Endothelial mediated enhancement of noradrenaline induced vasoconstriction in normal and varicose veins

Thulesius, Olav; Said, Sami I.; H, Shuhaiber; Neglén, Peter; Gjöres, J E

doi:10.1111/j.1475-097x.1991.tb00108.x

Cited by 25 publications

(18 citation statements)

References 13 publications

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“…The ultrasound diameter measurements in all subject groups were assessed by the same experienced vascular technologist (A.A) in a room at constant temperature (22±2°C). The pharmacological study confirmed the findings of Thulesius [7] in that there was contractile reduction in the maximal contractile force of varicose vein preparations to NA and 5-HT compared to controls. This was more evident when the endothelium was denuded.…”

Section: Discussionsupporting

confidence: 76%

“…Hypothermia cause vasoconstirction of normal veins while varicose veins are not affected [9]. Also Thulesius found in normal veins no endothelial-derived nitrous oxide (NO) relaxation upon acetylcholine stimulation, whereas NO was released from the endothelium of varicose veins [7]. However, capacitance veins have been shown to both release basal and stimulated NO [10].…”

Section: Introductionmentioning

confidence: 99%

“…Reduced contractile responses to noradrenaline [7] and imbalance between endothelial cell-derived contractile and vasodilator responses [8] have been described for varicose veins. Hypothermia cause vasoconstirction of normal veins while varicose veins are not affected [9].…”

Section: Introductionmentioning

confidence: 99%

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In Vivo and In Vitro Assessment of Human Saphenous Vein Wall Changes

Asbeutah¹,

Asfar²,

Mustafa³

et al. 2007

TOCMJ

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Abstract:Purpose: To investigate if noradrenaline (NA) and 5-hydroxyptamine (5-HT) drugs induce responses of isolated control and varicose veins are altered by removal of the endothelium. Subjects & Methods:Specimens of the great saphenous vein (GSV) were obtained from 12 subjects with primary varicose veins and 12 subjects from donor vessels at cardiac surgery. A total of 10 normal healthy volunteers were selected for comparison. The diameter changes of GSV during the resting phase, at the end of 5 minutes occlusion, and then every 30 seconds post deflation for five minutes were measured using B-mode ultrasound. Post-surgery the vein sample was collected in a tube of Krebs-Henseleit solution.Results: The repeated measure ANOVA test for the diameter, percent, and difference changes of GSV diameter from maximum diameter at different time intervals showed significance difference within and between all groups. NA and 5-HT produced concentration-dependent contractions of control and varicose saphenous vein segments. There was no significant difference in the potency of NA and for 5-HT, but the maximum response, normalized for tissue weight, was less in varicose vein segments. Removal of the endothelium had no effect on the potency of NA or 5-HT but significantly (p<0.05) reduced the maximum response to NA and 5-HT in varicose vein segments but not to 5-HT in control veins. Conclusion:The venous endothelial damage may cause vascular smooth muscle contractions dysfunction that favours dilatation and secondary valvular insufficiency.

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Section: Discussionsupporting

confidence: 76%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

In Vivo and In Vitro Assessment of Human Saphenous Vein Wall Changes

Asbeutah¹,

Asfar²,

Mustafa³

et al. 2007

TOCMJ

View full text Add to dashboard Cite

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“…Imbalance of these vasoactive substances may contribute to the overall relaxation of varicose veins 32 . For example, a reduction in factors contributing to vasoconstriction such as the noradrenaline, endothelin-1 binding and endothelin-B receptor density, probably due to endothelial injury, has also been shown in varicose compared with non-varicose veins 83,84 . Factors that contribute to vasodilatation, including nitric oxide, prostacyclin and hyperpolarization of the underlying SMCs by endothelium-derived hyperpolarizing factor, are upregulated in varicose compared with non-varicose veins 14,32 .…”

Section: Activation Of the Endotheliummentioning

confidence: 97%

Pathogenesis of primary varicose veins

Lim

Davies

2009

British Journal of Surgery

231

206

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Positive family history, age, sex and pregnancy are important risk factors for varicose vein formation. Areas of intimal hyperplasia and smooth muscle cell proliferation are often noted in varicose veins, although regions of atrophy are also present. The total elastin content in varicose as opposed to non-varicose veins is reduced; changes in overall collagen content are uncertain. Matrix metalloproteinases (MMPs), including MMP-1, MMP-2, MMP-3, MMP-7 and MMP-9, and tissue inhibitor of metalloproteinase (TIMP) 1 and TIMP-3 are upregulated in varicose veins. Activation of the endothelium stimulates the recruitment of leucocytes and the release of growth factors, leading to smooth muscle cell proliferation and migration. Dysregulated apoptosis has also been demonstrated in varicose veins. An understanding of the pathophysiology of varicose veins is important in the identification of potential therapeutic targets and treatment strategies.

