scholarly journals Importance of Endogenous Atrial and Brain Natriuretic Peptides in Murine Embryonic Vascular and Organ Development

Endocrinology ◽  
2016 ◽  
Vol 157 (1) ◽  
pp. 358-367 ◽  
Author(s):  
Takeshi Tokudome ◽  
Ichiro Kishimoto ◽  
Takayuki Shindo ◽  
Hayato Kawakami ◽  
Teruhide Koyama ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Umbilical Artery ◽  
Bone Development ◽  
Layer Structure ◽  
Vacuolar Degeneration ◽  
Organ Morphogenesis ◽  
Brain Natriuretic Peptides ◽  
Compact Zone ◽  
Ischemic Tissue ◽  
Embryonic Vascular Development

Abstract Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) bind to the receptor guanylyl cyclase (GC)-A, leading to diuresis, natriuresis, and blood vessel dilation. In addition, ANP and BNP have various angiogenic properties in ischemic tissue. When breeding mice devoid of GC-A, we noted significant skewing of the Mendelian ratio in the offspring, suggesting embryonic lethality due to knockout of GC-A. Consequently, we here investigated the roles of endogenous ANP and BNP in embryonic neovascularization and organ morphogenesis. Embryos resulting from GC-A−/− × GC-A+/− crosses developed hydrops fetalis (HF) beginning at embryonic day (E)14.5. All embryos with HF had the genotype GC-A−/−. At E17.5, 33.3% (12 of 36) of GC-A−/− embryos had HF, and all GC-A−/− embryos with HF were dead. Beginning at E16.0, HF-GC-A−/− embryos demonstrated poorly developed superficial vascular vessels and sc hemorrhage, the fetal side of the placenta appeared ischemic, and vitelline vessels on the yolk sac were poorly developed. Furthermore, HF-GC-A−/− embryos also showed abnormal constriction of umbilical cord vascular vessels, few cardiac trabeculae and a thin compact zone, hepatic hemorrhage, and poor bone development. Electron microscopy of E16.5 HF-GC-A−/− embryos revealed severe vacuolar degeneration in endothelial cells, and the expected 3-layer structure of the smooth muscle wall of the umbilical artery was indistinct. These data demonstrate the importance of the endogenous ANP/BNP-GC-A system not only in the neovascularization of ischemic tissues but also in embryonic vascular development and organ morphogenesis.

scholarly journals INFECTIOUS STUNTING SYNDROME ASSOCIATED WITH DISTURBANCES OF MINERAL METABOLISM AND BONE DEVELOPMENT IN BROILER CHICKENS

1999 ◽  
Vol 47 (3) ◽  
pp. 361-378 ◽  
Author(s):  
Glávits ◽  
G. Sályi ◽  
R. Glávits
Keyword(s):  
Growth Retardation ◽  
Broiler Chickens ◽  
Neuronal Degeneration ◽  
Bone Development ◽  
Mineral Metabolism ◽  
Digestive Enzyme ◽  
Small Intestinal Mucosa ◽  
Vacuolar Degeneration ◽  
Leg Weakness ◽  
Small Intestinal

On a broiler farm with a rearing capacity of about 200,000 chickens, a disease characterised by growth retardation, variability in chick size, 'leg weakness', diarrhoea and increased mortality at 3 weeks of age occurred repeatedly, in several successive broiler flocks. Gross and histopathological findings were dominated by widening of the hypertrophic and ossification layers of the physes of long bones as well as by thickening, unevenness and defective calcification of the cartilage trabeculae. In the parathyroid gland, vacuolar degeneration of the cytoplasm of glandular epithelial cells, connective tissue proliferation and, here and there, cyst formation were seen. Additional findings included severe cerebellar oedema and neuronal degeneration. The pancreatic, myocardial and intestinal changes typical of infectious stunting syndrome (ISS) occurred only in a mild form. Four-week-old chickens exhibiting 'leg weakness' had significantly lower blood inorganic phosphate concentration and tibial ash content as compared to healthy chickens. The disease was successfully transmitted by oral administration of small intestinal homogenate from affected chickens. In a second experiment, however, the disease could not be transmitted with intestinal homogenate sterilized by irradiation. Large doses of vitamin D3reduced the rate of growth retardation and defective calcification of bones. The digestive enzyme activities of the pancreas and small intestinal mucosa of 'infected' chickens were decreased as is typical of ISS.

