Autoradiographic localization of atrial and brain natriuretic peptide receptors in rat brain

1990 ◽  
Vol 258 (1) ◽  
pp. R57-R63 ◽  
Author(s):  
J. Brown ◽  
A. Czarnecki

Displacement of bound 125I-labeled atrial natriuretic peptide-(1-28) [alpha 125I-ANP-(1-28)] by alpha-ANP-(5-28) and porcine brain natriuretic peptide (BNP) was used to map receptors common to these peptides in rat brain by in vitro autoradiography. alpha-125I-ANP bound reversibly to subfornical organ, area postrema, median preoptic, supraoptic and paraventricular nuclei, and arachnoid mater. Binding at these sites was displaced similarly by 1 microM unlabeled alpha-ANP, alpha-ANP-(5-28), and BNP. Binding dissociation constants in the subfornical organ and arachnoid were 4.40 +/- 1.15 and 3.99 +/- 0.86 nM, respectively, for alpha-ANP, and 2.41 +/- 1.11 and 2.23 +/- 1.06 nM, respectively, for BNP. alpha-125I-ANP also bound to choroid plexus. Here 1 microM unlabeled alpha-ANP displaced significantly more radioligand than did 1 microM BNP, and the concentration displacing 50% of bound radioligand was 2.23 +/- 0.78 nM for alpha-ANP and 1.51 +/- 0.67 nM for BNP. alpha-ANP-(5-28) also displaced alpha 125I-ANP at all sites with significantly greater affinity than did unlabeled alpha-ANP. alpha-125I-ANP was not displaced by completely unrelated peptides. Therefore, both atrial and brain natriuretic peptides may be high-affinity ligands at common receptors in some cerebral localities.

1990 ◽  
Vol 258 (4) ◽  
pp. R1078-R1083
Author(s):  
J. Brown ◽  
A. Czarnecki

The presence and distribution of atrial natriuretic peptide (ANP) clearance receptors in rat brain were investigated by use of des[Gln18,Ser19,Gly20,Leu21,Gly22]ANP-(4-2 3) (C-ANP), a specific ligand of this receptor, to displace bound alpha-125I-labeled ANP. alpha-125I-ANP (200 pM) bound significantly to arachnoid mater, subfornical organ, choroid plexus, area postrema, median preoptic nucleus, and supraoptic and paraventricular nuclei. Binding was reversible at all sites with unlabeled alpha-ANP. Binding dissociation constants for alpha-ANP were measured for the first three sites and were all in the nanomolar range. C-ANP competed with alpha-125I-ANP only for binding sites on arachnoid mater, 1 microM C-ANP displacing radioligand from at least 60% of these sites. No alpha-125I-ANP was displaced by completely unrelated peptides. The reversible binding of 125I-Tyr0-ANP-(5-25), another relatively selective ligand of the clearance receptor, was also concentrated on arachnoid mater. Therefore, high-affinity binding sites for alpha-ANP on arachnoid mater may be clearance receptors for ANP.


1988 ◽  
Vol 66 (3) ◽  
pp. 288-294 ◽  
Author(s):  
Juan M. Saavedra

We have studied the localization, kinetics, and regulation of receptors for the circulating form of the atrial natriuretic peptide (99–126) in the rat brain. Atrial natriuretic peptide receptors were discretely localized in the rat brain, with the highest concentrations in circumventricular organs, the choroid plexus, and selected hypothalamic nuclei involved in the production of the antidiuretic hormone vasopressin and in blood pressure control. Spontaneously (genetic) hypertensive rats showed much lower numbers of atrial natriuretic peptide receptors than normotensive controls in the subfornical organ, the area postrema, the nucleus of the solitary tract, and in the choroid plexus. These changes are in contrast with those observed for receptors of angiotensin II, another circulating peptide with actions opposite to those of the atrial natriuretic peptide. In acute dehydration after water deprivation, as well as in chronic dehydration such as that present in homozygous Brattleboro rats, there was an up-regulation of atrial natriuretic peptide receptors in the subfornical organ. Thus, circumventricular organs contain atrial natriuretic peptide receptors that could respond to variations in the concentration of circulating peptide. The localization of atrial natriuretic peptide receptors and the alterations in their regulation present in hypertensive and dehydrated rats indicate that these brain receptors are related to fluid regulation, including the secretion of vasopressin, and to cardiovascular function. Atrial natriuretic peptide receptors in the choroid plexus may be related to the formation of cerebrospinal fluid.