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“…Previous measurements of the contractile response in isolated VarV segments have demonstrated variable results 3–6. The variability in the results could be related to differences in the vasoconstrictor stimulus used and/or the vein segment examined.…”

Section: Introductionmentioning

confidence: 99%

Functional adaptation of venous smooth muscle response to vasoconstriction in proximal, distal, and varix segments of varicose veins

Raffetto

Qiao

Beauregard

et al. 2010

Journal of Vascular Surgery

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Background Varicose Veins (VarV) is a common disorder of venous dilation and turtuosity with unclear mechanism. Although venous smooth muscle constitutes a significant component of the vein wall, the functional integrity and the ability of various regions of the VarV to constrict is unclear. The objective of this study was to test the hypothesis that the different degrees of venodilation in different regions of VarV reflect segmental differences in the responsiveness to receptor-dependent vasoconstrictive stimuli and/or in the post-receptor signaling mechanisms of vasoconstriction. Methods Varix segments and adjacent proximal and distal segments were obtained from patients undergoing VarV stripping. Control greater saphenous vein specimens were obtained from patients undergoing lower extremity arterial bypass and coronary artery bypass graft (CABG). Circular vein segments were equilibrated under 2 g of tension in a tissue bath, and the changes in isometric constriction in response to angiotensin II (AngII, 10−11−10−7 M), phenylephrine (PHE, 10−9−10−4 M), and KCl (96 mM) were recorded. The amount of angiotensin type 1 receptor (AT1R) was measured in vein tissue homogenate using Western blot analysis. Results AngII caused concentration-dependent constriction in control vein (max 35.3±9.6 mg/mg tissue, pED50 8.48±0.34). AngII caused less contraction and was less potent in proximal (max 7.9±2.5, pED50 6.85±0.61), distal (max 5.7±1.2, pED50 6.74±0.68) and varix segments of VarV (max 7.2±2.0, pED50 7.11±0.50), suggesting reduced AT1R-receptor-mediated contractile mechanisms. Western blot analysis revealed similar amount of AT1R in VarV compared to control veins. α-adrenergic receptor stimulation with PHE caused concentration-dependent constriction in control veins (max 73.0±13.9 mg/mg tissue, pED50 5.48±0.12), that was greater in magnitude than that of AngII. PHE produced similar constriction and was equally potent in varix and distal segments, but produced less constriction and was less potent in proximal segments of VarV (max 32.1±6.4 mg/mg tissue, pED50 4.89±0.13) as compared to control veins. Membrane depolarization by 96 mM KCl, a receptor-independent Ca2+-dependent response, produced significant constriction in control veins, and similar contractile response in proximal, distal and varix segments of VarV, indicating tissue viability and intact Ca2+-dependent contraction mechanisms. Conclusions Compared with control veins, different regions of VarV display reduced AngII-mediated venoconstriction, which may play a role in the progressive dilation in VarV. Post-receptor Ca2+-dependent contraction mechanisms remain functional in VarV. The maintained α-adrenergic responses in distal and varix segments, and the reduced constriction in the upstream proximal segments, may represent a compensatory adaptation of human venous smooth muscle to facilitate venous return from the dilated varix segments of VarV.

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Endothelial mediated enhancement of noradrenaline induced vasoconstriction in normal and varicose veins

Cited by 25 publications

References 13 publications

In Vivo and In Vitro Assessment of Human Saphenous Vein Wall Changes

In Vivo and In Vitro Assessment of Human Saphenous Vein Wall Changes

Pathogenesis of primary varicose veins

Functional adaptation of venous smooth muscle response to vasoconstriction in proximal, distal, and varix segments of varicose veins

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