Atrial Natriuretic Peptide Levels in Right Ventricle and Right Atrium following Chronic Hypoxia in Rats

1988 ◽  
Vol 74 (s18) ◽  
pp. 38P-39P
Author(s):  
R J D Winter ◽  
L Meleagros ◽  
S R Bloom
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Right Ventricle ◽  
Natriuretic Peptide ◽  
Right Atrium ◽  
Chronic Hypoxia ◽  
Atrial Natriuretic

scholarly journals Release of Atrial Natriuretic Peptide from the Isolated, Blood-Perfused Right Atrium of the Dog

1988 ◽  
Vol 47 (3) ◽  
pp. 285-291
Author(s):  
Shigeru MOTOMURA ◽  
Masanori OHTA ◽  
Kenji OHYAMA ◽  
Keitaro HASHIMOTO
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Right Atrium ◽  
Atrial Natriuretic

Effects of continuous infusion of atrial natriuretic peptide on the pulmonary hypertension induced by chronic hypoxia in rats

1991 ◽  
Vol 81 (3) ◽  
pp. 379-385 ◽  
Author(s):  
L. Zhao ◽  
R. J. D. Winter ◽  
T. Krausz ◽  
J. M. B. Hughes
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Pulmonary Artery Pressure ◽  
Chronic Hypoxia ◽  
Systemic Blood Pressure ◽  
Artery Pressure ◽  
Pulmonary Vascular Remodelling ◽  
Atrial Natriuretic

1. The effects of the continuous infusion of atrial natriuretic peptide on the development of pulmonary hypertension were studied in rats exposed to chronic hypoxia. 2. Continuous intravenous infusion of two doses of synthetic rat atrial natriuretic peptide, 300 ng/h per rat (0.10 pmol/h per rat) and 800 ng/h per rat (0.28 pmol/h per rat), attenuated the development of pulmonary hypertension in rats exposed to chronic hypoxia (fractional concentration of oxygen in inspired air = 10%) for 7 days: (i) the pulmonary artery pressure (mean ± sd) in the vehicle-treated hypoxic group was 45 ± 6 mmHg compared with 28 ± 6 mmHg in the vehicle-treated normotoxic group (n = 8, P < 0.001); (ii) treatment with atrial natriuretic peptide in normoxia did not alter the pulmonary artery pressure, systemic blood pressure or heart rate; (iii) treatment with atrial natriuretic peptide in hypoxia resulted in a lower pulmonary artery pressure in the group treated with 800 ng of atrial natriuretic peptide/h per rat (38 ± 8 mmHg, P < 0.05 compared with the vehicle-treated hypoxic group) without affecting the systemic blood pressure or heart rate. 3. Chronic hypoxia resulted in an extension of vascular smooth muscle towards the periphery of the lung with the development of muscle in normally non-muscularized vessels (remodelling). Quantitative assessment of the small pulmonary vessels (external diameter 25–55 μm) showed that atrial natriuretic peptide treatment reduced pulmonary vascular remodelling in hypoxia (the percentage of thick-walled vessels in the peripheral lung hypoxic vehicle-treated group was 25 ± 6 compared with 19 ± 4 in the group given 300 ng of atrial natriuretic peptide/h per rat and 17 ± 7 in the group given 800 ng of atrial natriuretic peptide/h per rat, means ± sd, both P < 0.01 compared with the vehicle-treated normoxic group). 4. These data show that infusion of synthetic atrial natriuretic peptide attenuated the pulmonary vascular remodelling and associated pulmonary hypertension produced by chronic hypoxia.

Bovine atrial natriuretic peptide in heart failure

1990 ◽  
Vol 124 (3) ◽  
pp. 463-467 ◽  
Author(s):  
N. Takemura ◽  
H. Koyama ◽  
T. Sako ◽  
K. Ando ◽  
S. Motoyoshi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Plasma Concentration ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Right Atrium ◽  
Left Ventricular ◽  
Atrial Pressure ◽  
Right Atrial ◽  
The Right ◽  
Atrial Natriuretic

