Hypophyseal hormone

Somatotropin (STH) (Growth hormone, GH somatotrophic hormone hypophyseal growth hormone) Structure Known and synthesized coiled, unbranched Promotes general growth of organism Promotes skeletal growth, protein anabolism, fat metabolism, carbohydrate metabolism, water, and salt meiabolism Relates with all vitamins in connection with growth actions... 

As discussed previously, the neurohypophysis has a direct anatomical connection to the hypothalamus. Therefore, the hypothalamus regulates the release of hormones from the neurohypophysis by way of neuronal signals. Action potentials generated by the neurosecretory cells originating in the hypothalamus are transmitted down the neuronal axons to the nerve terminals in the neurohypophysis and stimulate the release of the hormones into the blood. The tracts formed by these axons are referred to as hypothalamic-hypophyseal tracts (see Figure 10.2). The action potentials are initiated by various forms of sensory input to the hypothalamus. Specific forms of sensory input that regulate the release of ADH and oxytocin are described in subsequent sections in this chapter. 

The adenohypophysis does not have a direct anatomical connection with the hypothalamus therefore, regulation of hormone secretion by way of neuronal signals is not possible. Instead, these two structures are associated by a specialized circulatory system and the secretion of hormones from the adenohypophysis is regulated by hormonal signals from the hypothalamus (see Figure 10.2). Systemic arterial blood is directed first to the hypothalamus. The exchange of materials between the blood and the interstitial fluid of the hypothalamus takes place at the primary capillary plexus. The blood then flows to the adenohypophysis through the hypothalamic-hypophyseal portal veins. Portal veins are blood vessels that connect two capillary beds. The second capillary bed in this system is the secondary capillary plexus located in the adenohypophysis. 

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. 

The hypothalamic releasing hormones are peptides. They reach their target cells in the AH lobe by way of a portal vascular route consisting of two serially connected capillary beds. The first of these lies in the hypophyseal stalk, the second corresponds to the capillary bed of the AH lobe. Here, the hypothalamic hormones diffuse from the blood to their target cells, whose activity they control. Hormones released from the AH cells enter the blood, in which they are distributed to peripheral organs (1),... 

Thyroid hormones accelerate metabolism. Their release (A) is regulated by the hypophyseal glycoprotein TSH, whose release, in turn, is controlled by the hypothalamic tripeptide TRH. Secretion of TSH declines as the blood level of thyroid hormones rises by means of this negative feedback mechanism, hormone production is automatically adjusted to demand. 

I. Replacement therapy. The adrenal cortex (AC) produces the glucocorticoid cortisol (hydrocortisone) and the mine-ralocorticoid aldosterone. Both steroid hormones are vitally important in adaptation responses to stress situations, such as disease, trauma, or surgery. Cortisol secretion is stimulated by hypophyseal ACTH, aldosterone secretion by angiotensin 11 in particular (p. 124). In AC failure (primary AC insuffiency ... 

Effect of glucocorticoid administration on adrenocortical cortisol production (A). Release of cortisol depends on stimulation by hypophyseal ACTH, which in turn is controlled by hypothalamic corticotropin-releasing hormone (CRH). In both the hypophysis and hypothalamus there are cortisol receptors through which cortisol can exert a feedback inhibition of ACTH or CRH release. 

Mechanism of Action An antipsychotic that blocks postsynaptic dopamine receptor sites in brain. Has alpha-adrenergic blocking effects, and depresses the release of hypothalamic and hypophyseal hormones. Therapeutic Effect Suppresses psychotic behavior. 

For complete functional evaluation of the hypothalamic-hypophyseal-adrenal axis one can use synthetic corticorelin (corticotropin-releasing hormone), which is available in both human (hCRH) and ovine (oCRH) forms (1). 

Protirelin is a synthetic tripeptide that stimulates the hypophyseal secretion of thyrotrophin (thyroid-stimulating hormone, TSH). It is used mainly for diagnostic purposes in dynamic tests of pituitary and hypothalamic... 

Figure 16.1 Hypothalamic-pituitary system. The hypothalamus receives various types of impulses and responds by secreting appropriate release and release-inhibiting factors. These migrate to the anterior or intermediate pituitary via the hypophyseal portal vein system and elicit the secretion of various tropic or non tropic hormones. For instance, when the organism is exposed to cold, blood TSH levels increase when under stress, blood ACTH levels rise. In some animals, the absence of light causes the release of a-MSH.

Biotechnology-derived pharmaceuticals (biopharmaceuticals) appeared for the first time in the 1980s for medical treatment of diseases, such as diabetes mellitus and hypophysical dwarfism. Since then the number and types of biopharmaceuticals have climbed and continue to dramatically increase. One reason for the increase is the evolution of recombinant manufacturing of biopharmaceuticals. This has provided sufficient amounts of proteins for development and clinical use, whereas, for example, the amount of insulin or growth hormones extracted from animal or human tissues had been limited. Another... 

The adrenal cortex (AC) produces the glucocorticoid cortisol (hydrocortisone) in the zona fasciculata and the mineralocorticoid aldosterone in the zona glomerulosa. Both steroid hormones are vitally important in adaptation responses to stress situations, such as disease, trauma, or surgery. Cortisol secretion is stimulated by hypophyseal ACTH aldosterone secretion by angiotensin II in particular (p. 128). In AC failure (primary adrenocortical insuf ciency, Addison disease), both cortisol and aldosterone must be replaced when ACTH production is deficient (secondary adrenocortical insuf ciency), cortisol alone needs to be replaced. Cortisol is effective when given orally (30 mg/day, 2/3 a.m 1 /3 p.m.). In stress situations, the dose is raised 5- to 10-fold. Aldosterone is poorly effective via the oral route instead, the mineralocorticoid fludrocortisone (0.1 mg/day) is given. 

Thioxanthenes, such as flupenthixol and clopenthixol, are similar in structure to the phenothiazines. The therapeutic effects are similar to those of the piperazine group. Antipsychotic thioxanthenes are thought to benefit psychotic conditions by blocking postsynaptic dopamine receptors in the brain. They also produce an alpha-adrenergic blocking effect and depress the release of most hypothalamic and hypophyseal hormones. However, the concentration of prolactin is increased due to blockade of prolactin inhibitory factor (PIF), which inhibits the release of prolactin from the pituitary gland. 

Q1 Thyroid secretion is controlled by two feedback loops. Secretion of T3 and T4 is stimulated by TSH from the anterior pituitary gland. The secretion of TSH is controlled by the hypothalamus via production of TRH. TRH is secreted by the hypothalamus into the hypophyseal portal blood flow. Stimuli such as a very cold environment influence the secretion of thyroid hormones by affecting the hypothalamus and increasing the release of TRH. 

Q4 Glucocorticoid secretion is controlled by the hypothalamus and anterior pituitary gland. Corticotrophin releasing factor (CRF) is produced in the hypothalamus and travels in the hypophyseal portal blood vessels to the anterior pituitary to release ACTH (adrenocorticotrophic hormone). There is a daily (circadian) rhythm in CRF and ACTH secretion, with a peak in the morning between 7 and 9 a.m. and a low point during the night. 

Another case in point is the hypophyseal gland, which like the adrenal gland combines entodermal and neural gland cells in one organ both cell types secrete peptide hormones into the circulation. 

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