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Effect of Cardioprotective Drugs on the Cardiovascular System
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Effect of Cardioprotective Drugs on the Cardiovascular System

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

Deadline for manuscript submissions: 30 August 2024 | Viewed by 2433

Special Issue Editor

Prof. Dr. Ju-Tae Sohn

E-Mail Website
Guest Editor
Department of Anesthesiology and Pain Medicine, College of Medicine, Gyeongsang National University (GSNU), Jinju-si 52727, Republic of Korea
Interests: anesthetics; vascular pharmacology; lipid emulsion; local anesthetic toxicity; calcium; nitric oxide; smooth muscle contraction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alpha-2 adrenoceptor agonist dexmedetomidine is widely used for sedation, the reduction in opioid requirement, and the attenuation of hemodynamic response to surgery during the perioperative period. An excessive dose of dexmedetomidine produces vasoconstriction, which is mediated by calcium-dependent and calcium-sensitization mechanisms, produces a transient hypertensive crisis, and is followed by delayed hypotension. It is very important to elucidate the underlying mechanisms associated with vascular tone and hemodynamic change induced by cardioprotective drugs, including alpha-2 adrenoceptor agonist, which contributes to the understanding of the pathophysiology induced by various cardioprotective drugs and compounds. In this Special Issue, we welcome all research studies associated with vasoconstriction and vasodilation, and changes in myocardial contractility induced by various cardioprotective drugs and compounds including G protein-coupled receptor agonist.

Prof. Dr. Ju-Tae Sohn
Guest Editor

Manuscript Submission Information

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Keywords

  • alpha-2 adrenoceptor agonist
  • vascular smooth muscle
  • contraction
  • myocardial contractility
  • relaxation

Published Papers (3 papers)

