Urodilatin
(Synonyms: ANP 95-126) 目录号 : GC45130
A renal natriuretic peptide
Cas No.:115966-23-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Urodilatin is a renal natriuretic peptide first isolated from human urine. It is derived from the same precursor as atrial natriuretic peptide in kidney tubular cells and secreted luminally. Urodilatin regulates sodium and water reabsorption in the kidney. While it is not normally found in the circulation, systemic administration of urodilatin has pharmacological effects on renal, cardiovascular, and pulmonary parameters in animals.
| Cas No. | 115966-23-9 | SDF | |
| 别名 | ANP 95-126 | ||
| Canonical SMILES | [H]N[C@]([C@@H](C)O)([H])C(N[C@H](C(N1CCC[C@H]1C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CO)C(N[C@@H](CC(C)C)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CO)C(N[C@@H](CO)C(N[C@H](C(N[C@H](C(NCC(NCC(N[C@@H](CCCNC(N)=N)C(N[C@H](C(N[C@H](C(N[C@@H](CCCNC(N)= | ||
| 分子式 | C145H234N52O44S3 | 分子量 | 3506 |
| 溶解度 | DMF: 25 mg/ml,DMSO: 10 mg/ml,Ethanol: 0.3 mg/ml,PBS (pH 7.2): 10 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.2852 mL | 1.4261 mL | 2.8523 mL |
| 5 mM | 0.057 mL | 0.2852 mL | 0.5705 mL |
| 10 mM | 0.0285 mL | 0.1426 mL | 0.2852 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
The renal Urodilatin system: clinical implications
Cardiovasc Res 2001 Aug 15;51(3):450-62.PMID:11476735DOI:10.1016/s0008-6363(01)00331-5.
A renal natriuretic peptide and the 'renal Urodilatin system' were identified after the observation that immunoassayable ANP in urine may not be identical to the circulating cardiac hormone ANP, which is a peptide of 28 amino acids. Urodilatin (INN: Ularitide) is a natriuretic peptide isolated from human urine and belongs to the family of A-type natriuretic peptides. Urodilatin is differentially processed to a peptide of 32 amino acids from the same precursor as ANP. It is synthesized in kidney tubular cells and secreted luminally. After secretion from epithelial cells of the distal and/or connecting tubules, Urodilatin interacts downstream at distal segments of the nephron with luminally located receptors whereby it regulates Na(+) and water reabsorption. Thus, the physiological function of the renal Urodilatin system can be described as a paracrine intrarenal regulator for Na(+) and water homeostasis, considering Urodilatin as a real diuretic-natriuretic regulatory peptide. However, the regulation upon which the Urodilatin secretion depends is still not clear. Since Urodilatin has been discovered, a great number of pharmacological and clinical investigations have been carried out using Urodilatin as a drug for several indications. So far, clinical phase I and II studies for acute renal failure, congestive heart failure, and bronchial asthma have been performed.
ANP and Urodilatin: who is who in the kidney
Eur J Med Res 2006 Oct 27;11(10):447-54.PMID:17107879doi
Mounting evidence suggests that Urodilatin, not atrial natriuretic peptide (ANP) is the responsible peptide in regulation of renal Na superset+- and water homeostasis. Following the discovery of ANP this peptide was thought to be responsible for the induction of natriuresis and diuresis in the mammalian kidney. However, the isolation of Urodilatin from human urine and substantial work contributed to a better understanding of the renal physiology of these two natriuretic peptides. Indeed, subsequent elucidation supported that Urodilatin rather than ANP seems to be the natriuretic peptide responsible for the regulation of Na superset+- and water homeostasis in the kidney. Urodilatin - synthesized and secreted from the distal tubules of the kidney - may act as a paracrine mediator when secreted into the lumen. In contrast, while the role of ANP as regulator of the cardiovascular system is established, its physiological regulatory role on transport processes in the nephron is questionable. This review attempts to analyze the roles of both ANP and Urodilatin and to discuss new potential candidates which may also play a role in electrolyte and water handling in the kidney.
Urodilatin: a better natriuretic peptide?
Curr Heart Fail Rep 2007 Sep;4(3):147-52.PMID:17883990DOI:10.1007/s11897-007-0033-2.
