ArticleMicrocirculation (New York, N.Y. : 1994)2000
Hypoxia does not activate ATP-sensitive K+ channels in arteriolar muscle cells.
Article in Microcirculation (New York, N.Y. : 1994), 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- Review
- Hif1α-dependent mitochondrial acute ONature communications · 2024Article
- Acute oxygen sensing by vascular smooth muscle cells.Frontiers in physiology · 2023Review
- Ion channels and the regulation of myogenic tone in peripheral arterioles.Current topics in membranes · 2020Review
- Vascular KRespiratory physiology & neurobiology · 2017Article
- Conducted dilatation to ATP and KActa physiologica (Oxford, England) · 2017Article
- Arteriolar oxygen reactivity: where is the sensor and what is the mechanism of action?The Journal of physiology · 2016Review
- Potassium channels and uterine vascular adaptation to pregnancy and chronic hypoxia.Current vascular pharmacology · 2013Review
- Significance of K(ATP) channels, L-type Ca²⁺ channels and CYP450-4A enzymes in oxygen sensing in mouse cremaster muscle arterioles in vivo.BMC physiology · 2013Article
- Hypoxia. 4. Hypoxia and ion channel function.American journal of physiology. Cell physiology · 2011Review
- Development of an image-based system for measurement of membrane potential, intracellular Ca(2+) and contraction in arteriolar smooth muscle cells.Microcirculation (New York, N.Y. : 1994) · 2010Article
- Oxygen sensing and conducted vasomotor responses in mouse cremaster arterioles in situ.Pflugers Archiv : European journal of physiology · 2010Article
- Membrane hyperpolarization is not required for sustained muscarinic agonist-induced increases in intracellular Ca2+ in arteriolar endothelial cells.Microcirculation (New York, N.Y. : 1994) · 2005Article
- Hypoxia inhibits contraction but not calcium channel currents or changes in intracellular calcium in arteriolar muscle cells.Microcirculation (New York, N.Y. : 1994) · 2003Article
- Potassium channels in the peripheral microcirculation.Microcirculation (New York, N.Y. : 1994)Review
- K+-induced dilation of hamster cremasteric arterioles involves both the Na+/K+-ATPase and inward-rectifier K+ channels.Microcirculation (New York, N.Y. : 1994)Article
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Funding
Abstract
objectiveTo test the hypothesis that hypoxia activates ATP-sensitive K+ (KATP) channels in cremasteric arteriolar muscle cells, resulting in membrane hyperpolarization and inhibition of norepinephrine-induced contraction.
methodsArteriolar muscle cells were isolated enzymatically from second- and third-order arterioles that were surgically removed from hamster cremaster muscles. The effects of hypoxia (PO2 = 12-15 mm Hg) were then examined on norepinephrine-induced contraction, membrane currents, and membrane potential in these cells at room temperature. Whole-cell currents and membrane potential were recorded using the perforated patch technique.
resultsHypoxia (12-15 mm Hg PO2) reversibly inhibited norepinephrine-induced contraction to 52 +/- 6% of the response in normoxic solutions (156 mm Hg, n = 12 digests, p < 0.05). These effects of hypoxia could be prevented by superfusion of the cells with either solutions containing the KATP channel antagonist glibenclamide (1 microM) or solutions containing 35 mM K+ to reduce the electrochemical gradient for K+ diffusion. Cromakalim, an activator of KATP channels, also inhibited norepinephrine-induced contraction to a similar extent as hypoxia, and in a glibenclamide and 35 mM K(+)-sensitive manner. These results are consistent with the KATP channel hypothesis. In contrast, hypoxia had no effect on estimated whole-cell membrane conductance between -40 and -90 mV in voltage-clamp experiments; on holding current measured at -60 mV in cells superfused with 143 mM K+ under voltage-clamp conditions; or on membrane potential in current-clamp experiments, despite positive effects of cromakalim in all three protocols. These electrophysiological data lead to rejection of the hypothesis that hypoxia activates KATP channels.
conclusionsHypoxia inhibits norepinephrine-induced contraction of cremasteric arteriolar muscle cells by a mechanism that does not involve KATP channels. It is speculated that the inhibitory effects of glibenclamide and 35 mM K+ on the effects of hypoxia on contraction resulted from depolarization induced by these treatments rather than specific inhibition of KATP channels.
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10802856PMC1382022W2055611168What OpenQuestion holds
Registered trials
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