ABSTRACT The present study describes the concentration and molecular form of atrial natriuretic peptide (ANP) in Holstein dairy cattle with mild (bacterial endocarditis; BEC) or severe (dilated cardiomyopathy; DCM) heart failure. Significant increases in plasma concentration of ANP were observed in cattle with DCM (73·3 ± 16·02 pmol/l, n=4, P<0·01) and BEC (20·6± 3·45 pmol/l, n=7, P<0·05), when compared with those in control cattle (14·5± 1·84 pmol/l, n= 12). The concentration of ANP in cattle with DCM was significantly (P<0·01) higher compared with that in cattle with BEC. Plasma concentration of ANP correlated significantly with right atrial pressure (r =0·95, P<0·01) and left ventricular end-diastolic pressure (r= 0·84, P<0·01). Gel-permeation chromatography of ANP in plasma and the right atrium from control and cattle with BEC revealed a single peak corresponding to the elution position of authentic human ANP(99–126) in plasma, and two peaks corresponding to those of authentic human ANP(99–126) and pro-ANP in the atrial extract. In cattle with DCM, however, peaks corresponding to the elution positions of authentic human β-ANP and/or pro-ANP were detected in addition to the peak corresponding to ANP(99–126). The content of ANP in the right atrium of cattle with DCM was significantly (P<0·05) increased compared with that in control cattle and those with BEC. The present study therefore suggests that the synthesis and secretion of ANP might be stimulated by atrial distention induced by increased atrial pressure. This suggestion is supported by the fact that the middle molecular weight form of ANP, possibly corresponding to human β-ANP, was detected in both the plasma and atria of the cattle with severe heart failure. Journal of Endocrinology (1990) 124, 463–467

Atrial natriuretic peptide levels in plasma and in cardiac tissues after chronic hypoxia in rats

1989 ◽  
Vol 76 (1) ◽  
pp. 95-101 ◽  
Author(s):  
R. J. D. Winter ◽  
L. Meleagros ◽  
S. Pervez ◽  
H. Jamal ◽  
T. Krausz ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Right Ventricular ◽  
Natriuretic Peptide ◽  
Ventricular Hypertrophy ◽  
Chronic Hypoxia ◽  
Right Ventricular Hypertrophy ◽  
Right Atrial ◽  
Adult Rats ◽  
Cardiac Tissues ◽  
Atrial Natriuretic

1. Atrial natriuretic peptide (ANP) levels were measured in cardiac tissues and in plasma from adult rats exposed to chronic alveolar hypoxia for periods of 2 h, 24 h and 7 days. Levels were also measured in rats that were maintained in hypoxia for 7 days and then returned to air for 24 h. 2. Plasma ANP was not altered at 2 h but was significantly increased at both 24 h and at 7 days. Plasma ANP in animals exposed to hypoxia for 7 days was normal 24 h after returning to air breathing, despite the persistence of indices of pulmonary hypertension. 3. No significant right atrial hypertrophy was observed under these conditions of chronic hypoxia. A reduction in right atrial ANP content was found at 24 h and was accompanied by a decrease in the number of electrondense granules per right atrial muscle cell. After exposure to hypoxia for 7 days, right atrial ANP and granule number was not different from control, and no alteration was found in right atrial ANP level after removal from the hypoxic environment. 4. No significant right ventricular hypertrophy was produced by exposure to hypoxia for 2 or 24 h. In the former group ventricular ANP had decreased significantly compared with control. Right ventricular hypertrophy was found in both the hypoxic groups after exposure for 7 days, when selective increases in right ventricular ANP content were found. 5. These findings are consistent with the hypothesis that ANP release occurs on exposure to chronic hypoxia and is independent of the associated cardiac hypertrophy and pulmonary vascular remodelling. The findings may have relevance to the natriuresis and reported changes in the renin-angiotensin-aldosterone axis under hypoxic conditions.

Exaggerated Pulmonary Hypertensive Responses During Chronic Hypoxia in Mice With Gene-Targeted Reductions in Atrial Natriuretic Peptide

CHEST Journal ◽  
1998 ◽  
Vol 114 (1) ◽  
pp. 79S-80S ◽  
Author(s):  
James R. Klinger ◽  
R.R. Warburton ◽  
L.A. Pietras ◽  
R. Swift ◽  
S. John ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Chronic Hypoxia ◽  
Atrial Natriuretic

Downregulation of pulmonary atrial natriuretic peptide receptors in rats exposed to chronic hypoxia

1994 ◽  
Vol 77 (3) ◽  
pp. 1309-1316 ◽  
Author(s):  
J. R. Klinger ◽  
F. Arnal ◽  
R. R. Warburton ◽  
L. C. Ou ◽  
N. S. Hill
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Chronic Hypoxia ◽  
Binding Capacity ◽  
Specific Binding ◽  
Pulmonary Uptake ◽  
Anp Receptors ◽  
Atrial Natriuretic