2010 ◽  
Vol 235 (8) ◽  
pp. 941-951 ◽  
Author(s):  
Mario Torrado ◽  
Raquel Iglesias ◽  
Alberto Centeno ◽  
Eduardo López ◽  
Alexander T Mikhailov

1998 ◽  
Vol 95 (5) ◽  
pp. 547-555 ◽  
Author(s):  
J. G. LAINCHBURY ◽  
M. G. NICHOLLS ◽  
E. A. ESPINER ◽  
H. IKRAM ◽  
T. G. YANDLE ◽  
...  

1.The cardiac natriuretic peptides, atrial natriuretic peptide and brain natriuretic peptide, are degraded via clearance receptors and the enzyme neutral endopeptidase (EC 3.4.24.11). We studied the regional plasma concentrations of these peptides and their response to acute neutral endopeptidase inhibition in a consecutive series of patients with a broad spectrum of severity of cardiac dysfunction who were undergoing diagnostic right and left heart catheterization (24 patients, mean age 62.6 years). 2.Baseline blood samples were obtained for hormone analysis from femoral artery, femoral vein, renal vein, hepatic vein, superior vena cava, coronary sinus and pulmonary artery, and initial haemodynamic measurements were made. Twelve patients then received a neutral endopeptidase inhibitor (SCH 32615, 200 ;mg intravenously) and 12 received vehicle alone. The cardiac catheterization procedure was then completed and haemodynamic and hormone measurements were repeated. 3.Haemodynamic status was similar at baseline in both groups, and at repeated measurement (post-procedure after placebo or active drugs) haemodynamic variables were not significantly different from baseline values. Plasma levels of atrial and brain natriuretic peptides exhibited an arteriovenous increment (344% and 124% respectively) across the heart (femoral artery to coronary sinus) and decrement (by 28–54% and 9–16% respectively) across all other tissue beds (P< 0.05 for all) except the lung (no change). Final levels of atrial natriuretic peptide rose above initial levels at all sites in both groups (P< 0.05) except coronary sinus levels in the vehicle group (no change). The increase was consistently greater in the inhibitor group at all sites (P< 0.05 versus placebo). Levels of brain natriuretic peptide rose at all sites in the inhibitor group only (P< 0.05). The transcardiac step-up in atrial natriuretic peptide was markedly augmented after the administration of neutral endopeptidase inhibitor. Other tissue gradients were not significantly altered by neutral endopeptidase inhibitor. 4.Atrial and brain natriuretic peptides in plasma are degraded by a number of tissues, and respond differently to cardiac catheterization. Neutral endopeptidase has a significant role in determining plasma levels of natriuretic peptides, in part perhaps by influencing the amount of intact peptide reaching the circulation after secretion from the heart.


2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Pipin Ardhianto ◽  
Yoga Yuniadi

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmias and associated with the risk of stroke and death. Continuous development of the diagnostic tool and prognostic stratification may lead to optimal management of AF. The use of biomarkers in the management of AF has been grown as an interesting topic. However, the AF biomarkers are not yet well established in the major guidelines. Among these biomarkers, a lot of data show troponin and brain natriuretic peptides are promising for the prediction of future events. The troponin elevation in AF patients may not necessarily be diagnosed as myocardial infarction or significant coronary artery stenosis, and brain natriuretic peptide elevation may not necessarily confirm heart failure. Troponin T and troponin I may predict postoperative AF. Furthermore, troponin and brain natriuretic peptide gave better prognostic performance when compared with the risk score available today.


