KVchannels and the regulation of vascular smooth muscle tone

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Abstract

<div class="section"> <a class="named-anchor" id="S1">  </a> <h5 class="section-title" id="d802223e88">Objective</h5> <p id="P1">The objective of this brief review is to provide an overview of the expression and function of K <sub>V</sub> channels in VSMC of resistance arteries and arterioles. </p> </div><div class="section"> <a class="named-anchor" id="S2">  </a> <h5 class="section-title" id="d802223e96">Methods and Results</h5> <p id="P2">A review of the literature revealed that arterioles and resistance arteries express a diverse array of K <sub>V</sub> channels with members of the K <sub>V</sub>1, K <sub>V</sub>2 and K <sub>V</sub>7 families being particularly important. Members of the K <sub>V</sub> channel family: 1.) are highly expressed in VSMCs; 2.) are active at the resting membrane potential of VSMCs in vivo (-45 to −30 mV); 3.) contribute to the negative feedback regulation of VSMC membrane potential and myogenic tone; 4.) are activated by cAMP-related vasodilators, hydrogen sulfide and hydrogen peroxide; 5.) are inhibited by increases in intracellular Ca <sup>2+</sup> and vasoconstrictors that signal through G <sub>q</sub>-coupled receptors; 6.) are involved in the proliferative phenotype of VSMC; and 7.) are modulated by diseases such as hypertension, obesity, the metabolic syndrome and diabetes. </p> </div><div class="section"> <a class="named-anchor" id="S3">  </a> <h5 class="section-title" id="d802223e123">Conclusions</h5> <p id="P3">K <sub>V</sub> channels participate in every aspect of the regulation of VSMC function in both health and disease. </p> </div>

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Physiological roles and properties of potassium channels in arterial smooth muscle.

M T Nelson, J Quayle (1995)

This review examines the properties and roles of the four types of K+ channels that have been identified in the cell membrane of arterial smooth muscle cells. 1) Voltage-dependent K+ (KV) channels increase their activity with membrane depolarization and are important regulators of smooth muscle membrane potential in response to depolarizing stimuli. 2) Ca(2+)-activated K+ (KCa) channels respond to changes in intracellular Ca2+ to regulate membrane potential and play an important role in the control of myogenic tone in small arteries. 3) Inward rectifier K+ (KIR) channels regulate membrane potential in smooth muscle cells from several types of resistance arteries and may be responsible for external K(+)-induced dilations. 4) ATP-sensitive K+ (KATP) channels respond to changes in cellular metabolism and are targets of a variety of vasodilating stimuli. The main conclusions of this review are: 1) regulation of arterial smooth muscle membrane potential through activation or inhibition of K+ channel activity provides an important mechanism to dilate or constrict arteries; 2) KV, KCa, KIR, and KATP channels serve unique functions in the regulation of arterial smooth muscle membrane potential; and 3) K+ channels integrate a variety of vasoactive signals to dilate or constrict arteries through regulation of the membrane potential in arterial smooth muscle.

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Currents carried by sodium and potassium ions through the membrane of the giant axon ofLoligo

A. L. Hodgkin, A. F. Huxley (1952)

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Regulation of arterial diameter and wall [Ca2+] in cerebral arteries of rat by membrane potential and intravascular pressure.

Ken M. Nelson, J. Knot (1998)

1. The regulation of intracellular [Ca2+] in the smooth muscle cells in the wall of small pressurized cerebral arteries (100-200 micron) of rat was studied using simultaneous digital fluorescence video imaging of arterial diameter and wall [Ca2+], combined with microelectrode measurements of arterial membrane potential. 2. Elevation of intravascular pressure (from 10 to 100 mmHg) caused a membrane depolarization from -63 +/- 1 to -36 +/- 2 mV, increased arterial wall [Ca2+] from 119 +/- 10 to 245 +/- 9 nM, and constricted the arteries from 208 +/- 10 micron (fully dilated, Ca2+ free) to 116 +/- 7 micron or by 45 % ('myogenic tone'). 3. Pressure-induced increases in arterial wall [Ca2+] and vasoconstriction were blocked by inhibitors of voltage-dependent Ca2+ channels (diltiazem and nisoldipine) or to the same extent by removal of external Ca2+. 4. At a steady pressure (i.e. under isobaric conditions at 60 mmHg), the membrane potential was stable at -45 +/- 1 mV, intracellular [Ca2+] was 190 +/- 10 nM, and arteries were constricted by 41 % (to 115 +/- 7 micron from 196 +/- 8 micron fully dilated). Under this condition of -45 +/- 5 mV at 60 mmHg, the voltage sensitivity of wall [Ca2+] and diameter were 7.5 nM mV-1 and 7.5 micron mV-1, respectively, resulting in a Ca2+ sensitivity of diameter of 1 mum nM-1. 5. Membrane potential depolarization from -58 to -23 mV caused pressurized arteries (to 60 mmHg) to constrict over their entire working range, i.e. from maximally dilated to constricted. This depolarization was associated with an elevation of arterial wall [Ca2+] from 124 +/- 7 to 347 +/- 12 nM. These increases in arterial wall [Ca2+] and vasoconstriction were blocked by L-type voltage-dependent Ca2+ channel inhibitors. 6. The relationship between arterial wall [Ca2+] and membrane potential was not significantly different under isobaric (60 mmHg) and non-isobaric conditions (10-100 mmHg), suggesting that intravascular pressure regulates arterial wall [Ca2+] through changes in membrane potential. 7. The results are consistent with the idea that intravascular pressure causes membrane potential depolarization, which opens voltage-dependent Ca2+ channels, acting as 'voltage sensors', thus increasing Ca2+ entry and arterial wall [Ca2+], which leads to vasoconstriction.