Induction of Aortic and Coronary Athero-arteriosclerosis in Rats Fed a Hypervitaminosis D, Cholesterol-Containing Diet

Bajwa, G. S.; Morrison, Lester M.; Ershoff, Benjamin H.

doi:10.3181/00379727-138-36030

Cited by 53 publications

(15 citation statements)

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“…The endothelium-dependent relaxation to ACh was markedly impaired in the thoracic aortas iso lated from rats with excess VD-induced arteriosclerosis. The sclerotic aortas were characterized by calcification and degenerative changes in the media with cell pro liferation in the intima, as has been previously shown (18,19,26). Cholesterol feeding in addition to VD treatment facilitated the impairment of ACh-induced relaxation, along with aggravation of the morphological changes and the accumulation of aortic calcium and cholesterol.…”

Section: Discussionmentioning

confidence: 52%

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Impairment of Endothelium-Dependent Relaxation by Diesel Exhaust Particles in Rat Thoracic Aorta

Kitagawa

Yamaguchi

Kunitomo

et al. 1995

Japanese Journal of Pharmacology

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ABSTRACT-The present investigation was undertaken to characterize the relaxing responsiveness in aortic strips from rats with arteriosclerosis, which was produced by excess vitamin D2 (VD) administra tion followed by treatment with or without a high-cholesterol diet for 6 weeks (VD + CHOL and VD group, respectively). This arteriosclerotic aorta was characterized by medial calcification and intimal cell proliferation. Helical strips of thoracic aorta were suspended in oxygenated Krebs-Henseleit solu tion. Under precontraction with noradrenaline, endothelium-dependent relaxations to acetylcholine were significantly attenuated in the VD and VD + CHOL as compared with the control. Relaxation to calcium ionophore A23187 was also significantly attenuated in the VD + CHOL. However, the relax ing responses to acetylcholine and A23187 in aortas from rats fed a high-cholesterol diet alone re mained unaffected. Nitroglycerine caused an equal degree of relaxation in aortas from control and arteriosclerotic rats. There was a significant negative correlation between the relaxing response to acetylcholine and the calcium content in the aorta. These results indicate that in arteriosclerotic rat aor tas, the endothelium-dependent relaxation to acetylcholine is impaired in proportion to the degree of calcification, and such impairment is facilitated by cholesterol feeding but can not be attributed to hypercholesterolemia or vascular cholesterol deposition.

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Section: Discussionmentioning

confidence: 52%

“…Although degenerative arterial lesions could be de veloped in rats by the administration of excess vitamin D, the lesions are sclerotic rather than atheromatous in morphological features (18,19). Such arteriosclerosis is accompanied by calcification in the arterial media, which resembles Monckeberg's arteriosclerosis (20).…”

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confidence: 99%

Impairment of Endothelium-Dependent Relaxation by Diesel Exhaust Particles in Rat Thoracic Aorta

Kitagawa

Yamaguchi

Kunitomo

et al. 1995

Japanese Journal of Pharmacology

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“…Excess VD-induced arteriosclerosis in rat aortas is consi dered to be a model of Monkeberg's sclerosis (18), which is characterized by calcification and degenerative changes in the media (19,20). Cholesterol feeding in addition to excess VD treatment aggravates the morphological changes with an appreciable accumulation of cholesterol ester in the aorta (15).…”

Section: Discussionmentioning

confidence: 99%

Effects of SM-9018, a Potential Atypical Neuroleptic, on the Central Monoaminergic System in Rats

