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Multihormonal Control Of Melanotropin Secretion In Cold-Blooded Vertebrates
Published in Mac E. Hadley, The Melanotropic Peptides, 1988
Marie-Christine Tonon, Jean-Michel Danger, Marek Lamacz, Philippe Leroux, Saida Adjeroud, Ann C. Andersen, Kemenade Lidy Verburg-van, Bruce G. Jenks, Georges Pelletier, Lise Stoeckel, Arlette Burlet, Gotfryd Kupryszewski, Hubert Vaudry
The availability of synthetic CRF has allowed the generation of antirsera for radioimmunoassay and immunocytochemistry. CRF-containing neurons are widely distributed in the brain, including the telencephalon, mesencephalon, and metencephalon.359 In the rat, the great majority of CRF-immunoreactive perikarya are located in the parvocellular part of the paraventricular nucleus (PVN)360-363 as well as in the magnocellular perikarya of the PVN.364,365 In monkey and humans, CRF neurons are located in both the paraventricular and supraoptic nuclei of the hypothalamus.366-368 A close topographical relationship is generally found between neurophysin- and CRF-containing neurons,363,368-370 and the existence of CRF-like material in subpopulations of magnocellular neurons containing vasopressin or oxytocin has been reported. Dense bundles of CRF-containing processes terminate in the external zone of the median eminence362,363,365,371,372 and the presence of immunoreactive fibers has been observed in the neural lobe of the pituitary.363,373,374 Along these lines, significant amounts of CRF have been detected in the posterior lobe of the rat.375 The localization of CRF-neuronal systems has been determined in various submammalian vertebrates including birds,365,376,377 amphibians,365,378-380 and fishes.365,381-384 The distributional map of urotensin-I-like immunoreactivity in the fish brain has been recently provided.384 In the salmon, CRF-immunoreactive fibers terminate in the distal part of the neurohypophysis and in contact of adenohypophyseal corticotrophs.385 In amphibians, a large number of CRF- containing fibers are located in the external zone of the median eminence in close contact with the capillaries of the pituitary portal plexus.380 In Rana ridibunda, many fibers are present in the neurohypophysis and a few scattered fibers containing CRF-like material are found in the intermediate lobe of the pituitary,380 suggesting a possible role of CRF in the control of melanotropin secretion.
Genetic Basis of Blood Pressure and Hypertension
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Sandosh Padmanabhan, Alisha Aman, Anna F. Dominiczak
Vascular endothelial function also modulates vascular tone. The vascular endothelium synthesizes and releases a spectrum of vasoactive substances, including NO, a potent vasodilator. NO exerts vasodilating and antiproliferative effects on smooth muscle cells and inhibits thrombocyte aggregation and leukocyte adhesion. The synthesis of NO is controlled by the enzyme endothelial NO synthase (NOS3) and is induced by calcium-mobilizing agents and fluid shear stress. Other vascular relaxation factors include endothelins and prostacyclin. Endothelin-1 (EDN1) activates specific ETA receptors (EDNRA) on vascular smooth muscle cells to cause vasoconstriction and cell proliferation. In contrast, endothelial ETB receptors (EDNRB) mediate vasodilatation via release of NO and prostacyclin (PGI2). GWAS of coronary artery disease (CAD) showed the SNP rs9349379 G allele (frequency 36%) was associated with increased risk of CAD and coronary calcification but decreased risk for four conditions (migraine headache, cervical artery dissection, fibromuscular dysplasia and HTN [89,90]). This SNP is located within the third intron of the gene encoding phosphatase and actin regulatory protein 1 (PHACTR1). However, functional analysis of this variant show that it regulates expression of endothelin 1 (EDN1), a gene located 600 kb upstream of PHACTR1. The CAD risk associated with this allele is likely through increased endothelial production of ET-1 and subsequent binding to the ETA receptor, which promotes atherosclerosis. However, the association of the G allele with low systolic BP is thought to be through the action of ET-1 on the second endothelin receptor, ETB (91). In contrast to the coronary arteries where ETA receptors predominate, ETB receptors are more abundant in the large systemic arteries. The protective effect of this allele on BP is explained by action of ET1 on ETB receptors which predominate in large vessels. ET-1 binding to ETB triggers endothelium-dependent vasodilation through the production of NO, prostacyclins, and renal natriuresis. Interestingly, variants in the PHACTR1 gene have been associated with fibromuscular dysplasia (FMD), a nonatherosclerotic vascular disease leading to stenosis, dissection and aneurysm affecting mainly the renal and cerebrovascular arteries (92). Variants in the gene for vascular endothelial growth factor A (VEGFA) which induces proliferation, migration of vascular endothelial cells, and stimulates angiogenesis, is one of the replicated signals from GWAS. The GWAS locus containing urotensin-2 receptor (UTS2R) gene encodes a class A rhodopsin family G-protein—coupled receptor that upon activation by the neuropeptide urotensin II produces profound vasoconstriction. One of the GWAS loci is the relaxin gene, which encodes a G-protein—coupled receptor with roles in uterine relaxation, vasorelaxation and cardiac function which signals via phosphatidylinositol 3-kinase (PI3K).
