Hypothalamic Hormones Regulating the Secretions of the Anterior Pituitary

1979 ◽  
Vol 4 (7) ◽  
pp. 158-160 ◽  
Author(s):  
Fernand Labrie ◽  
Martin Godbout ◽  
Michèle Beaulieu ◽  
Pierre Borgeat ◽  
Nicholas Barden

Physiology ◽  
1999 ◽  
Vol 14 (2) ◽  
pp. 54-58
Author(s):  
W. R. Crowley

The hypothalamus regulates the secretion of anterior pituitary hormones via release of releasing hormones into the hypophysial portal vasculature. Additional neuromessengers act at the pituitary to modulate responses to the hypothalamic hormones. For example, neuropeptide Y enhances the effect of gonadotropin-releasing hormone and the response to the prolactin-inhibiting hormone dopamine.


1981 ◽  
Vol 7 (5) ◽  
pp. 225-237 ◽  
Author(s):  
F. Brambilla ◽  
D. Cocchi ◽  
P. Nobile ◽  
Eugenio E. Müller

Author(s):  
Sergio R. Ojeda

The hypothalamic-pituitary complex represents the core of the neuroendocrine system. The hypothalamus is composed of a diversity of neurosecretory cells arranged in groups, which secrete their products either into the portal blood system that connects the hypothalamus to the adenohypophysis (see later) or directly into the general circulation after storage in the neurohypophysis (see Chapter 6). Because of the nature of their actions, the hypothalamic hormones are classified as releasing or inhibiting hormones. The hypothalamic hormones delivered to the portal blood system are transported to the adenohypophysis, where they stimulate or inhibit the synthesis and secretion of different trophic hormones. In turn, these hormones regulate gonadal, thyroid, and adrenal function, in addition to lactation, bodily growth, and somatic development. No attempt will be made in this chapter to cover the actions of the different pituitary trophic hormones on their target glands, because they are discussed in detail in other chapters. An exception to this is growth hormone (GH). Although Chapter 11 considers several aspects of the control and actions of GH, a broader discussion of its physiological actions will be presented here because GH is the only anterior pituitary hormone that does not have a clear-cut target gland. The pituitary gland has two parts: the neurohypophysis, of neural origin (see Chapter 6), and the adenohypophysis, of ectodermal origin. In embryonic development, an evagination from the roof of the pharynx pushes dorsally to reach a ventrally directed evagination from the base of the diencephalon. The dorsally projecting evagination, known as Rathke’s pouch , forms the adenohypophysis, whereas the ventrally directed evagination of neural tissue forms the neurohypophysis. The neurohypophysis has three parts: the median eminence, the infundibular stem, and the neural lobe itself. The median eminence represents the intrahypothalamic portion and lies just ventral to the floor of the third ventricle protruding slightly in the midline. The main part of the neurohypophysis, the neural lobe, is connected to the median eminence by the infundibular stem.


2019 ◽  
Vol 8 (8) ◽  
pp. R131-R143 ◽  
Author(s):  
Arno Téblick ◽  
Lies Langouche ◽  
Greet Van den Berghe

Critical illness is hallmarked by major changes in all hypothalamic–pituitary–peripheral hormonal axes. Extensive animal and human studies have identified a biphasic pattern in circulating pituitary and peripheral hormone levels throughout critical illness by analogy with the fasting state. In the acute phase of critical illness, following a deleterious event, rapid neuroendocrine changes try to direct the human body toward a catabolic state to ensure provision of elementary energy sources, whereas costly anabolic processes are postponed. Thanks to new technologies and improvements in critical care, the majority of patients survive the acute insult and recover within a week. However, an important part of patients admitted to the ICU fail to recover sufficiently, and a prolonged phase of critical illness sets in. This prolonged phase of critical illness is characterized by a uniform suppression of the hypothalamic–pituitary–peripheral hormonal axes. Whereas the alterations in hormonal levels during the first hours and days after the onset of critical illness are evolutionary selected and are likely beneficial for survival, endocrine changes in prolonged critically ill patients could be harmful and may hamper recovery. Most studies investigating the substitution of peripheral hormones or strategies to overcome resistance to anabolic stimuli failed to show benefit for morbidity and mortality. Research on treatment with selected and combined hypothalamic hormones has shown promising results. Well-controlled RCTs to corroborate these findings are needed.


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