2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Aviva Peleg ◽  
Yonathan Hasin

Background: Contrast media (CM) administrated during percutaneous coronary intervention (PCI) is associated with endothelial dysfunction (ED) and systemic vascular injury. Brain natriuretic peptide (BNP) administration 24 hours post PCI decreases ED. Aims: To evaluate 1.The ability of human BNP (hBNP) infusion during PCI, to prevent ED in acute coronary syndrome's (ACS) patients post the PCI. 2. The effect of CM on human coronary microvascular endothelial cells (HCMEC).3. Explain ED by invitro study. Methods and results (in vivo): Non-ST elevation ACS patients who underwent PCI (111) were randomized into 2 groups: an hBNP group who received hBNP infusion during the procedure (n=44), and control group who received nitroglycerin (n=67). Flow mediated dilatation (FMD) (by ≥2.5%), BNP, corin, serum creatinine (sCr) and estimate Glomerular Filtration Rate (eGFR), before and 24 hr after operative were recorded, starting with the same baseline. The post PCI FMD and eGFR were significantly reduced in the control group (p=0.05, 0.002) but not in the hBNP group (p=0.16, 0.4). BNP, corin and sCr increased significantly in the control group (p=0.001, 0.003, 0.0002 respectively) but not in hBNP group (p=0.09, 0.07, 0.18). Methods and results (in vitro): HCMEC were treated with CM (10%) in the presence and absence of BNP. eNOS, corin and cGMP levels were measured by ELISA and the results were compared to untreated cells. In both treatments eNOS was significantly reduced (p=0.001) and corin was significantly increased (p=0.002). cGMP was not affected by CM treatment (p=0.278), but was increased significantly (p=0.001) by hBNP combination. cGMP immuno-flourescence staining of HCMEC showed distorted cellular cGMP appearance by CM treatment, that was corrected in the combination with hBNP with accentuated subsarcolemmal staining. Conclusions: CM reduces eNOS level in HCMEC. Therefore, reduced in NO-cGMP pathway's products, probably is the mechanism that induces ED in-vivo. BNP treatment reduces FMD diminution and kidney injury post PCI. A compensatory rise in corin that increases BNP as well as the hBNP administration, invivo and invitro, maintains cytosolic cGMP via NP-cGMP pathway, and compensates for NO-cGMP loss, (reduced sGC) and thus prevents ED.


1988 ◽  
Vol 254 (6) ◽  
pp. F912-F917 ◽  
Author(s):  
M. Crabos ◽  
D. A. Ausiello ◽  
G. T. Haupert ◽  
H. F. Cantiello

Tissue culture media from incubations of fragments of rat brain were collected and partially purified. These supernatants were effective in inhibiting the Na+-K+ pump as indicated by a 77% reduction of ouabain-sensitive 86Rb+ uptake into human erythrocytes. Release of the Na+-K+-ATPase inhibitor depended on the amount of tissue, the temperature, and the length of incubation. Atrial natriuretic peptide (ANP) injected intravenously, or included (10(-8) M) in the in vitro incubation of brain tissue, decreased the release of the Na+-K+-ATPase inhibitor by 74 and 42%, respectively. Control experiments using the neuropeptide arginine vasopressin showed no effect on release of the inhibitor. These studies indicate that ANP is capable of regulating the release from brain of a Na+-K+-ATPase inhibitor with similar chromatographic characteristics to the one previously obtained from extraction of bovine hypothalamus and raise the possibility that the two factors are interrelated in the regulation of fluid and electrolyte balance.


1989 ◽  
Vol 159 (3) ◽  
pp. 1420-1426 ◽  
Author(s):  
Masayasu Kojima ◽  
Naoto Minamino ◽  
Jenji Kangawa ◽  
Hisayuki Matsuo

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