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Hypothalamic Regulatory Hormones: a Review J Clin Pathol: first published as 10.1136/jcp.27.3.173 on 1 March 1974. Downloaded from J. clin. Path., 1974, 27, 173-184 Hypothalamic regulatory hormones: A review G. M. BESSER AND C. H. MORTIMER From the Medical Professorial Unit, St Bartholonew's Hospital, London It has long been suggested that the secretion of the aspects of their structure and function will be dis- anterior pituitary hormones is under the control of cussed in the light of recent knowledge. the hypothalamus (Green and Harris, 1947; Harris, 1955). Early studies of the vasculature of the hypo- Thyrotrophin-releasing Hormone (TRH) thalamic-hypophyseal system in birds and mammals described a portal system of capillaries in close The existence of a hypothalamic factor important for contact with neurosecretory cells of the median the regulation of thyrotrophin (TSH) release from eminence of the hypothalamus and draining to the the pituitary was first demonstrated in rats by anterior pituitary (Scharrer and Scharrer, 1954). It producing lesions in the median eminence of the was therefore assumed that neurosecretory trans- hypothalamus. These resulted in a decrease in mitters from the hypothalamus drained via this circulating TSH and thyroid hormone levels (Greer, portal system to their target cells in the pars anterior. 1951), and conversely electrical stimulation of sites The anatomical relationship between the hypothal- in the medial-basal and paraventricular areas of the amus and posterior pituitary was, however, recog- hypothalamus resulted in a rapid increase in circu- nized to be different since the nerve fibres were found lating levels of TSH (Martin and Reichlin, 1970; to extend from the supraoptic and paraventricular Guillemin, 1970). There followed a period of intense hypothalamic nuclei actually into the posterior search for the nature of thyrotrophin-releasing copyright. pituitary. These nerve endings are closely applied to hormone. Increasingly elaborate techniques of the capillaries and contain storage granules and purification of extracts of many hundreds of direct neurosecretion ofposterior pituitary hormones thousands of animal hypothalami yielded material into the systemic circulation occurs at these endings. of pure TSH-releasing activity. Finally the hypo- The absence of a significant neural connexion but thalamic origin of TRH was confirmed by the the presence of the portal capillary circulation linking isolation and subsequent synthesis of a tripeptide, the hypothalamus and anterior pituitary clearly pyro-GLU-HIS-PROamide (see table), with thyro- http://jcp.bmj.com/ suggested that the control of the secretion of the trophin-releasing properties (Schally, Bowers, anterior pituitary hormones was different from that Redding, and Barrett, 1966; Folkers, Enzman, Boler, of the posterior, and the alteration in function of the Bowers, and Schally, 1969; Schally, Redding, target organs when the pituitary stalk was cut Bowers, and Barrett, 1969a; Nair, Barrett, Bowers, leaving the pituitary intact implied that the hypo- and Schally, 1970; Burgus, Dunn, Desiderio, Ward, thalamus secreted regulatory substances. Despite Vale, and Guillemin, 1970). Porcine, ovine, bovine, the abundant evidence for the existence of hypo- and human TRH appear to have the same structures. on September 25, 2021 by guest. Protected thalamic substances controlling pituitary function, This major achievement-the isolation, analysis, and it is only recently that the chemical structures of synthesis of the first hypothalamic regulatory hor- some of these have been established and their mone-marked a major turning point in the under- effects demonstrated. They are conventionally standing of the control of the endocrine system. The referred to as factors (F) if the activity of simple biosynthesis in vitro of TRH from its three constitu- extracts of the hypothalamus is being studied, or as ent amino acids by fragments of the median emi- hormones (H) if their structures have been eluci- nence, as well as the ventral and dorsal hypothal- dated (Schally, Arimura, Bowers, Kastin, Sawano, amus, has been demonstrated. Its synthesis appears and Redding, 1968). Since they have been shown to to be under the influence of the non-ribosomal have either stimulatory or inhibitory effects the enzyme, TRH-synthetase, the activity of which is en- term 'hypothalamic regulatory hormones' would hanced by incubation with thyroxine, although a seem to be appropriate although early work resulted resulting increase in TRH production has not yet in the discovery mainly of releasing hormones. Each been demonstrated. Endogenous TRH also appears of the hormones will be considered individually and to be dependent on catecholaminergic and possibly monoaminergic neurones for its