Atrial natriuretic peptide lowers pulmonary arterial pressure in hypoxia-adapted rats

1988 ◽  
Vol 65 (4) ◽  
pp. 1729-1735 ◽  
Author(s):  
H. K. Jin ◽  
R. H. Yang ◽  
R. M. Thornton ◽  
Y. F. Chen ◽  
R. Jackson ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Vasculature ◽  
Vasodilator Effect ◽  
Pulmonary Arterial ◽  
Air Control ◽  
Atrial Natriuretic

To test the hypothesis that atrial natriuretic peptide (ANP) has a direct vasodilator effect on the pulmonary vasculature that is enhanced in hypoxia-induced pulmonary hypertension in the rat, we determined the effects of ANP on mean pulmonary (MPAP) and systemic arterial pressure (MSAP) in intact conscious Sprague-Dawley rats exposed to 10% O2 or room air for 4 wk. Catheters were placed in the pulmonary artery through the right jugular vein by means of a closed-chest technique. MPAP and MSAP were monitored before and after intravenous injections of graded doses of ANP. ANP produced dose-related decreases in MPAP that were greater in the hypoxic group than in air controls. There were no significant between-group differences in the systemic depressor responses to ANP or in the ANP-induced reduction in cardiac output. ANP lowered MPAP significantly in isolated perfused lungs from both hypoxia-adapted and air control rats, and this effect was significantly greater in the hypoxic than the air control lungs. These data indicate that ANP lowers pulmonary arterial pressure in rats with hypoxia-induced pulmonary hypertension, mainly by a direct vasodilator effect on the pulmonary vasculature.

Atrial natriuretic peptide correlates with pulmonary arterial pressure and cardiac output

Peptides ◽  
1987 ◽  
Vol 8 (2) ◽  
pp. 285-290 ◽  
Author(s):  
K. Naruse ◽  
M. Naruse ◽  
T. Honda ◽  
K. Obana ◽  
H. Sakurai ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Atrial Natriuretic

Atrial natriuretic peptide clearance receptor agonist lowers pulmonary pressure in hypoxic rats

1990 ◽  
Vol 68 (6) ◽  
pp. 2413-2418 ◽  
Author(s):  
H. Jin ◽  
Y. F. Chen ◽  
R. H. Yang ◽  
R. M. Jackson ◽  
S. Oparil
Keyword(s):  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Systemic Arterial Pressure ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Clearance Receptor ◽  
Air Control ◽  
Model C ◽  
Atrial Natriuretic

We demonstrated previously that intravenous administration of exogenous atrial natriuretic peptide (ANP) lowers mean pulmonary arterial pressure (MPAP) in hypoxia-adapted rats. To test the hypothesis that endogenous ANP may also lower MPAP in this model, C-ANP-(4-23), a ring-deleted analogue of ANP that binds to the biologically silent ANP clearance receptor (C-ANP receptor) but not to the ANP biological receptor (B-ANP receptor), was administered intravenously as a bolus injection (10 micrograms/kg) followed by an infusion (1 micrograms.kg-1.min-1 for 60 min) to rats adapted to hypoxia (10% O2) for 4 wk and to air control rats. C-ANP-(4-23) significantly lowered MPAP in hypoxic rats but not in air controls. A statistically insignificant reduction in mean systemic arterial pressure was found in both groups after C-ANP-(4-23) administration. C-ANP-(4-23) significantly (two- to threefold) increased endogenous plasma ANP levels in both groups; the increase was not significantly different between groups. Both basal and post-C-ANP-(4-23) levels of plasma ANP were greater in hypoxia-adapted animals than in air controls; the C-ANP-induced increase in plasma ANP was not significantly different between groups. These results suggest that the endogenous ANP may modulate pulmonary vascular tone in rats with hypoxic pulmonary hypertension.

scholarly journals Exposure of Stored Packed Erythrocytes to Nitric Oxide Prevents Transfusion-associated Pulmonary Hypertension

2016 ◽  
Vol 125 (5) ◽  
pp. 952-963 ◽  
Author(s):  
Stefan Muenster ◽  
Arkadi Beloiartsev ◽  
Binglan Yu ◽  
E Du ◽  
Sabia Abidi ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Erythrocyte Deformability ◽  
Pulmonary Vasculature ◽  
Prolonged Storage ◽  
Systemic Hemodynamic ◽  
Promising Therapeutic Approach ◽  
Erythrocyte Survival ◽  
Pulmonary Arterial

