<p>Influence of Ageing on Vascular Reactivity and Receptor Expression in Rabbit Aorta: A Complement to Elastocalcinosis and Smooth Muscle Mechanisms</p>

2020 ◽

Author(s):

Nelson Ivan Cupitra ◽

Juan C Calderón ◽

Raul Narvaez-Sanchez

Keyword(s):

Potassium Chloride ◽

Vascular Reactivity ◽

Thromboxane A2 ◽

Rabbit Aorta ◽

Time Frame ◽

Receptor Expression ◽

Optimal Time ◽

Maximum Effect ◽

Organ Bath ◽

Significant Deterioration

Abstract OBJECTIVES The mechanistic understanding of vascular functional impairment during preservation time helps determine the optimal time frame in which explanted arteries can be used. The method of choice is to measure vascular reactivity and receptor expression. Our goal was to study the influence of preservation for 24 and 48 h on vascular reactivity and receptor expression in rabbit aorta. METHODS Aortic rings preserved in Krebs–Henseleit solution were evaluated fresh (t0), 24 h (t24) and 48 h (t48) after harvest for (i) vascular reactivity as sensitivity (pD2) and maximum effect in response to potassium chloride, U46619 (thromboxane-A2 agonist), phenylephrine, carbachol and isoproterenol, in an organ bath; and for (ii) expression of α1, β2 and thromboxane-prostanoid receptors, by immunofluorescence. RESULTS Compared to the control, after 24 h of preservation, potassium chloride-induced pD2 increased a significant 3.6%, whereas U46619-induced vasoconstriction decreased 9%. None of the agonists affected vasodilation. Intimal and medial α1 receptor expression increased 2.5-fold. After 48 h of preservation, α1 expression and vasoconstrictor responses remained similar to those after 24 h of preservation, but in vasodilation the carbachol-induced maximum effect decreased 30% whereas isoproterenol-induced pD2 increased 4% and the maximum effect increased 10%. TP and β2 expression in the intima and media increased 1.8- and 2.5-fold, respectively. CONCLUSIONS Up to 48 h of preservation, the adrenergic pathway and its receptors support vasoconstriction and vasodilation, despite a significant deterioration in the prostanoid pathway.

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The Cellular Origin in Atheromatous Lesion

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s042482010006800x ◽

1970 ◽

Vol 28 ◽

pp. 202-203

Author(s):

T. M. Murad ◽

H. A. I. Newman ◽

K. F. Kern

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Rabbit Aorta ◽

Mixed Population ◽

The Other ◽

Cellular Origin ◽

Ultrastructural Studies ◽

Atherosclerotic Lesions ◽

Show Evidence ◽

Early Lesion

The origin of lipid containing cells in atheromatous lesion has been disputed. Geer in his study on atheromatous lesions of rabbit aorta, suggested that the early lesion is composed mainly of lipid-laden macrophages and the later lesion has a mixed population of macrophages and smooth muscle cells. Parker on the other hand, was able to show evidence that the rabbit lesion is primarily composed of lipid-laden cells of smooth muscle origin. The above studies and many others were done on an intact lesion without any attempt of cellular isolation previous to their ultrastructural studies. Cell isolation procedures have been established for atherosclerotic lesions through collagenase and elastase digestion Therefore this procedure can be utilized to identify the cells involved in rabbit atheroma.

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Medial Smooth Muscle Cell Proliferation in the Balloon Injured Rabbit Aorta: Effect of a Thiazole Compound with Platelet Inhibitory Activity

Thrombosis and Haemostasis ◽

10.1055/s-0038-1661024 ◽

1984 ◽

Vol 51 (01) ◽

pp. 075-078 ◽

Cited By ~ 8

Author(s):

R G Schaub ◽

C A Simmons

Keyword(s):

Smooth Muscle ◽

Platelet Aggregation ◽

Balloon Catheter ◽

Rabbit Aorta ◽

Surface Characteristics ◽

Inhibitory Effect ◽

Lesion Size ◽

Blue Staining ◽

Morphologic Characteristics ◽

Time Period

SummaryTwenty-seven adult male New Zealand rabbits (3–4 kgs) were used in this study. Six rabbits received vehicle, 3 groups of 6 each received doses of 4,5-bis(p-methoxyphenyl)-2-(trifluoromethyl)- thiazole, (U-53,059), at 0.3 mg/kg, 3.0 mg/kg and 30.0 mg/kg/day respectively. Drug and vehicle doses were given orally each day starting 3 days before balloon injury and continuing for the entire 2 week time period. Three rabbits were used as nontreated sham controls. In the vehicle and U-53,059 treated groups aortae were denuded of endothelial cells by balloon catheter injury. Two weeks after injury platelet aggregation to collagen was measured and the aortae removed for analysis of surface characteristics by scanning electron microscopy and lesion size by morphometry. All doses of U-53,059 inhibited platelet aggregation. The 3.0 and 30.0 mg/kg groups had the greatest inhibitory effect. All balloon injured aortae had the same morphologic characteristics. All vessels had similar extent and intensity of Evan’s blue staining, similar areas of leukocyte/platelet adhesion, and a myointimal cell cover of transformed smooth muscle cells. The myointimal proliferative response was not inhibited at any of the drug doses studied.