Urotensin-II, oxidative stress, and inflammation increase in hypertensive and resistant hypertensive patients
Published in Clinical and Experimental Hypertension, 2021
Eray Metin Guler, Mustafa Gokce, Ahmet Bacaksiz, Abdurrahim Kocyigit
Hypertension (HT) is a very common pathology which contributes to substantial risk factors for mortality and morbidity of cardiovascular disease (1). The etiology of HT is not completely understood. To date, a large amount of evidence has shown that vasoactive substances that played an essential role in HT pathophysiology. Urotensin-II (UII) is one of these vasoactives involved in the cardiovascular system in humans (2) by stimulating the proliferation of a series of cells (3) and regulating subendothelial inflammation (4). UII induces vasodilation or vasoconstriction on the condition of the endothelium (5) and dependently the vascular bed (6). This may be an explanation of why the correlation between HT and UII has been reported inconsistently in previous population-based studies. For example, elevated plasma UII was demonstrated in HT patients in comparison with normotensives (7,8).
Oxidative parameters, oxidative DNA damage, and urotensin-II in schizoaffective disorder patients
Published in Psychiatry and Clinical Psychopharmacology, 2019
Osman Hasan Tahsin Kilic, Ihsan Aksoy, Gulcin Cinpolat Elboga, Feridun Bulbul
Urotensin-II (U-II) is a neuropeptide which takes place in the oxidative system by increasing reactive oxygen species (ROS), inflammatory mediators, and pro-inflammatory cytokines [22]. Increased U-II levels have been demonstrated in the aetiology of many diseases such as diabetes mellitus, essential hypertension, and renal failure in which oxidative stress is also blamed [22,23]. U-II levels were found to be negatively correlated with TAS levels and positively correlated with oxidative stress index (OSI) levels in patients with diabetes mellitus [23]. U-II may be an important mediator in the central nervous system by means other than oxidative system. U-II was first isolated from the urophysis of teleost fish, which is an analogue of hypothalamic-pituitary axis and the receptor of U-II was found to be located throughout the central nervous system [24,25]. It has also been shown that U-II and its receptor may be a novel chemokine system that may influence the development of the central nervous system by recent studies [25]. The modulatory effect of U-II on behavioural, hormonal, oxidative, and inflammatory factors and its newly discovered migration regulatory effect suggest that U-II may play a role in the pathophysiology of psychotic disorders. U-II was researched only in schizophrenia patients with psychiatric disorders and it was found to be elevated [26]. Therefore, we investigated the levels of U-II in schizoaffective disorder patients and its association with oxidative status and oxidative DNA damage.
Expression of urotensin II is positively correlated with pyroptosis-related molecules in patients with severe preeclampsia
Published in Clinical and Experimental Hypertension, 2021
Ya-Jing Pan, Meng-Ze Zhang, Lin-Hui He, Jin Feng, Ai-Hua Zhang
Urotensin II is a vasoactive substance which is widely expressed in the placentas as well as other organs, such as kidney, small intestine, prostate et al. UII possesses the most potent endogenous vasoconstrictor discovered up to now. Our previous study (21) found that the expressions of UII and ER stress markers (GRP78 and CHOP) were significantly higher in patients with severe preeclampsia than that of normal controls. Moreover, UII expression was positively correlated with markers of ER stress. Moreover, UII is an inflammatory cytokine (22), so we hypothesize that UII may possess the potential to induce placental pyroptosis and amplify inflammation in severe preeclampsia.