Umbilical Artery N-Terminal Peptide of Proatrial Natriuretic Peptide in Hypertensive Pregnancies and Fetal Acidemia During Labor

2001 ◽  
Vol 97 (1) ◽  
pp. 23-28
Author(s):  
KAARIN MÄKIKALLIO ◽  
OLLI VUOLTEENAHO ◽  
PENTTI JOUPPILA ◽  
JUHA RÄSÄNEN
Keyword(s):  
Natriuretic Peptide ◽  
Umbilical Artery

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
Keyword(s):  
Brain Natriuretic Peptide ◽  
Rat Brain ◽  
Natriuretic Peptide ◽  
Dissociation Constants ◽  
Area Postrema ◽  
Subfornical Organ ◽  
Affinity Ligands ◽  
Paraventricular Nuclei ◽  
Brain Natriuretic Peptides

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.

Interactions of atrial and brain natriuretic peptides at pathophysiological levels in normal men

1995 ◽  
Vol 269 (6) ◽  
pp. R1397-R1403 ◽  
Author(s):  
P. J. Hunt ◽  
E. A. Espiner ◽  
A. M. Richards ◽  
T. G. Yandle ◽  
C. Frampton ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Urine Volume ◽  
Random Order ◽  
Normal Male ◽  
Metabolic Clearance ◽  
Physiological Effects ◽  
Brain Natriuretic Peptides ◽  
Normal Humans ◽  
Normal Men

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are both circulating plasma hormones that are secreted by the heart and have similar physiological effects. We have shown previously that abrupt increases in plasma BNP in normal humans impair the clearance of ANP from plasma and result in additive physiological effects. Because large increases in plasma ANP are reported to have no effect on plasma BNP levels in patients with heart failure, we have studied ANP-BNP interactions in eight normal male subjects receiving background infusions of BNP (2 pmol.kg-1.min-1 for 5 h). Each subject also received a coinfusion of ANP ("active" day, 2 pmol.kg-1.min-1 for 2 h) or vehicle ("placebo" day) using a balanced random order, single-blind design. Metabolic clearance rate of ANP (mean 4.1 +/- 0.6 l/min) and disappearance rate from the plasma (t1/2 3.4 +/- 0.3 min) were similar to values measured previously in the absence of exogenous BNP. In contrast, steady-state plasma BNP levels were reversibly increased (mean BNP increment 10 pmol/l) during the administration of ANP (P = 0.038). Associated with these changes were significant (additive) physiological effects. Thus the addition of ANP increased plasma and urine guanosine 3',5'-cyclic monophosphate (P < 0.001 for both) and lowered systolic blood pressure (P = 0.049). When ANP was coinfused, significant differences were also observed in urine volume (P = 0.001) and sodium excretion (P = 0.043) between the infusion period (when urine volume and sodium excretion were enhanced) and postinfusion period (when values decreased). Taken together, our findings of similar interactions between ANP-BNP and BNP-ANP infusions occurring at pathophysiological concentrations of these two peptides, suggest that the interactions result from dissociation of prebound hormone, presumably from biological or clearance receptors.

Regional plasma levels of cardiac peptides and their response to acute neutral endopeptidase inhibition in man

1998 ◽  
Vol 95 (5) ◽  
pp. 547-555 ◽  
Author(s):  
J. G. LAINCHBURY ◽  
M. G. NICHOLLS ◽  
E. A. ESPINER ◽  
H. IKRAM ◽  
T. G. YANDLE ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Coronary Sinus ◽  
Femoral Artery ◽  
Natriuretic Peptides ◽  
Plasma Levels ◽  
Neutral Endopeptidase ◽  
Brain Natriuretic Peptides ◽  
Atrial Natriuretic

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.

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