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Regulation of Scavenger Receptor Expression in Smooth Muscle Cells by Protein Kinase C

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/01.atv.17.5.969 ◽

1997 ◽

Vol 17 (5) ◽

pp. 969-978 ◽

Cited By ~ 52

Author(s):

Michele Mietus-Snyder ◽

Annabelle Friera ◽

Christopher K. Glass ◽

Robert E. Pitas

Keyword(s):

Smooth Muscle ◽

Protein Kinase C ◽

Protein Kinase ◽

Smooth Muscle Cells ◽

Scavenger Receptor ◽

Muscle Cells ◽

Receptor Expression ◽

Kinase C

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Regulation of 5-hydroxytryptamine2 (5-HT2) receptor expression in cultured rat aortic smooth muscle cells by SR 46349B, a selective 5-HT2 receptor antagonist.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(17)42363-5 ◽

1994 ◽

Vol 269 (1) ◽

pp. 396-401

Author(s):

M. Rinaldi-Carmona ◽

V. Prabonnaud ◽

M. Bouaboula ◽

C. Poinot-Chazel ◽

P. Casellas ◽

...

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Receptor Antagonist ◽

Muscle Cells ◽

Receptor Expression ◽

Aortic Smooth Muscle Cells ◽

Aortic Smooth Muscle ◽

Sr 46349B

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Mechanisms of Direct Inhibitory Action of Isoflurane on Vascular Smooth Muscle of Mesenteric Resistance Arteries

Anesthesiology ◽

10.1097/00000542-200309000-00023 ◽

2003 ◽

Vol 99 (3) ◽

pp. 666-677 ◽

Cited By ~ 18

Author(s):

Takashi Akata ◽

Tomoo Kanna ◽

Jun Yoshino ◽

Shosuke Takahashi

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Vascular Reactivity ◽

Channel Blocker ◽

Isometric Force ◽

Systemic Resistance ◽

Resistance Arteries ◽

Voltage Gated ◽

Fura 2 ◽

Force Relation

Background Isoflurane has been shown to directly inhibit vascular reactivity. However, less information is available regarding its underlying mechanisms in systemic resistance arteries. Methods Endothelium-denuded smooth muscle strips were prepared from rat mesenteric resistance arteries. Isometric force and intracellular Ca2+ concentration ([Ca2+]i) were measured simultaneously in the fura-2-loaded strips, whereas only the force was measured in the beta-escin membrane-permeabilized strips. Results Isoflurane (3-5%) inhibited the increases in both [Ca2+]i and force induced by either norepinephrine (0.5 microM) or KCl (40 mM). These inhibitions were similarly observed after depletion of intracellular Ca2+ stores by ryanodine. Regardless of the presence of ryanodine, after washout of isoflurane, its inhibition of the norepinephrine response (both [Ca2+]i and force) was significantly prolonged, whereas that of the KCl response was quickly restored. In the ryanodine-treated strips, the norepinephrine- and KCl-induced increases in [Ca2+]i were both eliminated by nifedipine, a voltage-gated Ca2+ channel blocker, whereas only the former was inhibited by niflumic acid, a Ca2+-activated Cl- channel blocker. Isoflurane caused a rightward shift of the Ca2+-force relation only in the fura-2-loaded strips but not in the beta-escin-permeabilized strips. Conclusions In mesenteric resistance arteries, isoflurane depresses vascular smooth muscle reactivity by directly inhibiting both Ca2+ mobilization and myofilament Ca2+ sensitivity. Isoflurane inhibits both norepinephrine- and KCl-induced voltage-gated Ca2+ influx. During stimulation with norepinephrine, isoflurane may prevent activation of Ca2+-activated Cl- channels and thereby inhibit voltage-gated Ca2+ influx in a prolonged manner. The presence of the plasma membrane appears essential for its inhibition of the myofilament Ca2+ sensitivity.

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Contractile and Endothelium-Dependent Dilatory Responses of Cerebral Arteries at Various Extracellular Magnesium Concentrations

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1991.20 ◽

1991 ◽

Vol 11 (1) ◽

pp. 161-164 ◽

Cited By ~ 21

Author(s):

Mária Faragó ◽

Csaba Szabó ◽

Eörs Dóra ◽

Ildikó Horváth ◽

Arisztid G. B. Kovách

Keyword(s):

Smooth Muscle ◽

Vascular Reactivity ◽

Calcium Influx ◽

Cerebral Arteries ◽

Inhibitory Effect ◽

Contractile Responses ◽

Middle Cerebral Arteries ◽

The Right ◽

Endothelial Receptor

To clarify the effect of extracellular magnesium (Mg2+) on the vascular reactivity of feline isolated middle cerebral arteries, the effects of slight alterations in the Mg2+ concentration on the contractile and endothelium-dependent dilatory responses were investigated in vitro. The contractions, induced by 10−8-10−5 M norepinephrine, were significantly potentiated at low Mg2+ (0.8 m M v. the normal, 1.2 m M). High (1.6 and 2.0 m M) Mg2+ exhibited an inhibitory effect on the contractile responses. No significant changes, however, in the EC50 values for norepinephrine were found. The endothelium-dependent relaxations induced by 108–10−5 M acetylcholine were inhibited by high (1.6 and 2.0 m M) Mg2+. Lowering of the Mg2+ concentration to 0.8 m M or total withdrawal of this ion from the medium failed to alter the dilatory potency of acetylcholine. The changes in the dilatory responses also shifted the EC50 values for acetylcholine to the right. The present results show that the contractile responses of the cerebral arteries are extremely susceptible to the changes of Mg2+ concentrations. In response to contractile and endothelium-dependent dilatory agonists, Mg2+ probably affects both the calcium influx into the endothelial and smooth muscle cells as well as the binding of acetylcholine to its endothelial receptor. Since Mg2+ deficiency might facilitate the contractile but not the endothelium-dependent relaxant responses, the present study supports a role for Mg2+ deficiency in the development of the cerebral vasospasm.

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