Hypophyseal portal system

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Hypophyseal portal system
Grays pituitary.png
Details
Latin Venae portales hypophysiales
Dorlands
/Elsevier
s_33/12787512
Anatomical terminology

The hypophyseal portal system is a system of blood vessels in the brain that connects the hypothalamus with the anterior pituitary. Its main function is the transport and exchange of hormones to allow a fast communication between both glands. The fenestrated structure of capillaries in the hypophyseal portal system facilitates a rapid exchange between the hypothalamus and the pituitary, with only a small amount of hormones needed to stimulate an accurate effect in the respective target organs in the body.

Peptides released near the median eminence from hypothalamic nuclei are transported to the anterior pituitary, where they apply their effects. Branches from the internal carotid artery provide the blood supply to the pituitary. The superior hypophyseal arteries form the primary capillary plexus that supplies blood to the median eminence. From this capillary system, the blood is drained in hypophyseal portal veins into the secondary plexus. The peptides released at the median eminence enter the primary plexus capillaries. From there, they are transported to the anterior pituitary via hypophyseal portal veins to the secondary plexus. The secondary plexus is a network of fenestrated sinusoid capillaries that provide blood to the anterior pituitary. The cells of the anterior pituitary express specific G protein-coupled receptors that bind to the neuropeptides, activating intracellular second messenger cascades that produce the release of anterior pituitary hormones.[1]

Structure[edit]

The blood supply and direction of flow in the hypophyseal portal system has been studied over several years on laboratory animals and human cadaver specimens with injection methods.[2][3] Results of these studies have shown that the neural hypophyseal stalk and ventromedial region of the hypothalamic arcuate nucleus receive arterial blood from ascending and descending infundibular branches and capillaries, coming from arteries of the superior hypophyseal arterial system.[3] Small ascending vessels arising from the anastomoses that connect the upper with the lower hypophyseal arterial system also supply blood to hypophyseal vessels. The majority of these branches penetrate into the neural tissue to break up into capillaries for rapid hormone exchange.[1][2][3]

Development[edit]

Proper hormone secretion in the developing fetus is crucial for its growth in the womb of the mother. In order to allow a controlled hormone secretion in the developing organs of the fetus, stimulating hormones must be exchanged in the regulating structures in the brain in early stages of the development. Hormone-exchanging blood vessels between the hypothalamus and the pituitary gland, similar to those of the hypophyseal portal system, can be observed in early developmental stages of the fetus. In the current literature, most research is conducted using mice as model species. In such studies, development of the hypophyseal portal system begins as early as 14.5 dpc (days post coitum). Two populations of pericytes arise from the mesoderm and the neuroectoderm and form at the approximate location of the portal system in what will eventually become the mature brain.[4] Additionally, in research involving human fetuses it has been observed that the hypophyseal portal system fully develops by week 11.5 of the human fetal gestation period. This was determined by injecting a silicone rubber compound into specimens of various stages of gestation. In a specimen at week 11.5, the median eminence and infundibular stem contained the compound, suggesting the existence of the fully developed portal system.[5] Further research in this area would help determine whether or not development could be complete at an even earlier stage.

Relevant Hormones[edit]

The following is a list of hormones that rely on the hypophyseal portal system to indirectly mediate their function by acting as a means of transportation from various nuclei of the hypothalamus to the anterior pituitary.[6]

  • Gonadotropin-releasing hormone (GnRH): regulates the release of follicle stimulating hormone and luteinizing hormone from the anterior pituitary; this pathway plays a critical role in reproductive activity and development
  • Corticotropin-releasing hormone (CRH): regulates the release of adrenocorticotropic hormone from the anterior pituitary; this cascade is primarily responsible for stress responses
  • Growth hormone-releasing hormone (GHRH): regulates the release of growth hormone from the anterior pituitary; as the name suggests, its main function is to help control cell growth, metabolism, and reproduction
  • Thyrotropin-releasing hormone (TRH): regulates the release of thyroid-stimulating hormone from the anterior pituitary; functions to mediate various responses in the thyroid gland, including additional hormone synthesis

Clinical significance[edit]

Over- or under-function as well as insufficiencies of the hypothalamus or the pituitary gland can cause a negative effect on the ability of the hypophyseal portal system to exchange hormones between both structures rapidly. This can have major effects on the respective target glands, making it impossible for them to carry out their functions properly. Occlusions and other issues in the blood vessels of the hypophysial portal system can also cause complications in the exchange of hormones between the hypothalamus and the pituitary gland.

