BNP-45 rat (Brain natriuretic peptide-45 rat)
(Synonyms: 大鼠脑钠素肽-45,BNP-45, rat) 目录号 : GC32612BNP-45 rat (Brain natriuretic peptide-45 rat) (BNP-45, rat) 是一种循环形式的大鼠脑利钠肽,从大鼠心脏中分离出来,具有强效降压和利钠作用。
Cas No.:123337-89-3
Sample solution is provided at 25 µL, 10mM.
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Animal experiment: | Rats[1]Male anesthetized spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) (20- to 25 week-old) are used in the assay. Isotonic saline (20 μL/min) is infused throughout the esperiment. After equilibration for at least 60 min, urine is collected every 10 min during a 20-min control period. Rat BNP-45 or rat α-ANP (0.1, O.2, 0.5, 1.0 and 2.0 nmol/kg) dissolved in saline containing 1% bacitracin is injected i.v., and urine is collected continuously for three to six 10-min periods following each dose. There is a 30- to 60-min rest interval between each injection, to allow the urine volume to return to a steady baseline value. Urine volume is determined by weight. Urinary sodium and potassium are measured by flame photometry. The concentration of cGMP in urine is measured by radioimmunoassay, using cGMP assay kit[1]. |
References: [1]. Kita T, et al. Effects of brain natriuretic peptide-45, a circulating form of rat brain natriuretic peptide, in spontaneously hypertensive rats. Eur J Pharmacol. 1991 Sep 4;202(1):73-9. |
BNP-45 (rat), a 45-amino acid brain natriurctic peptide isolated from rat heart, is a circulating hormone, with natriuretic andhypotensive activities.
BNP-45 (rat), a 45-amino acid brain natriurctic peptide isolated from rat heart, is a circulating hormone, with natriuretic andhypotensive activities[1].
BNP-45 (rat) (0.1, O.2, 0.5, 1.0 and 2.0 nmol/kg, i.v.) shows potent natriuretic and hypotensive activities in anesthetized spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). BNP-45 (rat) with high concentration decreases blood pressure in SHR. But WKY is more susceptible than SHR to BNP-45 for diuresis, natriuresis and urinary cGMP excretion. In addition, high dose of BNP-45 (rat) cuases prolonged lowering of blood pressure and urinary cGMP excretion in WKY[1].
[1]. Kita T, et al. Effects of brain natriuretic peptide-45, a circulating form of rat brain natriuretic peptide, in spontaneously hypertensive rats. Eur J Pharmacol. 1991 Sep 4;202(1):73-9.
Cas No. | 123337-89-3 | SDF | |
别名 | 大鼠脑钠素肽-45,BNP-45, rat | ||
Canonical SMILES | Ser-Gln-Asp-Ser-Ala-Phe-Arg-Ile-Gln-Glu-Arg-Leu-Arg-Asn-Ser-Lys-Met-Ala-His-Ser-Ser-Ser-Cys-Phe-Gly-Gln-Lys-Ile-Asp-Arg-Ile-Gly-Ala-Val-Ser-Arg-Leu-Gly-Cys-Asp-Gly-Leu-Arg-Leu-Phe(Disulfide bridge: Cys23-Cys39) | ||
分子式 | C213H349N71O65S3 | 分子量 | 5040.67 |
溶解度 | Soluble in Water | 储存条件 | Store at -20°C |
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Radioimmunoassay for rat B-type natriuretic peptide (BNP-45)
J Immunoassay 1993 Sep;14(3):167-82.PMID:8354718DOI:10.1080/15321819308019847.
rat BNP-45 is the main circulating form of BNP in rat plasma. To understand the role of BNP in physiological and pathophysiological conditions, a specific radioimmunoassay (RIA) for the quantitative determination of the peptide in plasma and tissues is necessary. An assay using rBNP-45 as the standard in conjunction with antisera directed against this peptide has not been described in the literature, though some investigators have reported values ranging from 0.73-2.0 pmol/L using either BNP-26 or BNP-32 as the standard peptide. Unfortunately, these forms of BNP do not exist in rat plasma. In our studies, we have developed a specific RIA for rBNP-45 using rBNP-45 as the standard peptide and Tyro-rBNP-45 as the radioligand. We have used two specific antisera for assay purposes; one against rBNP-45, and the second to a peptide composed of the first 20 amino acids of rBNP-45 (rBNP[1-20]). The recovery of various amounts of rBNP-45 added to control plasma was 50-80% depending on the method of extraction and purification. The interassay and intraassay coefficients of variation were 12% and 6% respectively. Values obtained were similar for blood sampled by either cardiac puncture, decapitation, or aortic puncture. The method was used to measure rBNP-45 in the plasma of normal (WKY) and Spontaneously Hypertensive (SHR) rats. The values obtained were 5.46 +/- 0.43 and 19.6 +/- 2.36 pmol/L respectively. The rat atrial natriuretic peptide (ANP[99-126]) values in the same extracts were 23.2 +/- 0.45 and 51.6 +/- 3.16 pmol/L.
Effects of brain natriuretic peptide-45, a circulating form of rat brain natriuretic peptide, in spontaneously hypertensive rats
Eur J Pharmacol 1991 Sep 4;202(1):73-9.PMID:1664804DOI:10.1016/0014-2999(91)90255-o.
