Physiological aspects of vascular endothelial cell interactions in hypertension and atherosclerosis

Dg, Harrison

doi:10.1111/j.1399-6576.1993.tb03817.x

Cited by 5 publications

(5 citation statements)

References 41 publications

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“…There is a growing speculation that inflammation may play a role in the development of hypertension . Systemic inflammation is involved in the pathogenesis of endothelial dysfunction, leading to structural and functional changes in the endothelium often apparent in the early stages of hypertension . Epidemiologic data are largely confined to cross‐sectional studies that reported elevations in C‐reactive protein (CRP), interleukin‐6 (IL‐6), and soluble intercellular adhesion molecule (sICAM‐1) with increases in blood pressure (BP) or hypertension.…”

Section: Introductionmentioning

confidence: 99%

“… 2 , 3 Systemic inflammation is involved in the pathogenesis of endothelial dysfunction, 4 leading to structural and functional changes in the endothelium often apparent in the early stages of hypertension. 5 , 6 Epidemiologic data are largely confined to cross-sectional studies that reported elevations in C-reactive protein (CRP), 7 – 16 interleukin-6 (IL-6), 9 , 13 , 17 , 18 and soluble intercellular adhesion molecule (sICAM-1) 14 , 17 with increases in blood pressure (BP) or hypertension. D-dimer is a hemostatic marker of coagulation activation and fibrinolysis 19 that might also indicate poor arterial health and adversely affect BP; however, existing findings from epidemiologic studies are inconsistent.…”

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confidence: 99%

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Plasma Inflammatory Markers and the Risk of Developing Hypertension in Men

Sesso

Jiménez

Wang

et al. 2015

JAHA

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BackgroundSeveral cross-sectional, but few prospective, studies suggest that inflammation may be involved in the development of hypertension. We examined markers of inflammation—high-sensitivity C-reactive protein, interleukin-6, and soluble intercellular adhesion molecule-1—and a marker of fibrinolysis, D-dimer, for their associations with incident hypertension in the Physicians’ Health Study.Methods and ResultsBaseline blood values and information on hypertension-related risk factors were collected in 1982. Incident hypertension was defined as self-reported initiation of antihypertensive treatment, systolic blood pressure ≥140 mm Hg, or diastolic blood pressure ≥90 mm Hg during follow-up. With use of a nested case-control design, 396 cases of incident hypertension and controls free of hypertension were matched 1:1 on age (mean 47.4 years) and follow-up time. In crude matched-pair analyses, the conditional relative risks of hypertension in the second through fourth versus the lowest quartiles for plasma high-sensitivity C-reactive protein were 1.27, 1.73, and 1.81 (Ptrend=0.01); for interleukin-6, 1.22, 1.02, and 1.51 (Ptrend=0.06); for soluble intercellular adhesion molecule-1, 1.00, 0.80, and 1.26 (Ptrend=0.37); and for D-dimer, 1.61, 1.81, and 1.52 (Ptrend=0.46). Multivariable adjustment attenuated the estimates. The multivariable relative risks of hypertension in the second through fourth compared to the lowest quartiles of high-sensitivity C-reactive protein were 1.24, 1.60, and 1.47 (Ptrend=0.20); for interleukin-6, 1.08, 0.92, and 1.36 (Ptrend=0.16); for soluble intercellular adhesion molecule-1, 0.89, 0.79, and 1.18 (Ptrend=0.55); and for D-dimer, 1.48, 1.68, and 1.38 (Ptrend=0.63).ConclusionsElevated plasma inflammatory markers and D-dimer were nonsignificantly associated with a higher risk of hypertension among initially healthy men.

