NAD(P)H oxidase inhibiting with apocynin improved vascular reactivity in tail-suspended hindlimb unweighting rat

Prolonged bed rest and exposure to weightlessness in humans result in cardiovascular alterations that are characterized by orthostatic intolerance and decreased exercise capacity. Modifications of cardiovascular function have been suggested to be causally related to changes in peripheral vascular reactivity. Rat hindlimb unweighting (HU) was used as an animal model to determine whether prolonged decreases in weight-bearing activity induce changes in vasoreactivity of peripheral arterial vessels. Responses to vasoactive compounds were examined in vitro using isolated abdominal and thoracic aortic rings. Maximal isometric contractile tension evoked by the vasoconstrictors KCl (10–100 mM), norepinephrine (NE; 10(-9)-10(-4) M), phenylephrine (10(-9)-10(-4) M), arginine vasopressin (10(-13)-3 x 10(-5) M), and CaCl2 (10(-6)-10(-2) M) was lower in abdominal aortic rings from HU rats. Sensitivity [agonist concentration that produced 50% of maximal vasoconstrictor response (EC50)] to KCl was enhanced in segments from HU animals but was not different for the other constrictors. Maximal contractile responses of thoracic aortic rings to KCl (10–100 mM) and NE (10(-9)-10(-4) M) were also attenuated by HU. In abdominal aortic rings preconstricted with 10(-4) M NE, maximal vasodilatory responses induced by sodium nitroprusside (10(-10)-10(-4) M) and 8-bromoguanosine 3',5'-cyclic monophosphate (10(-6)-10(-2) M) were greater in vessel rings from HU rats. However, with 10(-7) M NE preconstriction, maximal dilatory responses induced by sodium nitroprusside (10(-10)-10(-4) M) and acetylcholine (10(-9)-10(-4) M) were not different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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Blockade of AT1 receptor partially restores vasoreactivity, NOS expression, and superoxide levels in cerebral and carotid arteries of hindlimb unweighting rats

Journal of Applied Physiology ◽

10.1152/japplphysiol.01278.2007 ◽

2009 ◽

Vol 106 (1) ◽

pp. 251-258 ◽

Cited By ~ 35

Author(s):

Ran Zhang ◽

Yun-Gang Bai ◽

Le-Jian Lin ◽

Jun-Xiang Bao ◽

Yu-Yang Zhang ◽

...

Keyword(s):

Vascular Reactivity ◽

Carotid Arteries ◽

Cerebral Arteries ◽

Renin Angiotensin System ◽

Maximal Response ◽

Ang Ii ◽

Hindlimb Unweighting ◽

Basilar Arteries ◽

Receptor Signaling Pathway ◽

Oxide Synthase

Previous studies have demonstrated activation of the local renin-angiotensin system in hindlimb unweighting (HU) rat vasculature. The present study intended to identify the effects of blockade of angiotensin II (ANG II) type 1 (AT1) receptors with losartan on vascular reactivity, nitric oxide synthase (NOS) expression, and superoxide anion (O2•−) levels in 3-wk HU rat cerebral and carotid arteries. Three weeks later, vasoconstriction, vasodilatation, endothelial NOS (eNOS) and inducible NOS (iNOS) protein, as well as O2•− levels in rat cerebral and carotid arteries were examined. We found that HU enhanced maximal response to KCl/5-hydroxytryptamine ( P < 0.01) in basilar arteries and KCl/phenylephrine ( P < 0.05) in common carotid arteries from HU rats. Acetylcholine induced concentration-dependent vasodilatation in all the artery rings, but with significantly smaller amplitude in basilar ( P < 0.01) and common carotid ( P < 0.05) arteries from HU rats than those from control rats. Chronic treatment with losartan partially restored response to vasoconstrictors and acetylcholine-induced vasodilatation in basilar ( P < 0.01) and common carotid ( P < 0.05) arteries from losartan-treated HU rats. Furthermore, iNOS content in cerebral arteries and eNOS/iNOS content in carotid arteries were significantly ( P < 0.01) increased in HU rats. Meanwhile, HU increased O2•− levels in all the layers of these arteries. However, losartan restored NOS content and O2•− levels toward normal. These results suggested that the HU-induced enhancement of vasoconstriction and reduction in endothelium-dependent relaxation involved alterations in O2•− and NOS content through an ANG II/AT1 receptor signaling pathway.

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Cutaneous vascular reactivity in atopic children

Archives of Dermatology ◽

10.1001/archderm.92.6.621 ◽

1965 ◽

Vol 92 (6) ◽

pp. 621-624 ◽

Cited By ~ 1

Author(s):

L. A. Johnson

Keyword(s):

Vascular Reactivity

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History of vascular reactivity models and their involvement in hypertension pathogenesis

VASA ◽

10.1024/0301-1526/a000659 ◽

2017 ◽

Vol 46 (6) ◽

pp. 431-439 ◽

Cited By ~ 4

Author(s):

Ana Gabriela Conceição-Vertamatti ◽

Filipy Borghi ◽

Fernando Canova ◽

Dora Maria Grassi-Kassisse

Keyword(s):

Blood Pressure ◽

Adrenergic Receptors ◽

Vascular Reactivity ◽

Multifactorial Disease ◽

Pharmacological Treatments ◽

Beta Adrenergic Receptors ◽

Vascular Area ◽

History Of ◽

Record Blood Pressure ◽

Advance Knowledge

Abstract. Hypertension is a silent and multifactorial disease. Over two centuries ago, the first device to record blood pressure was developed, making it possible to determine normotension and to establish criteria for hypertension. Since then, several studies have contributed to advance knowledge in this area, promoting significant advances in pharmacological treatments and, as a result, increasing survival of hypertensive people. The main models developed for the study of hypertension and the main findings in the vascular area are included in this review. We considered aspects related to vascular reactivity, changes in the population, and action of beta adrenergic receptors in the pathogenesis of hypertension.

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