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Research

13 pages, 1357 KiB  
Article
Hypothermia Inhibits Dexmedetomidine-Induced Contractions in Isolated Rat Aortae
by Soohee Lee, Yeran Hwang, Kyeong-Eon Park, Sungil Bae, Seong-Ho Ok, Seung-Hyun Ahn, Gyujin Sim, Moonju Bae and Ju-Tae Sohn
Int. J. Mol. Sci. 2024, 25(5), 3017; https://doi.org/10.3390/ijms25053017 - 05 Mar 2024
Viewed by 518
Abstract
Dexmedetomidine is widely used to induce sedation in the perioperative period. This study examined the effect of hypothermia (33 and 25 °C) on dexmedetomidine-induced contraction in an endothelium-intact aorta with or without the nitric oxide synthase inhibitor NW-nitro-L-arginine methyl ester (L-NAME). [...] Read more.
Dexmedetomidine is widely used to induce sedation in the perioperative period. This study examined the effect of hypothermia (33 and 25 °C) on dexmedetomidine-induced contraction in an endothelium-intact aorta with or without the nitric oxide synthase inhibitor NW-nitro-L-arginine methyl ester (L-NAME). In addition, the effect of hypothermia on the contraction induced by dexmedetomidine in an endothelium-denuded aorta with or without a calcium-free Krebs solution was examined. The effects of hypothermia on the protein kinase C (PKC), myosin light chain (MLC20) phosphorylation, and Rho-kinase membrane translocation induced by dexmedetomidine were examined. Hypothermia inhibited dexmedetomidine-induced contraction in the endothelium-intact aorta with L-NAME or endothelium-denuded aorta. Hypothermia had almost no effect on the dexmedetomidine-induced contraction in the endothelium-denuded aorta with the calcium-free Krebs solution; however, the subsequent contraction induced by the addition of calcium was inhibited by hypothermia. Conversely, the transition from profound hypothermia back to normothermia reversed the hypothermia-induced inhibition of subsequent calcium-induced contractions. Hypothermia inhibited any contraction induced by KCl, PDBu, and NaF, as well as PKC and MLC20 phosphorylation and Rho-kinase membrane translocation induced by dexmedetomidine. These results suggest that hypothermia inhibits dexmedetomidine-induced contraction, which is mediated mainly by the impediment of calcium influx and partially by the attenuation of pathways involving PKC and Rho-kinase activation. Full article
(This article belongs to the Special Issue Effect of Cardioprotective Drugs on the Cardiovascular System)
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14 pages, 2286 KiB  
Article
Investigating the Cardiovascular Benefits of Dapagliflozin: Vasodilatory Effect on Isolated Rat Coronary Arteries
by Sooyeon Choi, Chae Eun Haam, Seonhee Byeon, Eun Yi Oh, Soo-Kyoung Choi and Young-Ho Lee
Int. J. Mol. Sci. 2023, 24(23), 16873; https://doi.org/10.3390/ijms242316873 - 28 Nov 2023
Viewed by 780
Abstract
Dapagliflozin, a sodium–glucose co-transporter 2 (SGLT2) inhibitor, is an antidiabetic medication that reduces blood glucose. Although it is well known that dapagliflozin has additional benefits beyond glycemic control, such as reducing blood pressure and lowering the risk of cardiovascular events, no sufficient research [...] Read more.
Dapagliflozin, a sodium–glucose co-transporter 2 (SGLT2) inhibitor, is an antidiabetic medication that reduces blood glucose. Although it is well known that dapagliflozin has additional benefits beyond glycemic control, such as reducing blood pressure and lowering the risk of cardiovascular events, no sufficient research data are available on the direct effect of dapagliflozin on cardiovascular function. Thus, in this study, we investigated the direct vascular effect of dapagliflozin on isolated rat coronary arteries. The left descending coronary arteries of 13-week-old male Sprague Dawley rats were cut into segments 2–3 mm long and mounted in a multi-wire myography system to measure isometric tension. Dapagliflozin effectively reduced blood vessel constriction induced by U-46619 (500 nM) in coronary arteries regardless of the endothelium. Treatment with an eNOS inhibitor (L-NNA, 100 μM), sGC inhibitor (ODQ, 5 μM), or COX inhibitor (indomethacin, 3 μM) did not affect the vasodilation induced by dapagliflozin. The application of a Ca2+-activated K+ channel (KCa) blocker (TEA, 2 mM), voltage-dependent K+ channel (KV) blocker (4-AP, 2 mM), ATP-sensitive K+ channel blocker (KATP) glibenclamide (3 μM), and inward-rectifier K+ channel (KIR) blocker (BaCl2, 30 μM) did not affect the dapagliflozin-induced vasodilation either. The treatment with dapagliflozin decreased contractile responses induced by the addition of Ca2+, which suggested that the extracellular Ca2+ influx was inhibited by dapagliflozin. Treatment with dapagliflozin decreased the phosphorylation level of the 20 kDa myosin light chain (MLC20) in vascular smooth muscle cells. In the present study, we found that dapagliflozin has a significant vasodilatory effect on rat coronary arteries. Our findings suggest a novel pharmacologic approach for the treatment of cardiovascular diseases in diabetic patients through the modulation of Ca2+ homeostasis via dapagliflozin administration. Full article
(This article belongs to the Special Issue Effect of Cardioprotective Drugs on the Cardiovascular System)
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11 pages, 1897 KiB  
Article
Ezetimibe Induces Vasodilation in Rat Mesenteric Resistance Arteries through Inhibition of Extracellular Ca2+ Influx
by Eun Yi Oh, Chae Eun Haam, Sooyeon Choi, Seonhee Byeon, Soo-Kyoung Choi and Young-Ho Lee
Int. J. Mol. Sci. 2023, 24(18), 13992; https://doi.org/10.3390/ijms241813992 - 12 Sep 2023
Viewed by 855
Abstract
Ezetimibe is a lipid-lowering agent that selectively inhibits cholesterol absorption by binding to the Niemann–Pick C1-like 1 (NPC1L1) protein. Although it is well known that administration of ezetimibe in hypercholesterolemia patients reduces the risk of cardiovascular events through attenuation of atherosclerosis, studies on [...] Read more.
Ezetimibe is a lipid-lowering agent that selectively inhibits cholesterol absorption by binding to the Niemann–Pick C1-like 1 (NPC1L1) protein. Although it is well known that administration of ezetimibe in hypercholesterolemia patients reduces the risk of cardiovascular events through attenuation of atherosclerosis, studies on the direct effect of ezetimibe on vascular function are not sufficient. The aim of the present study was to investigate the vascular effects of ezetimibe in rat mesenteric arteries. In the present study, 12-week-old male Sprague Dawley rats were used. After the rats were sacrificed, the second branches of the mesenteric arteries were isolated and cut into 2–3 mm segments and mounted in a multi-wire myography system to measure isometric tension. Ezetimibe reduced vasoconstriction induced by U46619 (500 nM) in endothelium-intact and endothelium-denuded arteries. Ezetimibe-induced vasodilation was not affected by the endothelial nitric oxide synthase (eNOS) inhibitor Nω-Nitro-L-arginine (L-NNA, 300 μM) or the non-selective potassium channel blocker, tetraethylammonium (TEA, 10 mM). Moreover, ezetimibe also completely blocked the contraction induced by an increase in external calcium concentration. Ezetimibe significantly reduced vascular contraction induced by L-type Ca2+ channel activator (Bay K 8644, 30 nM). Treatment with ezetimibe decreased the phosphorylation level of 20 kDa myosin light chain (MLC20) in vascular smooth muscle cells. In the present study, we found that ezetimibe has a significant vasodilatory effect in rat mesenteric resistance arteries. These results suggest that ezetimibe may have beneficial cardiovascular effects beyond its cholesterol-lowering properties. Full article
(This article belongs to the Special Issue Effect of Cardioprotective Drugs on the Cardiovascular System)
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