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%

Plasma Inflammatory Markers and the Risk of Developing Hypertension in Men

Sesso

Jiménez

Wang

et al. 2015

JAHA

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“…Hypertension has been shown to increase the risk of atherosclerosis in both clinical and animal studies [13,45]; however, the mechanisms of the enhanced or synergistic effect between these two disease entities are not yet clearly defined. Hypertension shares several vascular abnormalities with atherosclerosis, including interactions between blood cells and vascular cells, SMC migration and proliferation, as well as intimal thickening [1,12,13,16,22]. Our results suggest that the elevated migratory response of SHR-SMC could contribute to the increased risk that those with hypertension have for the development of atherosclerosis.…”

Section: Discussionmentioning

confidence: 63%

Migration of vascular smooth muscle cells is enhanced in cultures derived from spontaneously hypertensive rat

Hsieh

Lau

1997

Pfl�gers Archiv European Journal of Physiology

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Migration of vascular smooth muscle cells (SMC) constitutes a common step in neointimal formation which occurs in several vascular diseases. Whether the migratory response of SMC derived from hypertensive animals is different to that of controls may provide a clue to the link between hypertension and atherosclerosis. We examined the migratory responses of SMC from cell cultures and ring explants (thin aortic ring segment) and compared these responses between normotensive and hypertensive rats at two different ages. Both scrape-wound assay and transwell chambers from cultured aortic SMC as well as aortic ring explant cell outgrowth models were employed. The aortae were obtained from male spontaneously hypertensive rats (SHR) and their normotensive counterpart the Wistar-Kyoto rat (WKY) at 5 and 20 weeks of age. Migration was induced by fetal bovine serum or platelet-derived growth factor (PDGF) and migrated cells were counted at different times following stimulation. We found that SMC migration exhibited a high sensitivity to serum (range of ED50: 2.2-3.6%), migration of SMC from 20-week-old SHR exceeded (by 46%, P<0.025) that of SMC from age-matched WKY and the difference became significant as early as 8 h after stimulation by serum. Chemotaxis induced by PDGF (2 h) exhibited similar differences. An elevated migratory response in SHR-SMC was also found in cells derived from 5-week-old rats in whom the blood pressure was normal. In younger animals, cell outgrowth from SHR aortic ring explants also accumulated more cells compared with WKY without a higher growth rate, thus suggesting that SHR-SMC have a higher migratory response ex vivo. In conclusion, aortic SMC migration appeared to be enhanced in various preparations from SHR. This difference also existed in young animals before the elevation of blood pressure occurred and might contribute partly to the role of hypertension as a risk factor for atherosclerosis.

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“…The larger epicardial macrovessels are less sensitive to injury, whereas, the smaller intramyocardial microvessels-arterioles and capillaries-are extremely sensitive to injury because of their close proximity to the ischemic myocardium. The high sensitivity of the vascular endothelium to the detrimental inflammatory effects of ischemia and reperfusion (7) after myocadial revascularization is amplified in patients with such diseases as hypertension, hypercholesterolemia, and diabetes mellitus (8,9).…”

Section: Victims and Timing Of Surgical Ischemic-reperfusion Injurymentioning

confidence: 99%

Myocardial Protection: An Overview

Vinten-Johansen,

Thourani

2000

J Extra Corpor Technol

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The goals of myocardial protection during cardiac surgery are not only to facilitate the operation by providing a quiet bloodless field, thereby facilitating the precision of the operation, but also to avoid iatrogenic injury induced by cardiopulmonary bypass itself or by surgically imposed ischemia. In addition, myocardial protective strategies are geared to preventing reperfusion injury upon resolution of the coronary occlusion and the ultimate release of the aortic cross clamp. Cardioplegia plays a very important role in myocardial protection strategies. Acting as a selective perfusion agent, cardioplegia solutions can alter or inhibit ischemic injury by virtue of hypothermia and asystole. In addition, cardioplegia can be used to avoid reperfusion injury by altering the conditions of its delivery and the composition of the solution using various adjunctive agents and pharmacologic therapies for which cardioplegia solutions serve as a vector. Future strategies, particularly for off-pump surgical procedures, may incorporate systemic delivery of therapeutic agents to the heart directly either in conjunction with or without cardioplegia.

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Physiological aspects of vascular endothelial cell interactions in hypertension and atherosclerosis

Cited by 5 publications

References 41 publications

Plasma Inflammatory Markers and the Risk of Developing Hypertension in Men

Plasma Inflammatory Markers and the Risk of Developing Hypertension in Men

Migration of vascular smooth muscle cells is enhanced in cultures derived from spontaneously hypertensive rat

Myocardial Protection: An Overview

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