The kidney natriuretic peptide Urodilatin (ie, ularitide) decreases pulmonary capillary wedge pressure (PCWP) but does not cause diuresis in persons with congestive heart failure (CHF). Thirty-three percent of patients with CHF treated with 30 ng/kg/min ularitide develop hypotension with systolic blood pressures below 90 mmHg. Nesiritide and atrial natriuretic peptide lower PCWP and cause hypotension. They do not produce diuresis or natriuresis in patients with CHF. The best natriuretic peptide for treating CHF is the cardiac hormone vessel dilator which decreases PCWP and decreases systemic and pulmonary vascular resistance while simultaneously increasing cardiac output and cardiac index. What makes the vessel dilator markedly better than atrial natriuretic peptide, nesiritide, and ularitide for treatment of CHF is that it enhances sodium excretion fivefold and causes a fivefold enhanced diuresis in patients with CHF with its biologic effects lasting over 6 hours compared with less than 30 minutes for the above peptides.
Urodilatin, a natriuretic peptide with clinical implications
Eur J Med Res 1998 Feb 21;3(1-2):103-110.PMID:9512977doi
Natriuretic peptides (NP) constitute hormonal systems of great clinical impact. This report deals with Urodilatin (URO), a renal natriuretic peptide type A. From the gene of NP type A, a message for the preprohormone is transcribed in heart and kidney. The cardiac prohormone CDD/ANP-1-126 is synthesized in the heart atrium and processed during exocytosis forming the circulating hormone CDD/ANP-99-126. URO (CDD/ANP 95-126) is a product from the same gene, but differentially processed in the kidney and detected only in urine. Physiologically, URO acts in a paracrine fashion. After release from distal tubular kidney cells into the tubular lumen, URO binds to luminal receptors (NPR-A) in the collecting duct resulting in a cGMP-dependent signal transduction. cGMP generation is followed by an interaction with the amiloriode-sensitive sodium channel which induces diuresis and natriuresis. In this way, URO physiologically regulates fluid balance and sodium homeostasis. Moreover, URO excretion and natriuresis are in turn dependent on several physiological states, such as directly by sodium homeostasis. Pharmacologically, URO at low dose administered intravenously shows a strong diuretic and natriuretic effect and a low hypotensive effect. Renal, pulmonary, and cardiovascular effects evoked by pharmacological doses indicate that URO is a putative drug for several related diseases. Clinical trials show promising results for various clinical indications. However, the reduction in hemodialysis/hemofiltration in patients suffering from ARF following heart and liver transplantation, derived from preliminary trials recruiting a small number of patients, was not confirmed by a multicenter phase II study. In contrast, data for the prophylactic use of URO in this clinical setting suggest a better outcome for the patients. Furthermore, treatment of asthmatic patients showed a convincingly beneficial effect of URO on pulmonary function. Patients with congestive heart failure may also profit from URO treatment, as it increases stroke volume and PCWP. Moreover, preliminary results from recent studies indicate that URO may also be effective in patients suffering from hepato-renal syndrome.
Urodilatin regulates renal dopamine metabolism
J Nephrol 2013 Nov-Dec;26(6):1042-8.PMID:23661592DOI:10.5301/jn.5000279.
Background: Sodium and water transport across renal proximal tubules is regulated by diverse hormones such as dopamine and Urodilatin. We have previously reported that Urodilatin stimulates extraneuronal dopamine uptake in external renal cortex by activation of the type A natriuretic peptide receptor, coupled to cyclic guanylate monophosphate signaling and protein kinase G. Moreover, Urodilatin enhances dopamine-induced inhibition of Na+, K+-ATPase activity in renal tubules. The aim of the present study was to evaluate whether Urodilatin could also alter renal dopamine synthesis, release, catabolism and turnover. Methods: The effects of Urodilatin on dopamine synthesis, release, catabolism and turnover were measured in samples of renal cortex from Sprague Dawley rats. Results: The results indicate that Urodilatin increases L-DOPA decarboxylase activity and decreases catechol-o-methyl transferase and monoamine oxidase activity. Moreover, Urodilatin does not affect either dopamine basal secretion or potassium chloride-induced dopamine release in external renal cortex, and reduces amine turnover. Conclusions: Both the present results and previous findings show that Urodilatin modifies dopamine metabolism in external renal cortex of rats by enhancing dopamine uptake and synthesis and by decreasing catechol-o-methyl transferase and monoamine oxidase activity and dopamine turnover. Those effects taken together may favor dopamine accumulation in renal cells and increase its endogenous content and availability. This would permit D1 receptor recruitment and stimulation and, in turn, overinhibition of Na+, K+-ATPase activity, which results in decreased sodium reabsorption. Therefore, Urodilatin and dopamine enhance natriuresis and diuresis through a common pathway.