Determination of an Optimal Axial‐Length Tension for the Study of Isolated Resistance Arteries on a Pressure Myograph

Coats, Paul; Hillier, Chris

doi:10.1111/j.1469-445x.1999.01917.x

Cited by 13 publications

(6 citation statements)

References 14 publications

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“…The alteration of wall tension may activate or inactivate the contraction of vascular smooth muscle and the signal pathways of endothelial cells mediated by mechanotransductions such as integrins and G protein-coupled receptors (9, 17, 25, 26). It has been suggested that the change in distension or stretch affects vascular reactivity (3,6,22,27). In the present study, we extended the pressure and stretch to a pathological range (e.g., hypertensive pressures or stretches) and verified that the effect on the vasorelaxation of blood vessel is substantial (Fig.…”

Section: Discussionmentioning

confidence: 51%

Assessment of endothelial function of large, medium, and small vessels: a unified myograph

Kassab

2011

American Journal of Physiology-Heart and Circulatory Physiology

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Lu X, Kassab GS. Assessment of endothelial function of large, medium, and small vessels: a unified myograph. Am J Physiol Heart Circ Physiol 300: H94 -H100, 2011. First published November 12, 2010; doi:10.1152/ajpheart.00708.2010.-Endothelial dysfunction precedes the development of morphological atherosclerotic changes and can also contribute to lesion development in cardiovascular diseases. Currently, there is a lack of a single method to determine endothelial function of the entire range of vessel dimensions from aorta to arterioles. Here we assessed endothelial function of a large range of size arteries using a unified isovolumic myograph method. The method maintains a constant volume of fluid in the lumen of the vessel during contraction and relaxation, which are characterized by an increase and a decrease of pressure, respectively. Segments of six aortas, six common femoral arteries, and six mesenteric arteries from rats; six carotid arteries from mice; and six coronary and carotid arteries from pigs were used. The endothelium-dependent dose-response vasorelaxation was determined with endothelium-dependent vasodilators while arterial preconstriction was induced with vasoconstrictors at a submaximal dose. The circumferential midtension during vascular reactivity varied from 43.1 Ϯ 7.9 to 2.59 Ϯ 0.46 mN/mm (from large to small arteries), whereas the circumferential midstress showed a much smaller variation from 217 Ϯ 23.5 to 123 Ϯ 15.3 kPa (in the same range of vessels). We also found that overinflation and axial overelongation compromised endothelium-dependent vasorelaxation to underscore the significance of vessel preload. In conclusion, an isovolumic myograph was used to unify arterial vasoreactivity from large to small arteries and shows the uniformity of wall stress and %tension throughout the range of vessel sizes. isovolumic myograph; wire myograph; pressure myograph VASCULAR ENDOTHELIAL DYSFUNCTION is widely considered to be a consequence, a biomarker, and a mediator of the adverse effects of cardiovascular risk factors (2,4,5,11,15,18,21). Endothelial dysfunction precedes the development of morphological atherosclerotic changes and can also contribute to lesion development and later clinical complications (15,23,24). Endothelial dysfunction has also been shown to be a predictor of adverse outcomes in patients with coronary artery disease (10,11,20). Although endothelial dysfunction may be indicated by several biomarkers such as the expression of endothelial nitric oxide (NO) synthase, the expression of cyclooxygenase, and the production of nitric oxide or prostacyclin, the vasodilation of blood vessel in response to endothelium-dependent agonists is the gold standard.The wire and pressure myographs have been used extensively to study the vasoreactivity and pharmacology of large and small vessels, respectively (7-9, 12-16, 19, 26). The applicability of wire myograph is in vessels with a diameter range from large vessels (aorta) down to about 500 m. The attachment of vessel rings to hooks, however, ca...

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Section: Discussionmentioning

confidence: 51%

Assessment of endothelial function of large, medium, and small vessels: a unified myograph

Kassab

2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…20 To ensure optimal reactivity, the artery was pressurized (50 mm Hg) and stretched longitudinally by 20%. 21 After 30 minutes superfusion at 37°C, reactivity was assessed by contraction with 3 mol/L PE, followed by endothelium-dependent relaxation to 1 mol/L acetylcholine (ACh). Only vessels relaxing Ն90%, reflecting undamaged endothelium, were subsequently used.…”

Section: Measurement Of Diameter and Endothelial Cell Calcium In Presmentioning

confidence: 99%

Rapid Endothelial Cell–Selective Loading of Connexin 40 Antibody Blocks Endothelium-Derived Hyperpolarizing Factor Dilation in Rat Small Mesenteric Arteries