Rat brain natriuretic peptide-45 (rat BNP-45) has recently been isolated from rat heart and shown to be a circulating form of rat BNP. We investigated the effects of rat BNP-45 in anesthetized spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) and compared them with those of rat alpha-atrial natriuretic peptide (alpha-ANP). BNP-45 was a potent natriuretic and hypotensive agent in both strains. The effects were comparable with those of alpha-ANP and were far greater than those of porcine BNP-26 reported previously. In SHR blood pressure decreased more than in WKY following injection of the highest dose (2.0 nmol/kg) of BNP-45 or alpha-ANP. However, WKY were more susceptible than SHR to BNP-45 for diuresis, natriuresis and urinary cGMP excretion. Moreover, a high dose of BNP-45 led to a prolonged lowering of blood pressure and urinary cGMP excretion compared to alpha-ANP, and these features were prominent in WKY. BNP-45 disappeared more slowly than alpha-ANP when the two peptide (2.0 micrograms) were injected i.v. in WKY. Thus, rat BNP-45 and alpha-ANP had comparable hypotensive and natriuretic potency; however, the action and plasma half-life of rat BNP-45 were more prolonged.
Porcine brain natriuretic peptide-like immunoreactivity in rat tissues
Peptides 1991 Nov-Dec;12(6):1333-5.PMID:1815220DOI:10.1016/0196-9781(91)90216-c.
The presence of immunoreactive porcine brain natriuretic peptide in rat tissues was studied with a specific radioimmunoassay for porcine brain natriuretic peptide-26. The cross-reactivity of the antiserum used was less than 0.001% with rat atrial natriuretic peptide, rat brain natriuretic peptide-32 and Rat brain natriuretic peptide-45. Immunoreactive porcine brain natriuretic peptide was detectable in various tissues of the rat, and high concentrations of immunoreactive porcine brain natriuretic peptide were found in the brain and cardiac atrium, with the highest level in the hypothalamus (159 +/- 30 fmol/gram wet tissue, mean +/- SEM, n = 4). Reverse phase high performance liquid chromatography showed that the immunoreactive porcine brain natriuretic peptide of the whole brain and heart extracts eluted mainly at an identical position to synthetic porcine brain natriuretic peptide-26. These findings indicate that porcine brain natriuretic peptide-like substance, distinct from rat brain natriuretic peptide, is present in high concentrations in the rat brain and cardiac atrium.
Increased plasma levels and effects of brain natriuretic peptide in experimental nephrosis
Nephron 1993;65(3):454-9.PMID:8289999DOI:10.1159/000187529.
Rat brain natriuretic peptide-45 (BNP-45) is a new cardiac hormone secreted into the circulation. In order to evaluate the pathophysiologic role of BNP in the nephrotic syndrome, we investigated the plasma levels and effects of BNP in adriamycin (ADR)-induced nephrotic rats. Plasma levels of BNP rose with time and more than doubled in 3 weeks after injection. Plasma levels of BNP correlated significantly with urinary protein excretion (UPrV) and urinary protein/creatinine ratio (UPrV/UcrV). When rat BNP-45 was injected as a bolus, hypotensive, diuretic, and natriuretic effects were completely abolished in nephrotic animals even at a high dose (2.0 nmol/kg), whereas the peptide produced marked UPrV with an increase in UPrV/UcrV. These results indicate that in ADR-induced nephrosis, BNP secretion from the heart is increased. Remarkable resistance to some hemodynamic and renal effects, while prompt proteinuric effects of BNP, may contribute to the sodium and water retention and urinary protein characteristic of this disorder.
Atrial natriuretic peptide stimulates Na+-dependent Ca2+ efflux from freshly isolated adult rat cardiomyocytes
FEBS Lett 1997 Dec 15;419(2-3):255-8.PMID:9428645DOI:10.1016/s0014-5793(97)01470-1.
In the present study, we examined the effect of atrial natriuretic peptide (ANP) on Ca2+ efflux from freshly isolated adult rat cardiomyocytes. Rat ANP(1-28) stimulated the efflux of 45Ca2+ from the cells in a concentration-dependent manner (10(-8) M to 10(-6) M). The 45Ca2+ efflux was not affected by removal of extracellular Ca2+, but was dependent on the presence of extracellular Na+. In addition, rat ANP(1-28) caused 22Na+ influx into the cells. The 45Ca2+ efflux was also stimulated by C-type natriuretic peptide-22 (CNP-22), but not by Rat brain natriuretic peptide-45 (BNP-45). It was also observed that both rat ANP(1-28) and CNP-22 stimulated guanosine 3',5'-cyclic monophosphate production within the cells. These results indicate that ANP stimulates Na+-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through Na+/Ca2+ exchange, and that the stimulatory effect of ANP on Ca2+ efflux may be mediated via the natriuretic peptide receptor which has been shown to couple to guanylate cyclase. Since it is reported that Na+/Ca2+ exchange is important in calcium homeostasis within cells, ANP may play a role in the extrusion of intracellular Ca2+ from isolated adult rat cardiomyocytes.