Endothelium-Dependent Hyperpolarization (EDH) in Hypertension: The Role of Endothelial Ion Channels
<p>Diffusible and contact-mediated mechanisms of endothelium-dependent smooth muscle hyperpolarization. In certain vascular beds in specific conditions, diffusible factors such as epoxyeicosatrienoic acids (EETs), K<sup>+</sup> ions, and hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) hyperpolarize smooth muscle cells through the opening of potassium channels and/or Na<sup>+</sup>/K<sup>+</sup>-ATPase. In addition, endothelium-dependent hyperpolarization initiated in endothelial cells with a rise in intracellular calcium and the subsequent activation of small (SK<sub>Ca</sub>) and intermediate conductance (IK<sub>Ca</sub>) Ca<sup>2+</sup>-activated K<sup>+</sup> channels spreads to adjacent smooth muscle cells via myoendothelial gap junctions (MEGJs) in a number of vascular beds. In some vascular beds, combination of diffusible and contact-mediated mechanisms underpin smooth muscle hyperpolarization.</p> "> Figure 2
<p>Downregulation of transient receptor potential vanilloid type 4 channel (TRPV4) in hypertension. Representative tracing of GSK1016790A (GSK), a selective TRPV4 activator, induced hyperpolarization (<b>A</b>) and relaxation (<b>B</b>) in mesenteric arteries of Wistar–Kyoto (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP). GSK evoked hyperpolarization and relaxation in WKY but not in SHRSP arteries. Arteries were depolarized (<b>A</b>) or pre-contracted (<b>B</b>) with phenylephrine (10<sup>−5</sup> mol/L). Indomethacin (10<sup>−5</sup> mol/L) and N<sup>ω</sup>-nitro-<span class="html-small-caps">l</span>-arginine (<span class="html-small-caps">l</span>-NAME, 10<sup>−4</sup> mol/L) were present throughout the experiments. (<b>C</b>) Representative immunoblots of the expression of TRPV4 in mesenteric arteries from WKY and SHRSP. The expression of the TRPV4 protein was significantly decreased in the SHRSP mesenteric arteries compared with that from WKY. Modified from Seki et al. [<a href="#B46-ijms-19-00315" class="html-bibr">46</a>].</p> "> Figure 3
<p>Endothelial ion channels in normotension and hypertension. In normotension, in response to agonist stimulation of endothelial cells, a rise in intracellular Ca<sup>2+</sup> occurs due to the release from intracellular Ca<sup>2+</sup> stores and Ca<sup>2+</sup> entry via transient potential vanilloid type 4 channel (TRPV4). A rise in intracellular Ca<sup>2+</sup> subsequently generates endothelium-dependent hyperpolarization (EDH) through the activation of both small (SK<sub>Ca</sub>) and intermediate conductance (IK<sub>Ca</sub>) Ca<sup>2+</sup>-activated K<sup>+</sup> channels. In some arteries, K<sup>+</sup> released from endothelial K<sub>Ca</sub> channels activates endothelial Kir channels, which in turn amplifies EDH. EDH spreads to adjacent smooth muscle cells via myoendothelial gap junctions (MEGJs), resulting in vascular relaxation. In hypertension, alterations of endothelial ion channels additively reduce EDH; these alterations include downregulation of endothelial SK<sub>Ca</sub> and TRPV4 channels, upregulation of endothelial Ca<sup>2+</sup>-activated chloride channels (CaCCs), and functional loss of endothelial Kir channels.</p> ">
Abstract
:1. Introduction
2. Endothelium-Dependent Hyperpolarization (EDH) in Animal Models of Hypertension
3. Role of Endothelial Ion Channels in Reduced EDH during Hypertension
3.1. Ca2+-Activated K+ (KCa) Channels
3.2. Transient Receptor Potential (TRP) Channels
3.3. Inward Rectifier K+ (Kir) Channels
3.4. Voltage-Gated K+ (Kv) Channels and ATP-Sensitive K+ (KATP) Channels
3.5. Ca2+-Activated Chloride Channels (CaCCs)
4. Therapeutic Implications
5. Endothelium-Dependent Hyperpolarization (EDH) in Human Hypertension
6. Conclusions
Acknowledgments
Conflicts of Interest
Abbreviations
ACE | Angiotensin converting enzyme |
ACh | Acetylcholine |
AKAP150 | A-kinase anchoring protein 150 |
BKCa | Large conductance Ca2+-activated K+ |
CaCC | Ca2+-activated Cl− channel |
CYP | Cytochrome P450 |
DOCA | Deoxycorticosterone acetate |
EDH | Endothelium-dependent hyperpolarization |
EDHF | Endothelium-derived hyperpolarizing factor |
EETs | Epoxyeicosatrienoic acids |
eNOS | endothelial nitric oxide synthase |
GSK | GSK1016790A |
H2O2 | Hydrogen peroxide |
H2S | Hydrogen sulfide |
IKCa | Intermediate–conductance Ca2+-activated K+ |
KATP | ATP-sensitive K+ |
Kir | Inward rectifier K+ |
Kv | Voltage-gated K+ |
l-NAME | Nω-nitro-l-arginine |
MEGJs | Myoendothelial gap junctions |
MEPs | Myoendothelial projections |
NADPH | Nicotinamide adenine dinucleotide phosphate |
NO | Nitric oxide |
PKC | Protein kinase C |
RAS | Renin–angiotensin system |
SHR | Spontaneously hypertensive rats |
SHRSP | Stroke-prone spontaneously hypertensive rats |
SKCa | Small-conductance Ca2+-activated K+ |
TMEM16A | Transmembrane member 16A |
TRP | Transient receptor potential |
TRPC3 | TRP canonical type 3 |
TRPV4 | TRP vanilloid type 4 |
WKY | Wistar-Kyoto |
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Goto, K.; Ohtsubo, T.; Kitazono, T. Endothelium-Dependent Hyperpolarization (EDH) in Hypertension: The Role of Endothelial Ion Channels. Int. J. Mol. Sci. 2018, 19, 315. https://doi.org/10.3390/ijms19010315
Goto K, Ohtsubo T, Kitazono T. Endothelium-Dependent Hyperpolarization (EDH) in Hypertension: The Role of Endothelial Ion Channels. International Journal of Molecular Sciences. 2018; 19(1):315. https://doi.org/10.3390/ijms19010315
Chicago/Turabian StyleGoto, Kenichi, Toshio Ohtsubo, and Takanari Kitazono. 2018. "Endothelium-Dependent Hyperpolarization (EDH) in Hypertension: The Role of Endothelial Ion Channels" International Journal of Molecular Sciences 19, no. 1: 315. https://doi.org/10.3390/ijms19010315