Localization of the urotensin II receptor in the rat central nervous system

Jégou, Sylvie; Cartier, Dorthe; Dubessy, Christophe; Gonzalez, Bruno J.; Chatenet, David; Tostivint, Hervé; Scalbert, Elizabeth; Leprince, Jérôme; Vaudry, Hubert; Lihrmann, Isabelle

doi:10.1002/cne.20845

Cited by 65 publications

(71 citation statements)

References 46 publications

(93 reference statements)

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“…Central administration of UII has yielded more constant results, because in most species examined it evokes an increase in mean arterial pressure and heart rate through the activation of the peripheral sympathetic nervous system (Watson & May 2004, Le Mevel et al 2008. UTS2R1 mRNA can be detected in brainstem nuclei controlling cardiovascular homeostasis and in hypothalamic nuclei such as the paraventricular nucleus, which supports its role as a modulator of cardiovascular function (Jegou et al 2006). The URP mRNA is highly expressed in neurons that are intermingled with tyrosine hydroxylase-immunoreactive A1/C1 cells in the rostral ventrolateral medulla, indicating that URP may directly control adrenal sympathetic outflow.…”

Section: Uts2r5mentioning

confidence: 69%

“…A number of behavioral effects of UII have been reported (Do Rego et al 2008), in line with the broad distribution of UTS2R1 mRNA and radiolabeled UIIbinding sites in the CNS (Jegou et al 2006). It is well established that UII is involved in various mood and sleep processes.…”

Section: Uts2r5mentioning

confidence: 79%

“…It has been obvious for many years, ever since the discovery of UII in mammals, that UII and URP are involved in the control of motor functions, although their exact roles are not fully understood. A high density of UII-and URPbinding sites has been found in regions of the human and rat brains that are involved in motor control (Maguire et al 2000, Jegou et al 2006, Bucharles et al 2014, and i.c.v. administered UII and/or URP increases locomotion in mice, rats, and rainbow trout (Gartlon et al 2001, Lancien et al 2004, Do Rego et al 2005.…”

Section: Uts2r5mentioning

confidence: 99%

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MOLECULAR EVOLUTION OF GPCRS: Somatostatin/urotensin II receptors

Tostivint¹,

Daza²,

Bergqvist³

et al. 2014

Journal of Molecular Endocrinology

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Somatostatin (SS) and urotensin II (UII) are members of two families of structurally related neuropeptides present in all vertebrates. They exert a large array of biological activities that are mediated by two families of G-protein-coupled receptors called SSTR and UTS2R respectively. It is proposed that the two families of peptides as well as those of their receptors probably derive from a single ancestral ligand-receptor pair. This pair had already been duplicated before the emergence of vertebrates to generate one SS peptide with two receptors and one UII peptide with one receptor. Thereafter, each family expanded in the three whole-genome duplications (1R, 2R, and 3R) that occurred during the evolution of vertebrates, whereupon some local duplications and gene losses occurred. Following the 2R event, the vertebrate ancestor is deduced to have possessed three SS (SS1, SS2, and SS5) and six SSTR (SSTR1-6) genes, on the one hand, and four UII (UII, URP, URP1, and URP2) and five UTS2R (UTS2R1-5) genes, on the other hand. In the teleost lineage, all these have been preserved with the exception of SSTR4. Moreover, several additional genes have been gained through the 3R event, such as SS4 and a second copy of the UII, SSTR2, SSTR3, and SSTR5 genes, and through local duplications, such as SS3. In mammals, all the genes of the SSTR family have been preserved, with the exception of SSTR6. In contrast, for the other families, extensive gene losses occurred, as only the SS1, SS2, UII, and URP genes and one UTS2R gene are still present.

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Section: Uts2r5mentioning

confidence: 69%

Section: Uts2r5mentioning

confidence: 79%

Section: Uts2r5mentioning

confidence: 99%

See 1 more Smart Citation

MOLECULAR EVOLUTION OF GPCRS: Somatostatin/urotensin II receptors

Tostivint¹,

Daza²,

Bergqvist³

et al. 2014

Journal of Molecular Endocrinology

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“…Vasoconstriction is not its only effect because UT receptors have been found in other organs. 43,44 Urotensin-II has also been shown to function as a potent vasodilator in some isolated vessels. 45 Norepinephrine: VSMC are primarily innervated by the sympathetic nervous system through adrenergic receptors.…”

Section: Urotensin-iimentioning

confidence: 99%

The role of oxidative stress in the pathophysiology of hypertension

2011

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Hypertension is considered to be the most important risk factor in the development of cardiovascular disease. An increasing body of evidence suggests that oxidative stress, which results in an excessive generation of reactive oxygen species (ROS), has a key role in the pathogenesis of hypertension. The modulation of the vasomotor system involves ROS as mediators of vasoconstriction induced by angiotensin II, endothelin-1 and urotensin-II, among others. The bioavailability of nitric oxide (NO), which is a major vasodilator, is highly dependent on the redox status. Under physiological conditions, low concentrations of intracellular ROS have an important role in the normal redox signaling maintaining vascular function and integrity. However, under pathophysiological conditions, increased levels of ROS contribute to vascular dysfunction and remodeling through oxidative damage. In human hypertension, an increase in the production of superoxide anions and hydrogen peroxide, a decrease in NO synthesis and a reduction in antioxidant bioavailability have been observed. In turn, antioxidants are reducing agents that can neutralize these oxidative and otherwise damaging biomolecules. The use of antioxidant vitamins, such as vitamins C and E, has gained considerable interest as protecting agents against vascular endothelial damage. Available data support the role of these vitamins as effective antioxidants that can counteract ROS effects. This review discusses the mechanisms involved in ROS generation, the role of oxidative stress in the pathogenesis of vascular damage in hypertension, and the possible therapeutic strategies that could prevent or treat this disorder. Hypertension Research (2011) 34, 431-440; doi:10.1038/hr.2010.264; published online 13 January 2011Keywords: antioxidants; endothelial dysfunction; oxidative stress INTRODUCTION Hypertension is considered the most important risk factor for the occurrence of cardiovascular disease. 1 Oxidative stress has gained attention as one of the fundamental mechanisms responsible for the development of hypertension. Reactive oxygen species (ROS) have an important role in the homeostasis of the vascular wall; hence, they could be part of the mechanism that leads to hypertension. 2-4 Thus, increased ROS production, reduced nitric oxide (NO) levels and reduced antioxidant bioavailability were demonstrated in experimental and human hypertension. Vascular superoxide is primarily derived from nicotinamide adenine dineucleotide phosphate (NADPH) oxidase when stimulated by hormones, such as angiotensin II (AT-II), endothelin-1 (ET-1) and urotensin II. In addition, increased ROS production may be generated by mechanical stimuli on the vascular wall, which increase with hypertension. ROS-induced vasoconstriction results from increased intracellular calcium concentration, thereby contributing to the pathogenesis of hypertension. 2 Vasomotor tone is dependent on a delicate balance between vasoconstrictor and vasodilator forces that result from the interaction between the components of...

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“…In addition, this peptide may contribute to the physiological regulation of cardiovascular homeostasis in humans (21,22). It was suggested that urotensin II can be used as a marker of myocardial and ischemia reperfusion injuries (23,24).…”

mentioning

confidence: 99%