China
Africa
Explore chapters and articles related to this topic
Head and Neck
Published in Bobby Krishnachetty, Abdul Syed, Harriet Scott, Applied Anatomy for the FRCA, 2020
Bobby Krishnachetty, Abdul Syed, Harriet Scott
Arterial supply Superior and inferior hypophyseal arteries, which are branches of the internal carotid artery. They form a capillary network with the hypothalamo-hypophyseal portal system. The primary capillary network lies at the pituitary stalk, where the hypothalamic hormones are released. This capillary bed is drained by a set of long portal veins that give rise to the second capillary bed in the anterior pituitary. The veins originating in the neurohypophyseal capillary plexus give rise to the short portal veins that will also contribute to the adenohypophyseal capillary plexus and connect the two circulatory systems.This hypothalamo-hypophyseal portal system creates a communication between the endocrine and neural cells providing an easy short loop feedback between the two sets of cells.
Opioids and Induction of Ovulation: Mediation by Neuropeptide Y
Published in Craig A. Johnston, Charles D. Barnes, Brain-Gut Peptides and Reproductive Function, 2020
S.P. Kalra, L.G. Allen, A. Sahu, W.R. Crowley
Crowley et al. (1987) also explored the possibility that NPY may be released into the hypophyseal portal system for an effect at the level of the pituitary. Although a slight stimulatory effect of NPY on LH release from hemipituitaries in culture was observed, unlike the results of McDonald et al. (1985), we failed to observe any effect of NPY on LH release from dispersed pituitary cells (Fig. 10). However, an unexpected, novel outcome of these studies was a robust dose-dependent potentiation by NPY of the effects of LHRH on LH release from hemipituitaries and dispersed pituitary cells in culture (Fig. 10).
Distribution and Characteristics of Brain Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
The hypophysiotropic hormones of the hypothalamus (also called releasing and inhibiting hormones) collect in the median eminence and are secreted from there into the hypophyseal portal system, which vascularizes the pituitary gland [22]. The pars nervosa, a component of the posterior pituitary gland, forms a continuance with the median eminence via the pituitary stalk, or infundibulum. The stalk passes through the dura mater of the diaphragm sellae and carries dopaminergic and magnocellular axons down to the posterior pituitary. A detailed description of the neural and vascular connections between the hypothalamus and the pituitary is presented in Sections 3.4.5 and 3.4.6.
Hypothalamic-pituitary-adrenal axis activity in post-traumatic stress disorder and cocaine use disorder
Published in Stress, 2020
Natalie A. Hadad, Marek Schwendt, Lori A. Knackstedt
The HPA axis, a neuroendocrine system, responds to a variety of stimuli. One such stimulus is stress, which is defined as a circumstance that threatens homeostasis (de Kloet et al., 1998). Upon activation of the HPA axis, the parvocellular cells of the hypothalamic paraventricular nucleus synthesize and release corticotropin-releasing hormone (CRH; also known as corticotropin-releasing factor or CRF) and its co-secretagogue vasopressin into the primary plexus of the median eminence. From there, CRH and vasopressin travel along the hypophyseal portal system, to reach the secondary plexus of the anterior pituitary where they act synergistically to stimulate corticotroph cells to produce the polypeptide precursor proopiomelanocortin (POMC). POMC is then cleaved into several active peptides, including adrenocorticotropic hormone (ACTH; also known as corticotropin). In turn, ACTH circulates in the blood of the secondary plexus and is carried to the adrenal cortex. Binding of ACTH to its receptors within the zona fasciculata of the adrenal cortex promotes the local synthesis and release of glucocorticoids into the bloodstream. In humans and other primates, the main glucocorticoid secreted by the adrenal cortex is cortisol, while in many other species (including rodents and birds) it is corticosterone. Both glucocorticoids are abbreviated here and elsewhere as “CORT”. CRH and ACTH are secreted in bursts, with the frequency of bursts showing a circadian rhythm (Baum & Grunberg, 1995). As a result, under basal conditions, human CORT levels peak at approximately 8AM and decline throughout the day to reach the lowest levels around midnight (Baum & Grunberg, 1995). Under conditions of stress, CORT reaches its peak levels in the blood 15–30 min after the onset of the stressor and then declines to pre-stress levels after 60–90 min (Baum & Grunberg, 1995; de Kloet et al., 1998, 2005).
Pituitary adenoma and apoplexy during GnRH agonist treatment for IVF - case report
Published in Gynecological Endocrinology, 2020
Aneta Stefaniak, Jan Domitrz, Katarzyna Siewko, Małgorzata Szelachowska, Adam Krętowski, Alicja Stachura-Matyjewicz
GnRH is a decapeptide synthesized by neurons surrounding the septum pellucidum and the preoptic area of the hypothalamus. It travels through the hypophyseal portal system, bypassing systemic circulation, to reach the gonadotropic cells of the anterior pituitary gland. By binding to its cognate receptor on these cells, it stimulates the function of two gonadotropic hormones: follicle stimulating hormone (FSH) and luteinizing hormone (LH). Triptorelin, a synthetic GnRH analog, is a decapeptide whose structure was chemically modified by exchanging a glycine amino acid into a tryptophan at position six of the decapeptide. This change caused an increase in biological agonistic activity of the product toward GnRH receptors, improved stability, and a longer half-life of the drug molecule, owing to a longer binding time of the modified amino acids. Initially, its administration causes a substantial and sudden increase in the secretion of FSH and LH, leading to a rise in the number of GnRH receptors on the cells of the anterior pituitary (the flare-up effect). After a few days of drug use, these receptors become desensitized, and the drug causes a clear step-wise decrease in gonadotropin activity (a down-regulation effect) [1–3]. Currently, the effect of triptorelin on pituitary dysfunction has not been fully explored in humans as scientific reports are very sparse. The summary of product characteristics of triptorelin states that the use of GnRH agonists can, in very rare cases, reveal a hormonally inactive pituitary adenoma [https://www.leki-informacje.pl/content/gonapeptyl-daily; year of access: 2019]. These data are based on experiment performed in rats; however, these observations do not apply to humans due to differences in their endocrine systems [4–6]. In humans, a single case of pituitary adenoma has been described in a 78-year-old man treated with triptorelin due to prostate cancer. At the time, it was suggested that the adenoma occurrence may be due to a rapid stimulation of gonadotropic cells, leading to an increase in their volume and thus the volume of the tumor [4,7]. Causes of pituitary apoplexy in the vicinity of the adenoma are often attributed to the tumor’s rapid growth, which causes it to be insufficiently supplied with arterial blood. A different hypothesis suggests that the rapid filling of the sella turcica by the growing tumor puts pressure on the thin blood vessels in the area. This would lead to ischemia, necrosis around the entire anterior pituitary gland, explaining the violent clinical symptoms of all hormonal axes dependent on GnRH [2,4,7,8].