The hypophyseal portal system also plays an important role in several diseases involving the pituitary and central nervous system. In several cases of hypophyseal and pituitary metastatic tumors, the portal system acts as the pathway for metastasis from the hypothalamus to the pituitary. That is, cancerous cells from the hypothalamus multiply and spread to the pituitary using the hypophyseal portal system as a means of transportation. However, because the portal system receives an indirect supply of arterial blood, tumor formation in the anterior pituitary is less likely than in the posterior pituitary. This is because the posterior pituitary is vascularized by direct arterial blood flow.[7][8] Pituitary apoplexy is described as hemorrhaging or reduction of blood supply to the pituitary gland. The physiological mechanisms of this condition have not been clearly defined in current research.[9] It has been suggested, nonetheless, that damage to the pituitary stalk leads to an obstruction of blood flow in the hypophyseal portal system and contributes to this defective state.[10] In Erdheim-Chester Disease, cells of the immune system called histiocytes proliferate at an abnormal rate causing a plethora of symptoms and, in more severe cases, death. The disruption of the hypophyseal portal system has been implicated as the mechanism for several symptoms involving the central nervous symptom, most notably diabetes insipidus.[11]

See also[edit]

References[edit]

  1. ^ a b Molina, Patricia.E. (2010). Endocrine Physiology. Lange. (3, p. 31). ISBN 978-0-07-161301-9.
  2. ^ a b Shaver, S. W.; Pang, J. J.; Wainman, D. S.; Wall, K. M.; Gross, P. M. (1992). "Morphology and function of capillary networks in subregions of the rat tuber cinereum". Cell and Tissue Research. 267 (3): 437–48. PMID 1571958. 
  3. ^ a b c Ciofi, P; Garret, M; Lapirot, O; Lafon, P; Loyens, A; Prévot, V; Levine, J. E. (2009). "Brain-endocrine interactions: A microvascular route in the mediobasal hypothalamus". Endocrinology. 150 (12): 5509–19. PMC 2819742Freely accessible. PMID 19837874. doi:10.1210/en.2009-0584. 
  4. ^ Fiordelisio, Tatiana; Rizzoti, Karine; Samper, Patrick; Lafont, Chrstel; Davis, Shannon; Mollard, Patrice E. “Developmental Program of the Pituitary Portal System.” Endocrine Society’s 97th Annual Meeting and Expo. March 2015. San Diego, CA
  5. ^ Thliveris, James A.; Currie, R. William (1980-04-01). "Observations on the hypothalamo-hypophyseal portal vasculature in the developing human fetus". American Journal of Anatomy. 157 (4): 441–444. ISSN 1553-0795. doi:10.1002/aja.1001570411. 
  6. ^ 1948-, Silverthorn, Dee Unglaub,. Human physiology : an integrated approach. Johnson, Bruce R., Ober, William C., Ober, Claire E., Silverthorn, Andrew C. (Seventh ed.). [San Francisco]. ISBN 9780321981226. OCLC 890107246. 
  7. ^ Ravnik, Janez; Smigoc, Tomaz; Bunc, Gorazd; Lanisnik, Bostjan; Ksela, Ursa; Ravnik, Maja; Velnar, Tomaz. "Hypophyseal metastases: A report of three cases and literature review". Neurologia i Neurochirurgia Polska. 50 (6): 511–516. doi:10.1016/j.pjnns.2016.08.007. 
  8. ^ Komninos, John; Vlassopoulou, Varvara; Protopapa, Despina; Korfias, Stefanos; Kontogeorgos, George; Sakas, Damianos E.; Thalassinos, Nicolas C. (2004-02-01). "Tumors Metastatic to the Pituitary Gland: Case Report and Literature Review". The Journal of Clinical Endocrinology & Metabolism. 89 (2): 574–580. ISSN 0021-972X. doi:10.1210/jc.2003-030395. 
  9. ^ Briet, Claire; Salenave, Sylvie; Bonneville, Jean-François; Laws, Edward R.; Chanson, Philippe (2015-12-01). "Pituitary Apoplexy". Endocrine Reviews. 36 (6): 622–645. ISSN 0163-769X. doi:10.1210/er.2015-1042. 
  10. ^ Billeci, Domenico; Marton, Elisabetta; Giordan, Enrico. "Post-traumatic pituitary apoplexy: Case presentation and review of literature". Interdisciplinary Neurosurgery. 7: 4–8. doi:10.1016/j.inat.2016.10.006. 
  11. ^ Mazor, Roei D.; Manevich-Mazor, Mirra; Shoenfeld, Yehuda (2013-09-08). "Erdheim-Chester Disease: a comprehensive review of the literature". Orphanet Journal of Rare Diseases. 8: 137. ISSN 1750-1172. doi:10.1186/1750-1172-8-137. 

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