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尾加压素 ( Urotensin II)
Effect of chronic hypoxia on contents of urotensin II and its functional receptors in rat myocardium.
Zhang Y1, Li J1, Cao J1, Chen J1, Yang J2, Chang J2, Du J1, Tang C1
1Institute of Cardiovascular Research, First Hospital, Peking University, Beijing, People's Republic of China.
2 Phoenix Pharmaceuticals, Inc. Belmont, CA 94002, USA;

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The cyclic peptide urotensin II (UII) has recently been cloned in mammals and reported to constrict rat pulmonary arteries potently. An enhanced maximal response was shown in rats exposed to chronic hypoxia. The aim of this study was to investigate changes in plasma and myocardial UII levels and its receptor sites in crude sarcolemma of ventricles from chronic hypoxic rats. We observed that rats exposed to chronic hypoxia for 4 weeks developed pulmonary hypertension and right ventricular hypertrophy. Compared with controls, the UII content in hypoxic rats was increased by 97.5% (45.24 +/- 7.1 vs. 22.9 +/- 3.24pg/mg protein, P < 0.01) in the right ventricle and 33.2% (24.89 +/- 0.99 vs. 18.68 +/- 2.04pg/mg protein, P < 0.01) in the left ventricle, respectively. However, there was no significant difference in plasma (27.44 +/- 3.11 vs. 27.82 +/- 5.57pg/ml, P > 0.05) and lung tissue levels (34.03 +/- 4.63 vs. 33.74 +/- 4.06 pg/ mg protein, P > 0.05) between the control and hypoxic groups. The time course of the binding of [125I]UII to crude ventricular sarcolemma was specific and time dependent. Scatchard plot analysis of the data demonstrated that the maximal number of specific binding sites (Bmax) in both the right and left ventricles was upregulated in the hypoxic group. Moreover, Bmax in the right ventricular specimens was upregulated to a greater extent than in the left ventricle (increased by 114% and 25% in the right and left ventricles, respectively, compared with control group, P < 0.01). In contrast, the UII binding affinity in right and left ventricular membranes from hypoxic rats was decreased (the dissociation constant Kd) increased by 20% and 33%, respectively compared with controls, P < 0.01). These results indicate that UII may act as an autocrine and/or paracrine hormone rather than as a circulating hormone, playing important roles in the development of ventricular hypertrophy induced by chronic hypoxia, and that the pathophysiological significance of UII in pulmonary and cardiovascular alteration induced by chronic hypoxia deserves further investigation.
Heart Vessels 2002 Jan;16(2):64-8

Urotensin II-immunoreactivity in the brainstem and spinal cord of the rat
Dun SL1, Brailoiu GC1, Yang J2, Chang JK2, Dun NJ1.
1Department of Pharmacology, James H. Quillen College of Medicine, East Tennessee State University, PO Box 70577, 37614, Johnson City, TN, USA; 2 Phoenix Pharmaceuticals, Inc. Belmont, CA 94002, USA

The distribution of urotensin-II-immunoreactivity (irU-II) was studied in the rat brainstem and spinal cord with the use of an antiserum against the human urotensin II (U-II) peptide. A population of ventral horn neurons in the spinal cord, hypoglossal nucleus, dorsal motor nucleus of the vagus, facial motor nucleus, nucleus ambiguus, abducens nucleus and trigeminal motor nucleus exhibited irU-II of varying intensities. The number of irU-II motor neurons was higher in the lumbar segments as compared to that of cervical, thoracic and sacral segments. Double-labeling the sections with U-II- and choline acetyltransferase (ChAT)-antisera revealed that nearly all irU-II ventral horn and brainstem neurons were ChAT-positive. The result provides the first immunohistochemical evidence of the presence of irU-II in cholinergic motoneurons of the rat spinal cord and brainstem.
Neurosci Lett 2001 Jun 1;305(1):9-12

Adrenomedullin inhibits the endothelin production induced by urotensin II in rat vascular smooth muscle cells

