalk and interrupt tonic hypothalamic dopamine secretion, resulting in hyperprolactinemia. Increased thyroid-releasing hormone (TRH) concentrations in hypothyroidism can stimulate prolactin secretion and cause hyperprolactinemia. During conditions of renal or liver compromise, the... 

Hormones secreted in the hypothalamus, which releases pituitary hormones, are believed to bind to specific receptors of the membranes of the pituicyte. This action is dependent upon the presence of Ca Therefore, it has been proposed that the hormone depolarizes the cell membrane increasing the permeability to calcium which would, in turn, release the hormone. Whatever the role of calcium, it is known in the case of thyroid releasing hormone that it stimulates adenylcyclase and cAMP. 

The class III cytokine receptor family includes two TNE receptors, the low affinity NGE receptor and 7-ceU surface recognition sites that appear to play a role in proliferation, apoptosis, and immunodeficiency. TNE-a (- 17, 000 protein) is produced by astrocytes and microglia and can induce fever, induce slow-wave sleep, reduce feeding, stimulate prostaglandin synthesis, stimulate corticotrophin-releasing factor and prolactin secretion, and reduce thyroid hormone secretion. TNE-a stimulates IL-1 release, is cytotoxic to oligodendrocytes, and reduces myelination this has been impHcated in multiple sclerosis and encephalomyelitis. Astrocyte TNE-a receptors mediate effects on IL-6 expression and augment astrocytic expression of MHC in response to other stimulants such as lEN-y. 

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. 

Somatostatin inhibits secretion of growth hormone and other hormones such as prolactin from the anterior pituitary and is widely distributed in the brain in interneurons and projection pathways. All parts of the cortex contain local circuit somatostatin positive neurons, concentrated in layers V and VI, as does the amygdala and striatum. The nucleus accumbens and adjacent ventral putamen and caudate—designated limbic striatum—have particularly high concentrations of fibres. By contrast, TRH which regulates release of thyroid stimulating hormone and prolactin by the pituitary is generally confined to nuclei in and around the hypothalamus. 

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. 

TRH stimulates the anterior pituitary gland to release or secrete Thyroid-Stimulating-Hormone (TSH) (also referred to as Thyrotropin on some lab chem. Panels)... 

Anterior Lobe. The anterior pituitary, or adenohypophysis, secretes six important peptide hormones. The anterior pituitary releases growth hormone (GH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), and prolactin (Pr). The physiologic effects of these hormones are listed in Table 28-1. 

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. 

Correct answer = O. Propylthiouracil blocks the synthesis of the thyroid hormones, but does not affect the uptake of iodide, proteolytic cleavage of thyroglobulin, or the release of hormones from the thyroid gland. The thyroid hormones inhibit the secretion of thyroid-stimulating hormone from the anterior pituitary. ... 

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