Mather

Dora

Sandow

et al. 2005

Circulation Research

163

208

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Abstract-In resistance arteries, spread of hyperpolarization from the endothelium to the adjacent smooth muscle is suggested to be a crucial component of dilation resulting from endothelium-derived hyperpolarizing factor (EDHF). To probe the role of endothelial gap junctions in EDHF-mediated dilation, we developed a method, which was originally used to load membrane impermeant molecules into cells in culture, to load connexin (Cx)-specific inhibitory molecules rapidly (Ϸ15 minutes) into endothelial cells within isolated, pressurized mesenteric arteries of the rat. Validation was achieved by luminally loading cell-impermeant fluorescent dyes selectively into virtually all the arterial endothelial cells, without affecting either tissue morphology or function. The endothelial monolayer served as an effective barrier, preventing macromolecules from entering the underlying smooth muscle cells. Using this technique, endothelial cell loading either with antibodies to the intracellular carboxyl-terminal region of Cx40 (residues 340 to 358) or mimetic peptide for the cytoplasmic loop (Cx40; residues 130 to 140) each markedly depressed EDHF-mediated dilation. In contrast, multiple antibodies directed against different intracellular regions of Cx37 and Cx43, and mimetic peptide for the intracellular loop region of Cx37, were each without effect. Furthermore, simultaneous intra-and extraluminal incubation of pressurized arteries with inhibitory peptides targeted against extracellular regions of endothelial cell Cxs ( 43 Gap 26, 40 Gap 27, and 37,43 Gap 27; 300 mol/L each) for 2 hours also failed to modify the EDHF response. High-resolution immunohistochemistry localized Cx40 to the end of endothelial cell projections at myoendothelial gap junctions. These data directly demonstrate a critical role for Cx40 in EDHF-mediated dilation of rat mesenteric arteries. Key Words: endothelium-derived hyperpolarizing factor Ⅲ myoendothelial gap junctions Ⅲ endothelium-dependent dilation Ⅲ acetylcholine Ⅲ connexin 40 I n arterioles and some arteries, gap junctions between endothelial and smooth muscle cells (myoendothelial gap junctions [MEGJs]) enable changes in membrane potential to spread over considerable distances and, as a consequence, regulate blood flow by coordinating diameter change through the microcirculation. 1-3 For example, injection of hyperpolarizing current into a single endothelial cell can evoke extensive relaxation involving many smooth muscle cells throughout an isolated arteriole. 4,5 An important aspect of this response is that MEGJs may provide a crucial route for endothelial cell hyperpolarization to spread radially to the adjacent smooth muscle and evoke the dilation attributed to endothelium-derived hyperpolarizing factor (EDHF). 6 -8 In many arteries, there is more than 1 underlying mechanism for endothelium-dependent hyperpolarization of smooth muscle cells. In the rat mesenteric artery, during submaximal contraction to phenylephrine (PE), EDHF dilation appears to reflect hyperpolarizing current spread thro...

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“…Again, the technique of pressure myography has been has been described in detail elsewhere (29). Briefly, vessels were mounted on two glass pipettes in a pressure myograph system (Living Systems, Burlington VT, USA), and held in place with three strands of synthetic thread at either end.…”

Section: Assessment Of Vascular Reactivity Of Testosterone By Pressurmentioning

confidence: 99%

Altered circulating hormone levels, endothelial function and vascular reactivity in the testicular feminised mouse

Jones

Pugh²,

Hall³

et al. 2003

European Journal of Endocrinology

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Objective: Testicular feminised (Tfm) mice express a non-functional androgen receptor, and also have reduced levels of circulating testosterone. Recent studies support a cardio-protective role for testosterone since it elicits systemic and pulmonary vasodilatation. The aim of the present study was to determine whether androgen insensitivity and hypotestosteronaemia in the Tfm mouse are associated with abnormal vascular reactivity or hormone status. Methods: Adult male Tfm and littermate control mice were killed and the blood collected. Femoral (diameter range = 183 -508 mm) and pulmonary (diameter range = 320-816 mm) arteries were dissected and loaded in either a wire or pressure myograph, at 100 mmHg or 17.5 mmHg respectively. Pharmacological assessment of the vasoreactivity to potassium chloride (KCl, 80 mmol/l) and either noradrenaline (NA, 1 nmol/l -100 mmol/l) and acetylcholine (ACh, 0.1 -100 mmol/l) or testosterone (1 nmol/l -100 mmol/l) was then made. Results: Tfm mice had reduced levels of testosterone (1.8^0.3 nmol/l) compared with controls (9.3^2.0 nmol/l, P , 0:001Þ and elevated levels of cholesterol (3.6+0.1 mmol/l) compared with controls ð3:2 þ 0:1 mmol=l; P , 0:05Þ: Femoral arteries from Tfm mice exhibited reduced vasoconstriction to 80 mmol/l KCl ð3:27^0:23 mN=mmÞ compared with vessels from controls ð4:44^0:41 mN=mm; P , 0:05Þ; and reduced endothelial-dependent vasodilatation to 0.1-100 mmol/l ACh ð23:3^3:6% relaxation) compared with vessels from controls ð41:6^5:4% relaxation, P , 0:05Þ: Vasoconstriction to NA (1 nmol/l -100 mmol/l) and vasodilatation to testosterone were unaffected. Conclusions: Androgen receptor deficiency and hypotestosteronaemia in the Tfm mouse reduced endothelial function and impaired voltage-operated calcium channel activity, which may pre-dispose to cardiovascular disease. Testosterone-induced vasodilatation was unaffected, demonstrating no involvement of the androgen receptor in this response.

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Determination of an Optimal Axial‐Length Tension for the Study of Isolated Resistance Arteries on a Pressure Myograph

Cited by 13 publications

References 14 publications

Assessment of endothelial function of large, medium, and small vessels: a unified myograph

Assessment of endothelial function of large, medium, and small vessels: a unified myograph

Rapid Endothelial Cell–Selective Loading of Connexin 40 Antibody Blocks Endothelium-Derived Hyperpolarizing Factor Dilation in Rat Small Mesenteric Arteries

Altered circulating hormone levels, endothelial function and vascular reactivity in the testicular feminised mouse

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