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Journal ArticleDOI

Techniques to study the pharmacodynamics of isolated large and small blood vessels

TLDR
Techniques are described for the mounting of large artery and vein ring segments on wire hooks in an organ bath chamber, following the normalisation routine established by Mulvany and Halpern for small resistance arteries mounted under isometric conditions on a wire myograph.
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This article is published in Journal of Pharmacological and Toxicological Methods.The article was published on 2000-09-01. It has received 109 citations till now. The article focuses on the topics: Vasa vasorum.

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Endothelial dysfunction: from molecular mechanisms to measurement, clinical implications, and therapeutic opportunities.

TL;DR: This review combines evidence from cell-culture experiments, in vitro and in vivo animal models, and clinical studies to identify the variety of mechanisms involved in endothelial dysfunction in its broadest sense and highlight the importance of the process across many different conditions.
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Vasoconstrictor responses to vasopressor agents in human pulmonary and radial arteries: an in vitro study.

TL;DR: Findings provide some support for the use of vasopressin in patients with pulmonary hypertension, as sympathomimetics norepinephrine, phenylephrine, and metaraminol caused concentration-dependent vasoconstriction in the radial and pulmonary arteries with similar potency in each.
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A self-renewing, tissue-engineered vascular graft for arterial reconstruction.

TL;DR: The graft showed morphologic evidence of good in situ cellularization, satisfactory durability to withstand arterial pressure for 12 postoperative months, and the potential to acquire physiologic vasomotor responsiveness, suggesting that it shows promise as an arterial conduit prosthesis.
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Transdermal iontophoresis as an in-vivo technique for studying microvascular physiology.

TL;DR: How iontophoresis can be used as an in-vivo model for studying physiologic mechanisms and on the analysis and interpretation of dose-response data is focused on.
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Pharmacological models and approaches for pathophysiological conditions associated with hypoxia and oxidative stress.

TL;DR: This systematic review is a critical analysis of the advantages in the application of some experimental strategies and their contributions leading to novel pharmacological therapies.
References
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Journal ArticleDOI

The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine

TL;DR: It is demonstrated that relaxation of isolated preparations of rabbit thoracic aorta and other blood vessels by ACh requires the presence of endothelial cells, and that ACh, acting on muscarinic receptors of these cells, stimulates release of a substance(s) that causes relaxation of the vascular smooth muscle.
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Contractile Properties of Small Arterial Resistance Vessels in Spontaneously Hypertensive and Normotensive Rats

TL;DR: The direct measurement of the intrinsic mechanical and contractile properites of two categories of small arterial resistance vessels in the mesenteric bed of 5-month-old normotensive Wistar-Kyoto rats and spontaneously hypertensive rats suggests the disturbance to the cardiovascular regulatory system which results in hypertension produces similar cellular responses in both the myocardium and the peripheral vasculature.
Journal Article

The pharmacology of vascular smooth muscle.

TL;DR: As one of the part of book categories, pharmacology of vascular smooth muscle always becomes the most wanted book.
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Evidence that nitric oxide does not mediate the hyperpolarization and relaxation to acetylcholine in the rat small mesenteric artery

TL;DR: The data provide evidence that the acetylcholine responses in this artery, which are endothelium‐dependent, are not mediated by the release of NO, and that the hyperpolarization induced by NO is not involved in the responses to acetyl choline.
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Evidence for increased media thickness, increased neuronal amine uptake, and depressed excitation--contraction coupling in isolated resistance vessels from essential hypertensives.

TL;DR: The results suggest that the increased pressor response in essential hypertension can, to a large extent, be explained by altered vascular structure, while smooth muscle function is either unchanged or possibly depressed.
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