Abstract Background Transfusion of packed erythrocytes stored for a long duration is associated with increased pulmonary arterial pressure and vascular resistance. Prolonged storage decreases erythrocyte deformability, and older erythrocytes are rapidly removed from the circulation after transfusion. The authors studied whether treating stored packed ovine erythrocytes with NO before transfusion could prevent pulmonary vasoconstriction, enhance erythrocyte deformability, and prolong erythrocyte survival after transfusion. Methods Ovine leukoreduced packed erythrocytes were treated before transfusion with either NO gas or a short-lived NO donor. Sheep were transfused with autologous packed erythrocytes, which were stored at 4°C for either 2 (“fresh blood”) or 40 days (“stored blood”). Pulmonary and systemic hemodynamic parameters were monitored before, during, and after transfusion. Transfused erythrocytes were labeled with biotin to measure their circulating lifespan. Erythrocyte deformability was assessed before and after NO treatment using a microfluidic device. Results NO treatment improved the deformability of stored erythrocytes and increased the number of stored erythrocytes circulating at 1 and 24 h after transfusion. NO treatment prevented transfusion-associated pulmonary hypertension (mean pulmonary arterial pressure at 30 min of 21 ± 1 vs. 15 ± 1 mmHg in control and NO–treated packed erythrocytes, P < 0.0001). Washing stored packed erythrocytes before transfusion did not prevent pulmonary hypertension. Conclusions NO treatment of stored packed erythrocytes before transfusion oxidizes cell-free oxyhemoglobin to methemoglobin, prevents subsequent NO scavenging in the pulmonary vasculature, and limits pulmonary hypertension. NO treatment increases erythrocyte deformability and erythrocyte survival after transfusion. NO treatment might provide a promising therapeutic approach to prevent pulmonary hypertension and extend erythrocyte survival.

Hemodynamic effects of arginine vasopressin in rats adapted to chronic hypoxia

1989 ◽  
Vol 66 (1) ◽  
pp. 151-160 ◽  
Author(s):  
H. K. Jin ◽  
R. H. Yang ◽  
Y. F. Chen ◽  
R. M. Thornton ◽  
R. M. Jackson ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Pulmonary Arterial Pressure ◽  
Systemic Arterial Pressure ◽  
Systemic Hemodynamic ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Air Control

Acute and chronic pulmonary and systemic hemodynamic responses to arginine vasopressin (AVP) were examined in 4-wk hypoxia-adapted and air control rats. AVP, administered intravenously as bolus injections or sustained infusions, produced major dose-dependent V1-receptor-mediated reductions in mean pulmonary arterial pressure in hypoxia-adapted rats. These effects were comparable in pentobarbital-anesthetized, thoracotomized animals and in conscious, intact rats. Chronic infusions of AVP induced a sustained reduction in mean pulmonary arterial pressure and partially prevented the development of pulmonary hypertension without changing systemic arterial pressure. AVP induced significant decreases in cardiac output in both groups; the cardiac output response was not significantly different in hypoxia-adapted and air control animals. AVP induced almost no change in MPAP in air control rats. Furthermore the systemic pressor effects of AVP were significantly blunted in hypoxia-adapted rats compared with air controls. We conclude that the pulmonary depressor and blunted systemic pressor effects of AVP observed in hypoxia-adapted rats may be related to release of a vasodilator, such as endothelium-derived relaxing factor, vasodilator prostaglandins, or atrial natriuretic peptides. Further study is needed to elucidate these mechanisms and assess the usefulness of AVP and/or its analogues in the treatment and prevention of hypoxia-induced pulmonary hypertension.

Atrial natriuretic peptide in acute hypoxia-induced pulmonary hypertension in rats

1991 ◽  
Vol 71 (3) ◽  
pp. 807-814 ◽  
Author(s):  
H. Jin ◽  
R. H. Yang ◽  
Y. F. Chen ◽  
R. M. Jackson ◽  
H. Itoh ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Pressor Response ◽  
Acute Hypoxia ◽  
Treated Group ◽  
Pulmonary Vasculature ◽  
Hypoxic Exposure ◽  
Mean Pulmonary Arterial Pressure ◽  
Atrial Natriuretic

To test the hypothesis that exogenous atrial natriuretic peptide (ANP) prevents the acute pulmonary pressor response to hypoxia, ANP (20-micrograms/kg bolus followed by 1-microgram.kg-1.min-1 infusion) or vehicle was administered intravenously to conscious rats beginning 3 min before exposure to hypoxia or room air for 90 min. Exogenous ANP abolished the acute pulmonary pressor response to hypoxia in association with marked and parallel increases in plasma ANP and guanosine 5′-cyclic monophosphate (cGMP) and with a significant increase in lung cGMP content. To examine whether endogenous ANP modulates the acute pulmonary pressor response to hypoxia, rats were pretreated with a monoclonal antibody (Ab) to ANP and exposed to hypoxia. Mean pulmonary arterial pressure (MPAP) in the Ab-treated rats was not different from control over the first 6 h of hypoxic exposure. Thereafter, the Ab-treated group had significantly higher MPAP than control. Our data suggest that 1) exogenous ANP blocks the pulmonary pressor response to acute hypoxia via stimulation of cGMP accumulation in the pulmonary vasculature, and 2) endogenous ANP may modulate the subacute, but not acute, phase of hypoxic pulmonary hypertension.