Kitagawa

Yamaguchi

Kunitomo

et al. 1993

Japanese Journal of Pharmacology

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ABSTRACT-This investigation was undertaken to characterize the vasoconstrictor responsiveness in aortas isolated from a rat model of arteriosclerosis induced by vitamin D2 (VD) administration followed by feeding with a high-cholesterol diet. Cumulative contractile responses to KC1, noradrenaline and serotonin in thoracic aortic strips isolated from arteriosclerotic rats were slightly augmented in concentrations lower than the EC50 value of each agent and rather attenuated in their higher concentrations as compared with those from normal rats. Maximum contractions to the agonists were markedly attenuated in arteriosclerotic aortas; the degree of attenuation was greater in rats treated with a combination of VD and cholesterol than in those treated with VD alone. There was a significant negative correlation between the maximum contrac tion to KCI, noradrenaline or serotonin and the content of calcium or cholesterol ester in aortas. Removal of endothelium markedly enhanced sensitivity and contractility to the agonists in aortic strips from normal rats, whereas the same procedure only slightly enhanced them in aortic strips from arteriosclerotic rats. These results indicate that in arteriosclerotic rat aortas, contractile responsiveness to agonists of vascular smooth muscle cells is impaired with deposition of calcium and cholesterol, and they suggest that augmenta tion of contractile responses to the agonists in lower concentrations is due to impairment of endothelial func tion.Keywords: Arteriosclerosis, Vitamin D, High-cholesterol diet, Calcification, Contractile response Atherosclerosis accompanied with hypercholesterol emia results in altered responsiveness of blood vessels to vasoactive substances in parallel with smooth muscle cell proliferation and lipid deposition. A number of studies have shown augmented responses to serotonin, histamine or ergonovine (1-6), and impaired endothelium-depend ent relaxation to a variety of vasodilator agents (7 -12) in various regions of arteries with experimental or human atherosclerosis. These changes may predispose athero sclerotic arteries to vasospasm. On the other hand, only a limited number of studies have been carried out on the vascular reactivity of arteriosclerotic vessels without depo sition of lipids (13,14). Henrion et al. (14) have reported that in the aorta from a rat model of vascular calcium overload produced by treatment with vitamin D3 and nicotine, not only endothelium-dependent relaxation to carbachol but also the vasoconstrictive response to noradrenaline is attenuated, while the relaxing responses to sodium nitroprusside is unchanged. Studies in our laboratory have also shown attenuation of vasorelaxation to acetylcholine or the calcium ionophore A23187 in aortas from rats with arteriosclerosis produced by four consecutive doses of vitamin D2 (VD) (15). We also dem onstrated that such impairment of endothelium-depend ent relaxations to acetylcholine and A23187 was propor tional to the degree of calcium deposition and facilitated by cholesterol feeding ...

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“…The luminal narrowing due to atherosclerotic lesion in the coronary artery has been believed to be the major factor responsible for causing myocardial ischemia (Friedberg 1968;Bulkley and Roberts 1976). Such coronary arterial lesions have been produced in experimental animals by vitamin D and cholesterol diets (Bajwa et al 1971), epinephrine, and thyroxine administration with cholesterol cotton oil diet (Constantinidies 1958), a balloon endothelial cell denudation procedure, a cholesterol and butter fat diet (Lee and Lee 1975) and vitamin D, and cholesterol diets and total thyroidectomy (Shenk et al 1965). We noted similar pathological findings in the coronary arteries of swine without dietary fat additives, mechanical or surgical procedures.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D-induced coronary atherosclerosis in normolipemic swine: Comparison with human disease.

Taura¹,

Taura²,

Kamio

et al. 1979

Tohoku J. Exp. Med.

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Induction of Aortic and Coronary Athero-arteriosclerosis in Rats Fed a Hypervitaminosis D, Cholesterol-Containing Diet

Cited by 53 publications

References 0 publications

Impairment of Endothelium-Dependent Relaxation by Diesel Exhaust Particles in Rat Thoracic Aorta

Impairment of Endothelium-Dependent Relaxation by Diesel Exhaust Particles in Rat Thoracic Aorta

Effects of SM-9018, a Potential Atypical Neuroleptic, on the Central Monoaminergic System in Rats

Vitamin D-induced coronary atherosclerosis in normolipemic swine: Comparison with human disease.

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