Abstract   The aim of this study was to observe the effects of adrenomedullin (ADM) on endothelin (ET) production induced by urotensin II (U II) in rat vascular smooth muscle cells (VSMCs). Cultured VSMCs which were incubated with UII (10-8 mol/L) and with various concentrations of ADM were used to measure the VSMCs 3H-TdR incorpora- tion, the activity of extracellular signal-regulated kinase (ERK), the amount of ET mRNA and ET production in VSMCs. In this work we found that incubation with UⅡ(10-8 mol/L) increased obviously the amount of ET mRNA in VSMCs and ET production in medium, however, coincubation with ADM (10-10—10-8 mol/L) and UII(10-8 mol/L) reduced the amount of ET mRNA by 15%, 24% and 45% (P< 0.01) respectively, compared with UII alone. The content of ET in medium was 14.13, 11.38 and 11.00 pg/mL. ADM alone (10-8 mol/L) had no effect on ET production in VSMCs. UII (10-8 mol/L) promoted the 3H-TdR incorpo- ration and activity of ERK in VSMCs. ADM inhibited VSMCs 3H-TdR incorporation and activation of ERK in a concentration-dependent manner. Compared with UII group, after coincubation with ADM (10-10—10-8 mol/L) and UII (10-8 mol/L) the VSMCs 3H-TdR incorporation was decreased by 7% (P > 0.05), 32% (P < 0.05) and 41% (P < 0.01), respectively, and the activity of ERK  was decreased by 24% (P > 0.05), 32% (P < 0.05) and 36% (P < 0.05), re- spectively, in a concentration-dependent manner. The results show that in cultured VSMCs ADM inhibits ET mRNA expression, ET production and proliferation stimulated by UII, and that inhibitory effect of ADM on UⅡ bioaction could be mediated through inhibiting MAPK pathway.
QI Yongfen1, BU Dingfang1, YANG Jun2, ZHANG Zhaokang2, SHI Yanrong1, PANG Yongzheng1& TANG Chaoshu1,3  Chinese Science Bulletin  ISSN:1001-6538  2002 Vol.47 No.17       1457-1461

1. Institute of Cardiovascular Diseases, The First Hospital, Peking University, Beijing 100034, China;
2. Phoenix Pharmaceutical Inc. 2438 Wyandotte Street, Montain View, CA 94043, USA;
3. Department of Physiology, Heath Science Center, Peking University, Beijing 100083, China
Correspondence should be addressed to Tang Chaoshu (e-mail: tangchaoshu@263.net.cn)

 
Change and clinical implication of urotensin II in plasma and induced sputum of chronic obstructive pulmonary disease
OBJECTIVE: To investigate the roles of urotensin II (U-II) in chronic obstructive pulmonary disease (COPD). METHODS: Plasma and induced sputum were obtained from thirty four patients with stable COPD and ten healthy volunteers. The levels of U-II in plasma and induced sputum were measured by RIA kit. Lung function was performed routinely. Induced sputum cells were counted with hemacytometer and differentiated with Wright-Giemsa stain. RESULTS: The levels of U-II in induced sputum were 82 and 65 folds higher than those of plasma U-II in COPD patients and healthy controls (P<0.01). The levels of U-II in plasma were unrelated to those of induced sputum (r = 0.168, P>0.05). No difference was noted between COPD and healthy controls in the plasma U-II levels [1.46(1.15, 1.73) vs 1.61(1.31, 2.17) microg/L, medians with interquartile ranges, P>0.05]. Sputum U-II levels from COPD patients were 15% higher than those of healthy controls [119.87(105.03, 132.60) vs 104.44 (56.33, 122.24) microg/L, medians with interquartile ranges, P<0.05]. Induced sputum U-II levels of COPD patients had a trend of increase as lung function deteriorated and smoking index increases. Raised sputum total cell and neutrophil counts correlated strongly with the levels of U-II in induced sputum (r = 0.454, r = 0.431, both P<0.01). The levels of U-II in induced sputum correlated negatively with FEV(1)% predicted and p(O(2)) (r = -0.417, r = -0.518, both P<0.05). CONCLUSION: U-II may act locally, or, via paracrine or autocrine way, play a role in the mechanism of the airway inflammation and airway remodeling in COPD.
Lu M, et al. Beijing Da Xue Xue Bao. 2006 Apr 18;38(2):155-8.
 
