ArticleInvestigative ophthalmology & visual science2005
A-type potassium current in retinal arteriolar smooth muscle cells.
Article in Investigative ophthalmology & visual science, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- Myocardial Blood Flow Control by Oxygen Sensing Vascular Kvβ Proteins.Circulation research · 2021Article
- Isolation of Retinal Arterioles for Ex Vivo Cell Physiology Studies.Journal of visualized experiments : JoVE · 2018Article
- Potent block of potassium channels by MEK inhibitor U0126 in primary cultures and brain slices.Scientific reports · 2018Article
- KMicrocirculation (New York, N.Y. : 1994) · 2018Review
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- The role of K+ and Cl- channels in the regulation of retinal arteriolar tone and blood flow.Investigative ophthalmology & visual science · 2014Article
- Imaging of vascular wall fine structure in the human retina using adaptive optics scanning laser ophthalmoscopy.Investigative ophthalmology & visual science · 2013Article
- Fenamates block gap junction coupling and potentiate BKCa channels in guinea pig arteriolar cells.European journal of pharmacology · 2013Article
- Ca2+-activated Cl- current in retinal arteriolar smooth muscle.Investigative ophthalmology & visual science · 2009Article
- Ca2+-sparks constitute elementary building blocks for global Ca2+-signals in myocytes of retinal arterioles.Cell calcium · 2007Article
- Diabetes downregulates large-conductance Ca2+-activated potassium beta 1 channel subunit in retinal arteriolar smooth muscle.Circulation research · 2007Article
- Kv1.5 is a major component underlying the A-type potassium current in retinal arteriolar smooth muscle.American journal of physiology. Heart and circulatory physiology · 2007Article
- Selective downregulation of the BKbeta1 subunit in diabetic arteriolar myocytes.Channels (Austin, Tex.)Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
purposeBy their control of membrane potential and intracellular free Ca(2+) ([Ca(2+)](i)), K(+) currents are pivotal in the regulation of arterial smooth muscle tone. The goal of the present study was to identify and characterize the A-type K(+) current in retinal microvascular smooth muscle (MVSM) and to examine its role in modulating membrane potential and cellular contractility.
methodsWhole-cell perforated patch-clamp recordings were made from MVSM cells within intact isolated arteriolar segments. Before patch-clamping, retinal arterioles were anchored in the physiological recording bath and perfused with an enzyme cocktail to remove surface basal lamina and to uncouple electrically the endothelial cells from the overlying MVSM cells.
resultsK(+) currents were activated by depolarizing steps from -80 to +100 mV in 20-mV increments. A dominant, noninactivating current was elicited by depolarization to potentials positive of -50 mV. Inhibition of this current by 100 nM of the Ca(2+)-activated K(+) channel blocker, Penitrem A, revealed a rapidly inactivating K(+) current that resembled an A-type current. The A-type current was insensitive to tetraethylammonium (TEA) at 1 mM, but was partially suppressed by higher concentrations (10 mM). 4-Aminopyridine (10 mM; 4-AP) completely blocked the A-type current. The 4-AP-sensitive transient current was activated at a potential of -60 mV with peak current densities averaging 29.7 +/- 5.68 pA/pF at +60 mV. The voltage of half-inactivation was -28.3 +/- 1.9 mV, and the time constant for recovery from inactivation at +60 mV was 118.7 +/- 7.9 ms. Under current-clamp conditions 4-AP depolarized the membrane potential by approximately 3 to 4 mV and triggered small contractions and relaxations of individual MVSM cells within the walls of the arterioles.
conclusionsA-type current is the major voltage-dependent K(+) current in retinal MVSM and appears to play a physiological role in suppressing cell excitability and contractility.
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