We hypothesized that a downregulation in pulmonary atrial natriuretic peptide (ANP) receptors helps raise plasma ANP levels during chronic hypoxia. We measured in vivo pulmonary uptake and plasma clearance of 125I-ANP and in vitro pulmonary binding kinetics of 125I-ANP in normoxic and chronically hypoxic rats. Exposure to 21 days of hypobaric (0.5 atm) hypoxia did not decrease specific binding of 125I-ANP in the kidney, but pulmonary binding decreased 35 and 75% after 1 and 3 days of hypoxia, respectively, and increased 200% after 3 days of normoxic recovery from 21 days of hypoxia. The total binding capacity for ANP to lung membrane fractions from normoxic rats, chronically hypoxic rats, and rats that had recovered from hypoxia was 488 +/- 59, 109 +/- 17, and 338 +/- 48 fmol/mg, respectively (P < 0.05 for hypoxic vs. normoxic or recovered lung membranes). The area under the 125I-ANP plasma concentration curve for normoxic and hypoxic rats and normoxic rats that were infused with the ANP C-receptor ligand C-ANF-(4–23) was 3,292 +/- 216, 5,022 +/- 466, and 8,205 +/- 1,059 disintegrations.min-1.ml–1, respectively [P < 0.05 for hypoxic vs. normoxic or C-ANF-(4–23)-infused rats]. We conclude that pulmonary ANP clearance is reduced during chronic hypoxia secondary to a downregulation in pulmonary ANP clearance receptors. Reduced pulmonary clearance of ANP may represent an adaptation that contributes to increased plasma ANP levels during chronic hypoxia.

ATRIAL NATRIURETIC PEPTIDE CONCENTRATIONS IN BLOOD FROM RIGHT ATRIUM IN PATIENT WITH SEVERE RIGHT HEART FAILURE

The Lancet ◽  
1985 ◽  
Vol 326 (8446) ◽  
pp. 93-94 ◽  
Author(s):  
Engelbert Hartter ◽  
Michael Weissel ◽  
HansKrister Stummvoll ◽  
Wolfgang Woloszczuk ◽  
Christian Punzengruber ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Right Atrium ◽  
Right Heart Failure ◽  
Right Heart ◽  
Atrial Natriuretic

C-type natriuretic peptide expression and pulmonary vasodilation in hypoxia-adapted rats

1998 ◽  
Vol 275 (4) ◽  
pp. L645-L652 ◽  
Author(s):  
James R. Klinger ◽  
Farjaad M. Siddiq ◽  
Richard A. Swift ◽  
Cynthia Jackson ◽  
Linda Pietras ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricle ◽  
Natriuretic Peptide ◽  
Right Atrium ◽  
Chronic Hypoxia ◽  
Right Atrial ◽  
Mrna Levels ◽  
Hypoxic Pulmonary Hypertension ◽  
Pulmonary Arterial ◽  
The Right

Atrial and brain natriuretic peptides (ANP and BNP, respectively) are potent pulmonary vasodilators that are upregulated in hypoxia-adapted rats and may protect against hypoxic pulmonary hypertension. To test the hypothesis that C-type natriuretic peptide (CNP) also modulates pulmonary vascular responses to hypoxia, we compared the vasodilator effect of CNP with that of ANP on pulmonary arterial rings, thoracic aortic rings, and isolated perfused lungs obtained from normoxic and hypoxia-adapted rats. We also measured CNP and ANP levels in heart, lung, brain, and plasma in normoxic and hypoxia-adapted rats. Steady-state CNP mRNA levels were quantified in the same organs by relative RT-PCR. CNP was a less potent vasodilator than ANP in preconstricted thoracic aortic and pulmonary arterial rings and in isolated lungs from normoxic and hypoxia-adapted rats. Chronic hypoxia increased plasma CNP (15 ± 2 vs. 6 ± 1 pg/ml; P < 0.05) and decreased CNP in the right atrium (35 ± 14 vs. 65 ± 17 pg/mg protein; P < 0.05) and in the lung (3 ± 1 vs. 14 ± 3 pg/mg protein; P < 0.05) but had no effect on CNP in brain or right ventricle. Chronic hypoxia increased ANP levels fivefold in the right ventricle (49 ± 5 vs. 11 ± 2 pg/mg protein; P < 0.05) but had no effect on ANP in lung or brain. There was a trend toward decreased ANP levels in the right atrium (2,009 ± 323 vs. 2,934 ± 397 pg/mg protein; P = not significant). No differences in CNP transcript levels were observed between the two groups of rats except that the right atrial CNP mRNA levels were lower in hypoxia-adapted rats. We conclude that CNP is a less potent pulmonary vasodilator than ANP in normoxic and hypoxia-adapted rats and that hypoxia raises circulating CNP levels without increasing cardiopulmonary CNP expression. These findings suggest that CNP may be less important than ANP or BNP in protecting against hypoxic pulmonary hypertension in rats.

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