Depressor and regionally‐selective vasodilator effects of human and rat urotensin II in conscious rats

Gardiner, Sheila M.; March, J E; Kemp, P.A.; Davenport, Anthony P.; Bennett, T.

doi:10.1038/sj.bjp.0704051

Cited by 92 publications

(91 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These observations are consistent with Gardiner et al report of a modest reduction in RBF in conscious SD rats following either bolus injection (Gardiner et al 2001) or 6-h infusion (Gardiner et al 2006) of hUTS. The effects of hUTS on RBF were blocked by indomethacin and attenuated by L-NAME (Gardiner et al 2006) implying that cyclooxygenase products and nitric oxide were involved in the response to hUTS.…”

Section: Discussionsupporting

confidence: 82%

Renal haemodynamic and tubular actions of urotensin II in the rat

Abdel-Razik¹,

Forty²,

Balment³

et al. 2008

Journal of Endocrinology

View full text Add to dashboard Cite

Urotensin II (UTS) is a potent vasoactive peptide that was originally identified in teleost fish. Mammalian orthologues of UTS and its receptor (UTSR) have been described in several species, including humans and rats. We have shown previously that bolus injections of UTS caused a decrease in urine flow and sodium excretion rates in parallel with marked reductions in renal blood flow (RBF) and glomerular filtration rate (GFR). The aim of this study was to determine the effect of UTS infusion at a dose that has minimal impact upon renal haemodynamics in order to identify a potential direct tubular action of UTS. Infusion of rat UTS (rUTS) at 0 . 6 pmol/min per 100 g body weight in male Sprague-Dawley rats, which had no effect on RBF and caused a 30% reduction in GFR, resulted in a significant increase in the fractional excretion of sodium (vehicle 2 . 3G0 . 6 versus rUTS 0 . 6 pmol 4 . 5G0 . 6%, P!0 . 05) and potassium. At the higher dose of 6 pmol/min per 100 g body weight, haemodynamic effects dominated the response. rUTS induced a marked reduction in RBF and GFR (vehicle 1 . 03G 0 . 06 versus rUTS 6 pmol 0 . 31G0 . 05 ml/min per 100 g body weight, P!0 . 05) resulting in an anti-diuresis and antinatriuresis, but no change in fractional excretion of sodium or potassium. Uts2d and Uts2r mRNA expression were greater in the renal medulla compared with the cortex. Together, these data support an inhibitory action of Uts2d on renal tubule sodium and potassium reabsorption in the rat, in addition to its previously described renal haemodynamic effects.

show abstract

Section: Discussionsupporting

confidence: 82%

Renal haemodynamic and tubular actions of urotensin II in the rat

Abdel-Razik¹,

Forty²,

Balment³

et al. 2008

Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…In vivo, systemic administration of U-II to the anesthetized primate results in profound renal vasoconstriction (Ames et al 1999). In contrast to the primate, systemic U-II administration to the conscious rat is associated with renal hyporemia secondary to its effects on arterial blood pressure (Gardiner et al 2001).…”

Section: Discussionmentioning

confidence: 99%

Localization of Urotensin-II Immunoreactivity in Normal Human Kidneys and Renal Carcinoma

Shenouda

Douglas

Ohlstein

et al. 2002

J Histochem Cytochem.

103

View full text Add to dashboard Cite

S U M M A R Y Human urotensin-II (U-II) is a cyclic 11-amino-acid residue peptide with a wide range of vasoactive properties dependent on the anatomic site and the species studied. The purpose of this study was to determine the localization of human U-II in normal human kidneys and in renal carcinoma. Normal human kidneys ( n ϭ 11) and eight cases of clear-cell carcinoma were immunostained with a polyclonal antibody to human U-II. In normal human kidneys, U-II was mostly present in the epithelial cells of tubules and ducts, with greater intensity in the distal convoluted tubules. Moderate U-II immunoreactivity was seen in the endothelial cells of renal capillaries, but only focal immunoreactivity was found in the endothelial cells of the glomeruli. No staining was found in the veins. All tumors expressed moderate U-II immunoreactivity in the cancer cells and vasculature. Here we demonstrate abundant expression of U-II in normal human kidneys and renal carcinoma. These findings suggest that the vasoactive and growth-mediator peptide U-II may contribute to the pathophysiology of the human renal system.

