ArticlePulmonary circulation
Depolarization-dependent contraction increase after birth and preservation following long-term hypoxia in sheep pulmonary arteries.
Article in Pulmonary circulation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Long-term hypoxia modulates depolarization activation of BKFrontiers in physiology · 2024Article
- Long-Term Hypoxia Negatively Influences CaFrontiers in physiology · 2021Article
- Enhanced Vasoconstriction Mediated by αFrontiers in physiology · 2021Article
- Long-Term High-Altitude Hypoxia and Alpha Adrenoceptor-Dependent Pulmonary Arterial Contractions in Fetal and Adult Sheep.Frontiers in physiology · 2019Article
- Gestational Hypoxia and Developmental Plasticity.Physiological reviews · 2018Review
- Long-term hypoxia uncouples CaAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Long-term high-altitude hypoxia influences pulmonary arterial L-type calcium channel-mediated CaAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Muscarinic Receptor Activation Affects Pulmonary Artery Contractility in Sheep: The Impact of Maturation and Chronic Hypoxia on Endothelium-Dependent and Endothelium-Independent Function.High altitude medicine & biology · 2016Article
- Developmental acceleration of bradykinin-dependent relaxation by prenatal chronic hypoxia impedes normal development after birth.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Prenatal programming of pulmonary hypertension induced by chronic hypoxia or ductal ligation in sheep.Pulmonary circulation · 2013Review
- Antenatal hypoxia and pulmonary vascular function and remodeling.Current vascular pharmacology · 2013Review
- Optimization of isolated perfused/ventilated mouse lung to study hypoxic pulmonary vasoconstriction.Pulmonary circulation · 2013Article
- Effect of chronic perinatal hypoxia on the role of rho-kinase in pulmonary artery contraction in newborn lambs.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
- Maternal high-altitude hypoxia and suppression of ryanodine receptor-mediated Ca2+ sparks in fetal sheep pulmonary arterial myocytes.American journal of physiology. Lung cellular and molecular physiology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Membrane depolarization is critical to pulmonary arterial (PA) contraction. Both L-type Ca(2+) channels (Ca(L)) and Rho-kinase are important signaling components of this process and mitochondrial and non-mitochondrial generated superoxides can be part of the signaling process. Maturation and long-term hypoxia (LTH) each can modify depolarization-dependent contraction and the role of superoxides. By the use of wire myography, we tested the hypothesis that maturation and LTH increase pulmonary arterial reactivity to high-K(+)-induced membrane depolarization through enhancements in the importance of Ca(L)and Rho-kinase-dependent pathways. The data show that maturation, but not LTH, increases contraction to 125 mM KCl (high-K(+)) without altering the EC(50). High-K(+)-dependent contraction was inhibited to a similar extent in fetal and adult PA by multiple Ca(L) blockers, including 10 μM diltiazem, 10 μM verapamil, and 10 μM nifedipine. Postnatal maturation increased the role for 10 μM nifedipine-sensitive Ca(L), and decreased that for 10 μM Y-27632-sensitive Rho-kinase. In all groups, the combination of nifedipine and Y-27632 effectively inhibited high-K(+) contraction. Tempol (3 mM) but not 100 μM apocynin slightly reduced contraction in arteries from fetal hypoxic and adult normoxic and hypoxic sheep, indicating a limited role for non-mitochondrial derived superoxide to high-K(+)-induced contraction. Western immunoblot for alpha smooth muscle actin indicated small increases in relative abundance in the adult. The data suggest that while Ca(L) therapies more effectively vasodilate PA in adults and rho-kinase therapies are more effective in newborns, combination therapies would provide greater efficacy in both young and mature patients regardless of normoxic or hypoxic conditions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.