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Aging, ion channel expression, and vascular function
Abstract
Cardiovascular disease remains the leading cause of death in the United States, and aging is one of the main risk factors for its development. Coronary arteries nurture the heart, but as age progresses, they suffer changes that make them stiffer, thicker, and with higher spontaneous contractile activity. Even in the absence of pathological atherosclerotic lesions, these changes make the coronary arteries at risk for vasospasm and the individual at risk for myocardial ischemia and heart failure. Thus, knowledge of the molecular mechanisms involved in the vascular physiology, disease, and aging of the coronary circulation is required to develop strategies to preserve the quality of life of an increasingly aging population. One of the key factors that regulate coronary arterial tone is the activity of K+ channels in the vascular smooth muscle cells (SMCs). In particular, voltage-dependent and Ca(2+)-activated K+ (BKCa) channels, which are abundant in the coronary SMCs, are targets of vasoconstrictors and vasorelaxants, and play a key role in determining arterial tone and diameter. Aging induces a reduction in the density of the alpha-subunit of BKCa channels in coronary smooth muscle, lowers baseline endothelial release of the relaxant nitric oxide (NO), and increases the response to endothelial constrictor factors and K+. Thus, aging induces the remodeling of important proteins involved in the excitability and contractility of the coronary circulation. Altogether, these changes…
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“Candidate mechanisms include age-related changes in vascular physiology, including increased arterial stiffness [58], diminished endothelial cell release of nitric oxide, enhanced vascular responsivity to endothelial constriction factors, increases in circulating catecholamines, and attenuated vasodilator responses to circulating epinephrine due to decreased beta-adrenergic sensitivity in vascular”
From Loneliness matters: a theoretical and empirical review of consequences and mechanisms (2010) · cites this paper as [61]
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Loneliness matters: a theoretical and empirical review of consequences and mechanisms
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“smooth muscle [59–61].”
Metadata
- Authors
- Toro, L., Marijic, J., Nishimaru, K., Tanaka, Y., Song, M., & Stefani, E.
- Affiliations
- University of California, Los Angeles (US)
- Toho University (JP)
- Corresponding author
- Toro, Ligia
- ORCID
- Tanaka, Yoshio
- Venue
- Vascular Pharmacology
- Publisher
- Elsevier BV
- Published
- 2002-01
- Volume
- 38
- Issue
- 1
- Pages
- 73-80
- ISSN
- 1537-1891 (ISSN-L)
- OpenAlex
- W1970135079
- Cited by
- 73
- References
- 0
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 3 · 2022: 3 · 2021: 1 · 2020: 1 · 2019: 3 · 2018: 3 · 2017: 1 · 2016: 5 · 2014: 2 · 2013: 4 · 2012: 6
- FWCI
- 0.32
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Vascular Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL-47382, R01HL054970)
- National Institute of General Medical Sciences (R01GM052203)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD038983)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Keywords
- aging, BKCa channels, potassium channels, coronary artery smooth muscle, vascular function, coronary vasospasm, myocardial ischemia, nitric oxide, endothelial dysfunction, vascular remodeling, ion channel expression, cardiovascular risk
- MeSH terms
- Aging, Animals, Arteries, Humans, Ion Channels, Muscle, Smooth, Vascular, Nitric Oxide, Vasoconstriction, Vasodilation, Myocytes, Smooth Muscle, Rats
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- Toro, L., Marijic, J., Nishimaru, K., Tanaka, Y., Song, M., & Stefani, E. (2002). Aging, ion channel expression, and vascular function. Vascular Pharmacology. https://doi.org/10.1016/s0306-3623(02)00128-3