synthesis and release Received for publication 11 January 1974. (Reichlin, Martin, Mitnick, Boshans, Grimm, 173 J Clin Pathol: first published as 10.1136/jcp.27.3.173 on 1 March 1974. Downloaded from 174 G. M. Besser and C. H. Mortimer Releasing hormones or factorsI for: TSH PYRO-GLU-HIS-PRO-NH, TRH (Prolactin FSHI) LH and FSH PYRO-GLU-HIS-TRP-SER-TYR-GLY-LEU-ARG-PRO-GLY-NH2 LH/FSH-RH GH Structure uncertain GRH (?F) ACTH Structure uncertain CRF MSH Structure uncertain MRF Prolactin Structure uncertain PRF Release-inhibiting hormones or factors for: GH H-ALA-GLY-CYS-LYS-ASN-PHE-PHE-TRP-LYS-THR-PHE-THR-SER-CYS-OH (TSH, FSH, glucagon, 1, GH-RIH insulin)2 MSH ? PRO-LEU-GLY-NH2 MIH (?F) Prolactin Structure uncertain PIF Table Hypothalamic regulatory hormones andfactors 'Hypothalamic regulatory substances are called 'hormones' (H) when their structures have been elucidated; otherwise they are referred to as 'factors' (F). 'Anterior pituitary hormones which are secondarily affected-see text. Bollinger, Gordon, and Malacra, 1972). Recently it single dose orally or intravenously (Hall, Amos, has been shown that tritiated TRH is specifically Garry, and Buxton, 1970; Ormston, 1972), and to bound by pituitary membrane receptors (Wilber and result in elevation of circulating T3 and T4 (Lawton, Seibel, 1973) and, since the adenyl cyclase system is 1972). also associated with these structures, it seems likely A standard intravenous TRH test has been that cyclic AMP may be the mediator of the actions developed which will differentiate both hyper- of the tripeptide on the pituitary thyrotrophs. thyroidism and hypothyroidism from normality. Further evidence for this is the demonstration of an When 200 ,ug TRH is given intravenously the serum increase in pituitary adenyl cyclase activity pro- TSH normally rises to reach a peak at about 20copyright. duced by TRH (Kaneko, Saito, Oka, Oda, and minutes and then falls again. In the TRH test, serum Yanaihara, 1972). The stimulatory effect of TRH is immunoreactive TSH is measured at 0, 20, and 60 blocked by an increase in circulating thyroid minutes; unfortunately TSH rather than serum hormone levels acting directly on the pituitary. thyroxine or protein-bound iodine has to be Although the mechanisms involved in hypothalamic- measured since the changes in circulating thyroid pituitary thyroid regulation are complex it seems hormone levels are too small to be easily followed likely that the thyrotroph is primarily regulated by and the effects are delayed for up to eight hours. http://jcp.bmj.com/ circulating levels of triiodothyronine (T3) and The TSH responses to TRH are slightly, but thyroxine (TA, or possibly by T3 only. These provide significantly, greater in women than in men unless a negative feedback at the pituitary level. The the latter are treated with oestrogens (Ormston, inhibitory actions of the thyroid hormones modulate Garry, Cryer, Besser, and Hall, 1971; Faglia, and oppose the stimulatory effects of thyrotrophin- Beck-Pecioz, Ferrari, Ambrosi, Spada, and releasing hormone. It is not yet certain whether Travaglini, 1973). TRH secretion is altered by the level of circulating In hyperthyroidism, whether due to Graves' on September 25, 2021 by guest. Protected thyroid hormones but it seems likely that the disease or to an autonomous thyroid nodule, the negative feedback also operates at the hypothalamic high circulating T3 and T4 levels interfere with the level so that TRH secretion increases when thyroid action of TRH on the pituitary thyrotroph cell and hormone levels fall, and viceversa. Variousanalogues impair the TSH response (seefig.). Usingthe standard of TRH have been synthesized, including a proline intravenous 200 jig TRH test, we have never seen methyl derivative with enhanced biological action. a significant (> 1 uU/ml) TSH response in a thyro- This appears to be due to increased binding proper- toxic patient, although it has been reported that ties at the pituitary cell receptor site (Burgus, with very large doses of TRH some TSH secretion Monahan, Rivier, Vale, Ling, Grant, Amoss, and may occur. Clearly this simple test is most valuable Guillemin, 1973). since it provides confirmatory evidence of the Apart from the fascinating theoretical considera- clinically suspected diagnosis even when other tions of the biosynthesis and mode of action of thyroid function tests are normal or equivocal such TRH at the cellular level, the wide availability of as in T3-toxicosis or borderline T4-toxicosis. Before this material has enabled extensive clinical observa- the advent of this test the only equivalent test pro- tions to be made. It has been shown to cause a cedure was the T3-suppression test which required a dose-related TSH response when administered as a radioactive iodine uptake study
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