Nifedipine inhibits pulmonary hypertension but does not prevent decreased lung eNOS in hypoxic newborn pigs

1999 ◽  
Vol 277 (3) ◽  
pp. L449-L456 ◽  
Author(s):  
Candice D. Fike ◽  
Mark R. Kaplowitz
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Untreated Control ◽  
Pulmonary Arterial Pressure ◽  
Vascular Responses ◽  
Pulmonary Arterial ◽  
Air Control ◽  
Endothelial Nitric Oxide

Therapies to prevent the onset or progression of pulmonary hypertension in newborns have received little study compared with those in adult models. We wanted to determine whether nifedipine treatment prevents the increased pulmonary vascular resistance, blunted pulmonary vascular responses to acetylcholine, and reduced lung endothelial nitric oxide synthase (eNOS) amounts that we have found in a newborn model of chronic hypoxia-induced pulmonary hypertension. Studies were performed with 1- to 3-day-old piglets raised in room air (control) or 10% O2 (hypoxia) for 10–12 days. Some piglets from each group were given nifedipine (3–5 mg/kg sublingually three times a day). Pulmonary arterial pressure, pulmonary wedge pressure, and cardiac output were measured in anesthetized animals. Pulmonary vascular responses to acetylcholine and eNOS amounts were assessed in excised lungs. The calculated value of the pulmonary vascular resistance for nifedipine-treated hypoxic piglets (0.09 ± 0.01 cmH2O ⋅ ml−1 ⋅ min ⋅ kg) was almost one-half of the value for untreated hypoxic piglets (0.16 ± 0.01 cmH2O ⋅ ml−1 ⋅ min ⋅ kg) and did not differ from the value for untreated control piglets (0.05 ± 0.01 cmH2O ⋅ ml−1 ⋅ min ⋅ kg). Pulmonary arterial pressure responses to acetylcholine and whole lung homogenate eNOS amounts were less for both nifedipine-treated and untreated hypoxic piglets than for untreated control piglets. Nifedipine treatment attenuated pulmonary hypertension in chronically hypoxic newborn piglets despite the persistence of blunted responses to acetylcholine and reduced lung eNOS amounts.

BMPR-II heterozygous mice have mild pulmonary hypertension and an impaired pulmonary vascular remodeling response to prolonged hypoxia

2004 ◽  
Vol 287 (6) ◽  
pp. L1241-L1247 ◽  
Author(s):  
Hideyuki Beppu ◽  
Fumito Ichinose ◽  
Noriko Kawai ◽  
Rosemary C. Jones ◽  
Paul B. Yu ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Primary Pulmonary Hypertension ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arteries ◽  
Pulmonary Vasculature ◽  
Wild Type ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Alveolar Capillary

Heterozygous mutations of the bone morphogenetic protein type II receptor ( BMPR-II) gene have been identified in patients with primary pulmonary hypertension. The mechanisms by which these mutations contribute to the pathogenesis of primary pulmonary hypertension are not fully elucidated. To assess the impact of a heterozygous mutation of the BMPR-II gene on the pulmonary vasculature, we studied mice carrying a mutant BMPR-II allele lacking exons 4 and 5 ( BMPR-II+/− mice). BMPR-II+/− mice had increased mean pulmonary arterial pressure and pulmonary vascular resistance compared with their wild-type littermates. Histological analyses revealed that the wall thickness of muscularized pulmonary arteries (<100 μm in diameter) and the number of alveolar-capillary units were greater in BMPR-II+/− than in wild-type mice. Breathing 11% oxygen for 3 wk increased mean pulmonary arterial pressure, pulmonary vascular resistance, and hemoglobin concentration to similar levels in BMPR-II+/− and wild-type mice, but the degree of muscularization of small pulmonary arteries and formation of alveolar-capillary units were reduced in BMPR-II+/− mice. Our results suggest that, in mice, mutation of one copy of the BMPR-II gene causes pulmonary hypertension but impairs the ability of the pulmonary vasculature to remodel in response to prolonged hypoxic breathing.

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