Urotensin II and biomarkers of endothelial activation and atherosclerosis in end-stage renal disease
BACKGROUND: Urotensin II (UTN), a cyclic undecapeptide widely distributed in various organs and tissues, is found in high concentration in atheromatous lesions. Because UTN accumulates in patients with chronic renal failure, the association between plasma UTN and biomarkers of atherosclerosis and endothelial activation needs to be better understood. METHODS: We tested by a robust statistical approach (Holm method) the association between plasma UTN and biomarkers of atherosclerosis and endothelial activation in a population of 191 patients undergoing chronic hemodialysis. RESULTS: Plasma UTN was significantly higher in patients with end-stage renal disease (median: 6.5 ng/mL) than in healthy subjects (median: 3.1 ng/mL) (P < .001), and in both patients and control subjects it was independent of age and sex. Interestingly, UTN was inversely related to fibrinogen (r = -0.50, P < .004), intracellular adhesion molecule-1 (r = -0.24, P < .004) and with NO synthesis inhibitor asymmetric dimethyl-arginine (r = -0.40, P < .004). These links were paralleled by direct correlations with albumin (r = 0.21, P < .006) and with transforming growth factor-beta1 (TGFbeta1) (r = 0.36, P < .004). Of note, on multiple regression analysis, these associations remained highly significant also after data adjustment for potential confounders. CONCLUSIONS: The inverse links between UTN with biomarkers of atherosclerosis and endothelial activation suggest that downregulation of UTN may be a counter-regulatory response aimed at mitigating cardiovascular damage or that UTN itself is a protective factor.
Mallamaci F, et al. Am J Hypertens. 2006 May;19(5):505-10
 
Urotensin II in end-stage renal disease: An inverse correlate of sympathetic function and cardiac natriuretic peptides
Urotensin II (UTN) is a peptide highly conserved across species with disparate effects on the vascular system and it is currently unclear whether high plasma UTN levels play a vasculotoxic or a vasculoprotective role. Methods: In this study, we investigated the relationship between plasma UTN and sympathetic activity and cardiac natriuretic hormones in 191 hemodialysis (HD) patients without clinical evidence of heart failure. Results: Plasma UTN was significantly higher in patients with end-stage renal disease (ESRD) (median: 6.5 ng/mL) than in age matched healthy subjects (median: 3.1 ng/mL) (p<0.001). On univariate analysis, UTN was inversely related to heart rate (r=-0.24), dialysis treatment duration (r=-0.27), norepinephrine (r=-0.28), neuropeptide Y (NPY) (r=-0.66), brain natriuretic peptide (BNP) (r=-0.41) and atrial natriuretic peptide (ANP) (r=-0.28) (all p<0.008). Of note, in multiple regression analyses these associations maintained strength similar to that of the corresponding unadjusted correlation coefficients. Conclusions: The inverse links between UTN and neuro-hormonal factors indicate that UTN down-regulation in the presence of high sympathetic activity and high BNP could be a counter-regulatory response aimed at mitigating cardiovascular (CV) damage or that UTN itself acts as a protective factor.
F. Mallamaci et al. J NEPHROL 2005; 18: 727-732
 
Circulating urotensin II levels in moderate to severe congestive heart failure: Its relations with myocardial function and well established neurohormonal markers
Urotensin II (UII) is a potent vasoactive cyclic peptide thought to play a role in myocardial hypertrophy and remodelling. We therefore determined UII plasma levels in congestive heart failure (CHF) patients and its relationship with the severity of the disease and well-established markers of left ventricular function. UII was significantly higher in CHF patients (n=57) than in controls (n=48) [geometric mean (pg/ml), 95% PI: 1.32 (0.67-2.59) versus 0.84 (0.31-1.61), p<0.0001], was related to the functional class of the disease and correlated negatively with left ventricular ejection fraction (r=-0.316, P=0.016). Furthermore, UII correlated significantly with Big-ET1 (r=0.32, p=0.03), BNP (r=0.42, p=0.005) but poorly with Nt-proANP (r=0.28, p=0.07). Our results suggest that UII could play a role in worsening the course of congestive heart failure and is associated with established markers of cardiovascular dysfunction.
Gruson D, et al. Peptides. 2006 Jun;27(6):1527-31. Epub 2005 Dec 20.