show abstract

“…Using helically cut strips from major arteries of male Sprague-Dawley rats, UII was shown to produce concentration-dependant contractions, with EC 50 obtained at a concentration of 6.8 ϫ 10 Ϫ10 M. This effect was greatest in the thoracic aorta. The action of UII was found to be independent of endothelial cells and to work via mobilization of intracellular calcium as well as through stimulation of extracellular calcium influx (39).…”

Section: Physiological Actions Of Uii In Various Organ Systemsmentioning

confidence: 99%

“…At low concentrations (3 pmol/kg), neither rUII nor hUII administration seemed to have any effect. At a 30 pmol/kg dose, however, rUII was shown to cause transient mesenteric vasodilation, while at 300 and 3,000 pmol/kg, dose-dependent tachycardia and mesenteric and hindquarter hyperemic vasodilation was noted (39).…”

mentioning

confidence: 99%

Role of urotensin II in health and disease

Ross

McKendy

Giaid

2010

American Journal of Physiology-Regulatory, Integrative and Comp

128

107

View full text Add to dashboard Cite

Urotensin II (UII) is an 11 amino acid cyclic peptide originally isolated from the goby fish. The amino acid sequence of UII is exceptionally conserved across most vertebrate taxa, sharing structural similarity to somatostatin. UII binds to a class of G protein-coupled receptor known as GPR14 or the urotensin receptor (UT). UII and its receptor, UT, are widely expressed throughout the cardiovascular, pulmonary, central nervous, renal, and metabolic systems. UII is generally agreed to be the most potent endogenous vasoconstrictor discovered to date. Its physiological mechanisms are similar in some ways to other potent mediators, such as endothelin-1. For example, both compounds elicit a strong vascular smooth muscle-dependent vasoconstriction via Ca 2ϩ release. UII also exerts a wide range of actions in other systems, such as proliferation of vascular smooth muscle cells, fibroblasts, and cancer cells. It also 1) enhances foam cell formation, chemotaxis of inflammatory cells, and inotropic and hypertrophic effects on heart muscle; 2) inhibits insulin release, modulates glomerular filtration, and release of catecholamines; and 3) may help regulate food intake and the sleep cycle. Elevated plasma levels of UII and increased levels of UII and UT expression have been demonstrated in numerous diseased conditions, including hypertension, atherosclerosis, heart failure, pulmonary hypertension, diabetes, renal failure, and the metabolic syndrome. Indeed, some of these reports suggest that UII is a marker of disease activity. As such, the UT receptor is emerging as a promising target for therapeutic intervention. Here, a concise review is given on the vast physiologic and pathologic roles of UII.UT receptor; somatostatin; human; experimental animals; autocrine/paracrine UROTENSIN II (UII) was initially isolated from the urophysis of the goby fish (Gillichthys mirabilis) (97). The peptide was subsequently isolated from the white sucker (Catostomus commersoni) and the carp (Cyprinus carpio). Although there were variations in the amino acid sequence near the amino terminus, in both species the UII molecule retained the COOH-terminal cyclic sequence: -Cys

show abstract

Depressor and regionally‐selective vasodilator effects of human and rat urotensin II in conscious rats

Cited by 92 publications

References 19 publications

Renal haemodynamic and tubular actions of urotensin II in the rat

Renal haemodynamic and tubular actions of urotensin II in the rat

Localization of Urotensin-II Immunoreactivity in Normal Human Kidneys and Renal Carcinoma

Role of urotensin II in health and disease

Contact Info

Product

Resources

About