ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Large-conductance Ca2+-activated K+ channel beta1-subunit knockout mice are not hypertensive.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 45 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Inhibition of big-conductance CaPflugers Archiv : European journal of physiology · 2021Article
- Role of Ryanodine Type 2 Receptors in Elementary CaJournal of the American Heart Association · 2019Article
- Regulation of BK Channels by Beta and Gamma Subunits.Annual review of physiology · 2019Review
- Association between potassium channel SNPs and essential hypertension in Xinjiang Kazak Chinese patients.Experimental and therapeutic medicine · 2017Article
- High-fat diet-induced obesity alters nitric oxide-mediated neuromuscular transmission and smooth muscle excitability in the mouse distal colon.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Aging is associated with changes to the biomechanical properties of the posterior cerebral artery and parenchymal arterioles.American journal of physiology. Heart and circulatory physiology · 2016Article
- BK channel β1-subunit deficiency exacerbates vascular fibrosis and remodelling but does not promote hypertension in high-fat fed obesity in mice.Journal of hypertension · 2015Article
- Two-pore domain potassium channels in the adrenal cortex.Pflugers Archiv : European journal of physiology · 2015Review
- Western blot analysis of BK channel β1-subunit expression should be interpreted cautiously when using commercially available antibodies.Physiological reports · 2014Article
- Altered L-type Ca2+ channel activity contributes to exacerbated hypoperfusion and mortality in smooth muscle cell BK channel-deficient septic mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Smooth muscle BK channel activity influences blood pressure independent of vascular tone in mice.The Journal of physiology · 2014Article
- DiBAC₄(3) hits a "sweet spot" for the activation of arterial large-conductance Ca²⁺-activated potassium channels independently of the β₁-subunit.American journal of physiology. Heart and circulatory physiology · 2013Article
- Reduced vascular smooth muscle BK channel current underlies heart failure-induced vasoconstriction in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Ion channel remodeling in vascular smooth muscle during hypertension: Implications for novel therapeutic approaches.Pharmacological research · 2013Review
- BK Channels in Cardiovascular Diseases and Aging.Aging and disease · 2013Article
- A process-based review of mouse models of pulmonary hypertension.Pulmonary circulation · 2012Article
- Function and regulation of large conductance Ca(2+)-activated K+ channel in vascular smooth muscle cells.Drug discovery today · 2012Review
- Impaired propulsive motility in the distal but not proximal colon of BK channel β1-subunit knockout mice.Neurogastroenterology and motility · 2012Article
- Penitrem A as a tool for understanding the role of large conductance Ca(2+)/voltage-sensitive K(+) channels in vascular function.The Journal of pharmacology and experimental therapeutics · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Large-conductance Ca2+-activated K+ (BK) channels are composed of pore-forming α-subunits and accessory β1-subunits that modulate Ca2+ sensitivity. BK channels regulate arterial myogenic tone and renal Na+ clearance/K+ reabsorption. Previous studies using indirect or short-term blood pressure measurements found that BK channel β1-subunit knockout (BK β1-KO) mice were hypertensive. We evaluated 24-h mean arterial pressure (MAP) and heart rate in BK β1-KO mice using radiotelemetry. BK β1-KO mice did not have a higher 24-h average MAP when compared with wild-type (WT) mice, although MAP was ∼10 mmHg higher at night. The dose-dependent peak declines in MAP by nifedipine were only slightly larger in BK β1-KO mice. In BK β1-KO mice, giving 1% NaCl to mice to drink for 7 days caused a transient (5 days) elevation of MAP (∼5 mmHg); MAP returned to pre-saline levels by day 6. BK β1-KO mesenteric arteries in vitro demonstrated diminished contractile responses to paxilline, increased reactivity to Bay K 8644 and norepinephrine (NE), and maintained relaxation to isoproterenol. Paxilline and Bay K 8644 did not constrict WT or BK β1-KO mesenteric veins (MV). BK β1-subunits are not expressed in MV. The results indicate that BK β1-KO mice are not hypertensive on normal or high-salt intake. BK channel deficiency increases arterial reactivity to NE and L-type Ca2+ channel function in vitro, but the L-type Ca2+ channel modulation of MAP is not altered in BK β1-KO mice. BK and L-type Ca(2+) channels do not modulate murine venous tone. It appears that selective loss of BK channel function in arteries only is not sufficient to cause sustained hypertension.
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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.