More Urotensin II related publications

   
 
Urotensin II
urotensin II
QC Data / Protocol
QC Data / Protocol
urotensin II
   
QC Data / Protocol
QC Data / Protocol
Code Product Name Quantity USD Euro
071-16 Urotensin II (3-11) (Human) 200 ug 90.00 85.50
071-27 Urotensin II (4-11) (Human) 200 ug 80.00 76.00
071-28 Urotensin II (5-11) (Human) 200 ug 80.00 76.00
071-23 Urotensin II, Prepro (41-68) (Human) 100 ug 180.00 171.00
071-22 Urotensin II, Prepro (71-84) (Human) 200 ug 120.00 114.00
071-24 Urotensin II, Prepro (21-40) (Human) 200 ug 120.00 114.00
071-06 Urotensin II, Prepro (87-110) (Human) 200 ug 150.00 143.00
071-21 Urotensin II, Prepro (87-104) (Rat) 200 ug 120.00 114.00
071-17 Urotensin II Related Peptide 200 ug 90.00 86.00
071-15 SB-710411, Urotensin II Receptor Antagonist 100 ug 120.00 114.00
071-29 BIM 23127 200 ug 80.00 76.00
 
U II
Relationship between plasma UTN and biochemical score calculated as sum of three variables (norepinephrine, NPY and BNP) defined in categorical terms (0=below and 1=above the 75th percentile of the relative data distribution). Data are median and inter-quartile range. F. Mallamaci et al. J NEPHROL 2005; 18: 727-732
Urotensin II
Urotensin II
Relationship between plasma UTN with plasma norepinephrine, plasma NPY and plasma BNP. Data are correlation coefficients and PHolm values. F. Mallamaci et al. J NEPHROL 2005; 18: 727-732
Urotensin II
Relationship between plasma UTN and HR. Data are correlation coefficient and PHolm value. F. Mallamaci et al. J NEPHROL 2005; 18: 727-732

Plasma UTN was significantly higher in patients with ESRD (median: 6.5 ng/mL, range 1.1-66.0 ng/mL) than in age matched healthy subjects (median: 3.1 ng/mL, range 1.3-12.8 ng/mL) (p<0.001). Both in patients (p>0.50) and in controls (p>0.56) plasma UTN was uninfluenced by age and sex. Plasma UTN was determined by a specific, commercially available, high sensitivity enzyme immunoassay ( EK-071-05, Phoenix Pharmaceuticals, Belmont, CA, USA). The antibody employed in this assay does not cross react with ET-1, angiotensin II, adrenomedullin, CGRP and brain natriuretic peptide (BNP). F. Mallamaci et al. J NEPHROL 2005; 18: 727-732

Anti-Urotensin II Antibody For Your  Immunohistochemistry Mapping

A section of rat lumbar spinal cord was labeled with Phoenix's Anti-Urotensin II antibody (1:2,500 dilution).

Dr. Nae J. Dun's Lab.,  Department of Pharmacology
James H. Quillen College of Medicine
East Tennessee State University

Fluorescein Labeled Urotensin II Enables to Visualize Urotensin II Receptor (GPR14) Dynamic Trafficking in Living Cell

 Human Plasma Levels of Urotensin II
 
Urotensin II (Human) 5.5 ± 0.2 pg/ml  (extracted plasma) Dr. Chao-Shu Tang, 1st Hospital, Peking University, P.R.China
Urotensin II (Human) 45.5 ± 3.1 pg/ml (non-extracted plasma) Dr. Chao-Shu Tang, 1st Hospital, Peking University, P.R.China
Urotensin II (Human) 7.70 ± 0.97 pg/ml (extracted plasma) Phoenix Pharmaceuticals
Urotensin II (Human) 12 ± 3 pmol/L (16.6 ± 4.1 pg/ml) Wilkinson IB, et al. Cardiovasc Res 2002 Feb 1;53(2):341-7
 

 




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