ArticleProceedings of the National Academy of Sciences of the United States of America1996
NO hyperpolarizes pulmonary artery smooth muscle cells and decreases the intracellular Ca2+ concentration by activating voltage-gated K+ channels.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 153 citations in OpenAlex.
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- Pathophysiology and pathogenic mechanisms of pulmonary hypertension: role of membrane receptors, ion channels, and CaPhysiological reviews · 2023Review
- Protective role of perivascular adipose tissue in the cardiovascular system.Frontiers in endocrinology · 2023Review
- Mechanosensitive channel Piezo1 is required for pulmonary artery smooth muscle cell proliferation.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Artemisinin and Its Derivate Alleviate Pulmonary Hypertension and Vasoconstriction in Rodent Models.Oxidative medicine and cellular longevity · 2022Article
- A TOR2A Gene Product: Salusin-β Contributes to Attenuated Vasodilatation of Spontaneously Hypertensive Rats.Cardiovascular drugs and therapy · 2021Article
- Vasorelaxant-Mediated Antihypertensive Effect of the Leaf Aqueous Extract fromBioMed research international · 2021Article
- Improvement of Vascular Function by Knockdown of Salusin-β in Hypertensive Rats via Nitric Oxide and Reactive Oxygen Species Signaling Pathway.Frontiers in physiology · 2021Article
- Activation of KBritish journal of pharmacology · 2019Article
- Calcitonin gene-related peptide hyperpolarizes mouse pulmonary artery endothelial tubes through KAmerican journal of physiology. Lung cellular and molecular physiology · 2018Article
- Overview of the Microenvironment of Vasculature in Vascular Tone Regulation.International journal of molecular sciences · 2018Review
- Isolation, culture and identification of pulmonary arterial smooth muscle cells from rat distal pulmonary arteries.Cytotechnology · 2017Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Isometric Stretch Alters Vascular Reactivity of Mouse Aortic Segments.Frontiers in physiology · 2017Article
- SGLT inhibitors attenuate NO-dependent vascular relaxation in the pulmonary artery but not in the coronary artery.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Article
- High k(+)-induced relaxation by nitric oxide in human gastric fundus.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2012Article
- Hypoxic pulmonary vasoconstriction.Physiological reviews · 2012Review
- Nitric Oxide-mediated Relaxation by High K in Human Gastric Longitudinal Smooth Muscle.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2011Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
NO causes pulmonary vasodilation in patients with pulmonary hypertension. In pulmonary arterial smooth muscle cells, the activity of voltage-gated K+ (Kv) channels controls resting membrane potential. In turn, membrane potential is an important regulator of the intracellular free calcium concentration ([Ca2+]i) and pulmonary vascular tone. We used patch clamp methods to determine whether the NO-induced pulmonary vasodilation is mediated by activation of Kv channels. Quantitative fluorescence microscopy was employed to test the effect of NO on the depolarization-induced rise in [Ca2+]i. Blockade of Kv channels by 4-aminopyridine (5 mM) depolarized pulmonary artery myocytes to threshold for initiation of Ca2+ action potentials, and thereby increased [Ca2+]i. NO (approximately 3 microM) and the NO-generating compound sodium nitroprusside (5-10 microM) opened Kv channels in rat pulmonary artery smooth muscle cells. The enhanced K+ currents then hyperpolarized the cells, and blocked Ca(2+)-dependent action potentials, thereby preventing the evoked increases in [Ca2+]i. Nitroprusside also increased the probability of Kv channel opening in excised, outside-out membrane patches. This raises the possibility that NO may act either directly on the channel protein or on a closely associated molecule rather than via soluble guanylate cyclase. In isolated pulmonary arteries, 4-aminopyridine significantly inhibited NO-induced relaxation. We conclude that NO promotes the opening of Kv channels in pulmonary arterial smooth muscle cells. The resulting membrane hyperpolarization, which lowers [Ca2+]i, is apparently one of the mechanisms by which NO induces pulmonary vasodilation.
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