Phenotypic differences between microvascular and macrovascular smooth muscle cells and their contribution to coronary microvascular dysfunction

Riches-Suman, Kirsten

doi:10.20517/2574-1209.2021.45

Cited by 2 publications

(5 citation statements)

References 61 publications

(74 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Such a thrombogenic effect was reported for the contrast agent 5-Fluorouracil as a consequence of the initially direct disruption of the endothelial barrier. In addition, drug-related impaired cardiac microvasculature SMC function, namely impaired vasodilation or microvascular spasms, could result in defective adaptation in the case of changing oxygen demand and thus decreased myocardial blood supply 30 .…”

Section: Discussionmentioning

confidence: 99%

Amphetamine increases vascular permeability by modulating endothelial actin cytoskeleton and NO synthase via PAR-1 and VEGF-R

Böttner,

Fischer-Schaepmann,

Werner

et al. 2024

Sci Rep

View full text Add to dashboard Cite

Abuse of amphetamine-type stimulants is linked to cardiovascular adverse effects like arrhythmias, accelerated atherosclerosis, acute coronary syndromes and sudden cardiac death. Excessive catecholamine release following amphetamine use causes vasoconstriction and vasospasms, over time leading to hypertension, endothelial dysfunction or even cardiotoxicity. However, immediate vascular pathomechanisms related to amphetamine exposure, especially endothelial function, remain incompletely understood and were analyzed in this study. Pharmaco-pathological effects of acute d-amphetamine-sulfate (DAM) were investigated ex vivo using contraction–force measurements of rat carotid artery rings and in vitro using label-free, real-time electrochemical impedance spectroscopy (EIS) on endothelial and smooth muscle cells. Specific receptor and target blocking was used to identify molecular targets and to characterize intracellular signaling. DAM induced vasodilation represented by 29.3±2.5% decrease in vascular tone (p<0.001) involving vascular endothelial growth factor receptor (VEGF-R) and protease activated receptor 1 (PAR-1). EIS revealed that DAM induces endothelial barrier disruption (−75.9±1.1% of initial cellular impedance, p<0.001) also involving VEGF-R and PAR-1. Further, in response to DAM, Rho-associated protein kinase (ROCK) mediated reversible contraction of actin cytoskeleton resulting in endothelial barrier disruption. Dephosphorylation of Serine1177 (−50.8±3.7%, p<0.001) and Threonine495 (−44.8±6.5%, p=0.0103) of the endothelial NO synthase (eNOS) were also observed. Blocking of VEGF-R and PAR-1 restored baseline eNOS Threonine495 phosphorylation. DAM induced vasodilation, enhanced vascular permeability and actin cytoskeleton contraction and induced eNOS hypophosphorylation involving VEGF-R, PAR-1 and ROCK. These results may contribute to a better understanding of severe adverse cardiovascular effects in amphetamine abuse.

show abstract

Section: Discussionmentioning

confidence: 99%

Amphetamine increases vascular permeability by modulating endothelial actin cytoskeleton and NO synthase via PAR-1 and VEGF-R

Böttner,

Fischer-Schaepmann,

Werner

et al. 2024

Sci Rep

View full text Add to dashboard Cite

show abstract

“…This alters them from mature cells that control contraction and relaxation to synthetic cells that causes them to proliferate and migrate. This proliferation and migration of immature cells results in hypertrophy [8] . The impaired coronary microvascular flow eventually leads to concentric hypertrophy and diastolic dysfunction in the left ventricle (LV) [8] .…”

Section: Pathophysiology Of Microcirculatory Dysfunctionmentioning

confidence: 99%

“…This proliferation and migration of immature cells results in hypertrophy [8] . The impaired coronary microvascular flow eventually leads to concentric hypertrophy and diastolic dysfunction in the left ventricle (LV) [8] .…”

Section: Pathophysiology Of Microcirculatory Dysfunctionmentioning

confidence: 99%

“…Initially the RV-PA system can adapt and preserve efficient blood flow through the ventricle and into the lungs, but as PA load increases the system uncouples and becomes less efficient, leading to first diastolic then systolic RVF [18] , [19] . CMD, through diastolic dysfunction of the LV, can also lead to group 2 PH and RV dysfunction [8] ; high left-sided pressures cause pulmonary vascular congestion, increased pulmonary venous pressure, and hypoxic vasoconstriction and endothelial dysfunction in the pulmonary vascular system [20] . RV dysfunction in the two entities (PAH and left sided heart failure associated with PH) does have distinct phenotypes.…”

Section: Pathophysiology Of Microcirculatory Dysfunctionmentioning

confidence: 99%

“…Impaired vasodilation secondary to [8] : arteriole smooth muscle hypertrophy collagen deposition intimal thickening …”

Section: Pathophysiology Of Microcirculatory Dysfunctionmentioning

confidence: 99%

See 2 more Smart Citations

A review of cardio-pulmonary microvascular dysfunction in pulmonary hypertension

Vahdatpour¹,

Epstein²,

Jones³

et al. 2023

American Heart Journal Plus: Cardiology Research and Practice

View full text Add to dashboard Cite

Phenotypic differences between microvascular and macrovascular smooth muscle cells and their contribution to coronary microvascular dysfunction

Abstract: How to cite this article: Riches-Suman K. Phenotypic differences between microvascular and macrovascular smooth muscle cells and their contribution to coronary microvascular dysfunction.

Cited by 2 publications

References 61 publications

Amphetamine increases vascular permeability by modulating endothelial actin cytoskeleton and NO synthase via PAR-1 and VEGF-R

Amphetamine increases vascular permeability by modulating endothelial actin cytoskeleton and NO synthase via PAR-1 and VEGF-R

A review of cardio-pulmonary microvascular dysfunction in pulmonary hypertension

Contact Info

Product

Resources

About