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Molecular Mechanisms of Various Diseases and Drugs Involved in Vascular Tone Regulation in Cardiovascular Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 September 2025 | Viewed by 188

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Guest Editor
Department of Anesthesiology and Pain Medicine, College of Medicine, Gyeongsang National University (GSNU), Jinju, Republic of Korea
Interests: anesthetics; vascular pharmacology; lipid emulsion; local anesthetic toxicity; calcium; nitric oxide; smooth muscle contraction
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Special Issue Information

Dear Colleagues,

Vascular tone regulation is crucial for maintaining homeostasis. The contraction of vascular smooth muscle is controlled by calcium-dependent and calcium-sensitizing mechanisms. The calcium-dependent mechanism is mediated by calcium influx through voltage-operated and receptor-operated calcium channels or by calcium release from the sarcoplasmic reticulum, leading to myosin light chain (MLC20) phosphorylation. Additionally, calcium sensitization occurs through the inhibition of myosin light chain phosphatase via protein kinase C phosphorylation and Rho-kinase membrane translocation, resulting in MLC20 phosphorylation.Furthermore, vasodilation is induced by nitric oxide, endothelium-derived hyperpolarizing factors, and prostaglandins, which activate cyclic guanosine monophosphate- and adenosine monophosphate-dependent protein kinases, stimulate potassium channels, and inhibit calcium influx. However, the pathophysiological mechanisms of various diseases, such as hypertension, involve the dysregulation of calcium sensitization, calcium-dependent contraction, nitric oxide release, and endothelium-derived hyperpolarizing factors.Understanding the underlying mechanisms of vascular tone regulation and hemodynamic changes caused by various diseases and pharmacological agents—including antihypertensive drugs and vasopressors—is essential for advancing our knowledge of disease pathophysiology and drug effects. This Special Issue welcomes research related to vasoconstriction and vasodilation in the context of diseases and therapeutic compounds, including G protein-coupled receptor agonists. 

Prof. Dr. Ju-Tae Sohn
Guest Editor

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Keywords

  • vasoconstriction
  • vasodilation
  • calcium
  • protein kinase C
  • Rho-kinase
  • hypertension
  • nitric oxide

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Published Papers (1 paper)

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Research

16 pages, 2571 KiB  
Article
Chloroquine Inhibits Contraction Elicited by the Alpha-1 Adrenoceptor Agonist Phenylephrine in the Isolated Rat Aortas
by Soo Hee Lee, Kyeong-Eon Park, Seong-Chun Kwon, Seong-Ho Ok, Seung Hyun Ahn, Gyujin Sim and Ju-Tae Sohn
Int. J. Mol. Sci. 2025, 26(10), 4556; https://doi.org/10.3390/ijms26104556 - 9 May 2025
Viewed by 102
Abstract
Although chloroquine appears to inhibit the alpha-1 adrenoceptor, whether the chloroquine-mediated inhibition of phenylephrine-induced contraction is associated with the blockade of alpha-1 adrenoceptors remains unknown. This study examined the effect of chloroquine on contractions elicited by the alpha-1 adrenoceptor agonist phenylephrine in isolated [...] Read more.
Although chloroquine appears to inhibit the alpha-1 adrenoceptor, whether the chloroquine-mediated inhibition of phenylephrine-induced contraction is associated with the blockade of alpha-1 adrenoceptors remains unknown. This study examined the effect of chloroquine on contractions elicited by the alpha-1 adrenoceptor agonist phenylephrine in isolated rat aortas and determined the underlying mechanism. The effects of chloroquine and the alpha-1 adrenoceptor inhibitor prazosin on phenylephrine-elicited contractions were examined. The effects of the irreversible alpha-adrenoceptor inhibitor phenoxybenzamine followed by washout with fresh Krebs solution, as well as combined treatment with chloroquine and phenoxybenzamine followed by washout with fresh Krebs solution, on phenylephrine-induced contraction were investigated. Chloroquine and prazosin inhibited phenylephrine-induced contractions. However, pretreatment with prazosin eliminated the chloroquine-induced inhibition of contractions elicited by phenylephrine. Additionally, pretreatment with chloroquine and phenoxybenzamine followed by washout produced a higher contraction elicited by phenylephrine than pretreatment with phenoxybenzamine alone followed by washout. Although chloroquine did not affect the contraction induced by KCl in the endothelium-denuded aorta, it inhibited phenylephrine-induced protein kinase C (PKC) and myosin light-chain (MLC20) phosphorylation and Rho-kinase membrane translocation. These results suggest that chloroquine inhibits vasoconstriction elicited by phenylephrine via alpha-1 adrenoceptor inhibition, which is mediated by decreased MLC20 phosphorylation, the attenuation of PKC phosphorylation, and Rho-kinase membrane translocation. Full article
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