Urotensin II is a nitric oxide-dependent vasodilator and natriuretic  peptide in the rat kidney

Zhang, Andrew Y.; Chen, Yafei; Zhang, David X.; Feng, Yi; Qi, Jenson; Andrade‐Gordon, Patricia; Garavilla, Lawrence de; Li, Pin‐Lan; Zou, Ai-Ping

doi:10.1152/ajprenal.00342.2002

Cited by 92 publications

(87 citation statements)

References 37 publications

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“…Other groups have reported a variety of renal responses to UTS infusion in the rat. Zhang et al (2003) observed an increase in fractional sodium excretion following intra-renal infusion of hUTS, but this was seen against a rather different background of diuresis and natriuresis accompanied by no change in GFR. By contrast, Ovcharenko et al (2006) observed no change in sodium excretion or fractional excretion of sodium in response to bolus injections of hUTS in Wistar rats.…”

Section: Discussionmentioning

confidence: 90%

“…Previous clearance studies in rats have injected bolus doses systemically at 1-100 nmol/kg (Ovcharenko et al 2006) or infused at 2 . 5-20 ng/kg per min directly into the renal artery (Zhang et al 2003), which potentially exposed the kidney to supraphysiological doses of the hormone. The heterologous nature of the peptides used in these studies is unlikely to have had a significant impact on the outcome, as the UTSR is unable to distinguish between UTS from a number of species, including humans and rats (Labarrere et al 2003).…”

Section: Discussionmentioning

confidence: 99%

“…bolus dose; this was associated with and driven by renal haemodynamic effects leading to a marked reduction in glomerular filtration rate (GFR) (Song et al 2006). By contrast, Zhang et al (2003) observed an increased renal blood flow (RBF) when UTS was infused directly into the renal artery, this time associated with a diuresis and natriuresis. These contradictory observations highlight the profound, possibly pharmacological influence of UTS on renal haemodynamics.…”

Section: Introductionmentioning

confidence: 99%

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Renal haemodynamic and tubular actions of urotensin II in the rat

Abdel-Razik¹,

Forty²,

Balment³

et al. 2008

Journal of Endocrinology

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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.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Renal haemodynamic and tubular actions of urotensin II in the rat

Abdel-Razik¹,

Forty²,

Balment³

et al. 2008

Journal of Endocrinology

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“…The role of UII in the kidney is not clear at present. It has been shown to promote endothelial NO-mediated vasodilation in rat renal arteries accompanied by a dosedependent increase in renal blood flow and an increased urinary water and sodium excretion, but opposite effects have also been reported (Zhang et al 2003, Ashton 2006, Song et al 2006. It has been suggested that these discrepancies might result from the limited amounts of unoccupied receptors for binding exogenous UII (Qi et al 2005).…”

Section: Uts2r5mentioning

confidence: 99%

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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“…Continuous infusion of U-II into the renal artery of anesthetized rats caused nitric oxide-dependent increases in GFR, urinary water excretion, and urinary sodium excretion. 5 This effect may be possibly explained by reduced renal functions and fluid overload association. In a model of arteriovenous fistula induced high-output heart failure, incremental injection of U-II caused mean arterial pressure lowering, both in failing heart and in healthy controls.…”

Section: Introductionmentioning

confidence: 99%

Decrease of Urotensin II activity can impact on the volume status in predialysis chronic kidney disease

Yılmaz

Sarı

et al. 2015

Renal Failure

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Urotensin II (U-II) was thought to be one of the mediators of primary renal sodium retention due to effects on renal sodium excretion. For this purpose, the relationship between U-II and overhydration was investigated. A total of 107 patients were enrolled in the study. According to body compositor monitor analysis, fluid overload up to 1.1 L, was considered normohydration. Patients were divided according to hydration status; overhydrate (n ¼ 42) and normohydrate (n ¼ 65) were studied in both groups. Pulse waveform velocity propagation for arterial stiffness and blood pressure analysis and echocardiographic left ventricular and left atrial indices were performed with known fluid overload-related parameters. U-II levels were measured by using Human ELISA kit. In overhydrated group, U-II levels were significantly lower. All parameters (blood pressure, arterial stiffness parameters, echocardiographic data, age, gender, diabetes, U-II, hemoglobin) correlated with overhydration, were determined by linear regression model (method ¼ enter), when considered together, U-II was found to be an independent predictor from other conventional overhydration-related parameters. Male sex, left ventricular mass index, left atrial volume index, hemoglobin value were found to be independent predictors for overhydration. Considering the association of low U-II levels with adverse cardiovascular events and its role in sodium retention, we think that low U-II levels can be accepted as a potential therapeutic target in patients with hypervolemic cardio-renal syndrome.

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Urotensin II is a nitric oxide-dependent vasodilator and natriuretic peptide in the rat kidney

Cited by 92 publications

References 37 publications

Renal haemodynamic and tubular actions of urotensin II in the rat

Renal haemodynamic and tubular actions of urotensin II in the rat

MOLECULAR EVOLUTION OF GPCRS: Somatostatin/urotensin II receptors

Decrease of Urotensin II activity can impact on the volume status in predialysis chronic kidney disease

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