Effects of hypertension on hypercholesterolemia-induced changes in contraction of rabbit aorta and carotid artery

Moreland, Robert S.; Lichtenstein, Alice H.; Chobanian, Aram V.

doi:10.1016/0014-2999(96)00232-4

Cited by 2 publications

(3 citation statements)

References 32 publications

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“…Thus, alterations in vascular responses to contractile agents may be related to the duration of cholesterol feeding and lesion size. 21 On the other hand, in the present study, sensitivity but not maximum relaxant responses to acetylcholine has been found to be impaired in rings from cholesterol-fed rabbits. However, cholesterol loading has decreased maximum relaxant responses to ACh in the Data are presented as mean AE SD.…”

Section: Discussioncontrasting

confidence: 61%

“…showed that cholesterol feeding had no effect on 5‐HT responses of aorta from 0.3% cholesterol for 8 weeks. Thus, alterations in vascular responses to contractile agents may be related to the duration of cholesterol feeding and lesion size . On the other hand, in the present study, sensitivity but not maximum relaxant responses to acetylcholine has been found to be impaired in rings from cholesterol‐fed rabbits.…”

Section: Discussioncontrasting

confidence: 48%

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Different responses of fluvastatin to cholesterol‐induced oxidative modifications in rabbits: evidence for preventive effect against DNA damage

Sevin

Yasa

Akcay

et al. 2012

Cell Biochemistry & Function

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Hypercholesterolemia is a major risk factor for atherosclerosis and related occlusive vascular diseases. We investigated the effect of low-dose fluvastatin (2 mg kg(-1) day(-1)) on antioxidant enzyme activities [superoxide dismutase (SOD), catalase], vascular reactivity changes and oxidatively induced DNA damage in early stage of atherosclerosis in hypercholesterolemic rabbits. The animals were divided into three groups each composed of 10 rabbits. The control group received a regular rabbit chow diet, and the cholesterol group had hypercholesterolemic diet (2%, 4 weeks). The fluvastatin group was given hypercholesterolemic diet plus fluvastatin. Dietary intake of cholesterol significantly increased total cholesterol levels in rabbits (control, 0.85 ± 0.29; cholesterol, 12.04 ± 4.61; fluvastatin, 8.07 ± 2.72 mmol l(-1)). Hypercholesterolemic diet revealed discernible fatty streaks in arcus aortae. Fluvastatin significantly reduced the areas of the lesions. The diet significantly increased SOD activities in both erythrocyte and tissue. Treatment with fluvastatin normalized the increased activity of SOD in both erythrocyte and aortic tissues from the cholesterol group. Cholesterol feeding decreased the sensitivity to acetylcholine, and treatment with fluvastatin significantly restored the diminished sensitivity to acetylcholine in thoracic aortae. Cholesterol feeding caused oxidatively induced DNA damage in liver tissues determined by the increased levels of 8-hydroxyguanine (8-OH-Gua) and 2,6-diamino-4-hydroxy-5-formamidopyrimidine (FapyGua). Fluvastatin decreased only FapyGua level in liver. In conclusion, our results may suggest that fluvastatin seems to play a protective role on high cholesterol-induced oxidative stress and DNA damage.

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Section: Discussioncontrasting

confidence: 61%

Section: Discussioncontrasting

confidence: 48%

Different responses of fluvastatin to cholesterol‐induced oxidative modifications in rabbits: evidence for preventive effect against DNA damage

Sevin

Yasa

Akcay

et al. 2012

Cell Biochemistry & Function

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“…Recently, it was suggested that cholesterol: increases vascular sensitivity by increasing Ca 2+ permeability [22], increases calcium sensitization through the Rho-kinase (ROCK)-mediated pathway [21], influences vascular reactivity to endothelin-1 and 5-HT [22, 23], decreases the expression of LTCC [24], and regulates the expression levels of specific inward rectifier and ATP-sensitive potassium channel subtypes [25]. On the other hand, farnesol, a nonsterol mevalonate derivative from the cholesterol synthesis pathway, was reported to inhibit L-type calcium channels (LTCC) in vascular smooth muscle cells [26, 27] and it also induces relaxation of contracted rat aortic and human mesenteric arteries [28].…”

Section: Introductionmentioning

confidence: 99%

Testosterone and Cholesterol Vasodilation of Rat Aorta Involves L-Type Calcium Channel Inhibition

Álvarez

Cairrão

Morgado

et al. 2010

Advances in Pharmacological Sciences

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Testosterone has rapid nongenomic vasodilator effects which could be involved in protective cardiovascular actions. Several authors suggested specific mechanisms to explain this effect, but this matter was not clarified yet. We studied the actions of testosterone and cholesterol on endothelium-denuded rat aorta and their effects on the L-type Ca2+ current (ICa,L) and potassium current (IK). Testosterone (1–100 μM) totally relaxed, in a rapid and concentration-dependent way, the aortic rings contracted by KCl or by (−)-Bay K8644 (BAY). Cholesterol also fully relaxed the contractions induced by KCl. None of the potassium channel antagonists tested (glibenclamide, tetraethylammonium and 4-aminopyridine) modified significantly the relaxant effect of testosterone. The antagonist of classic testosterone receptors, flutamide, did not modify the vasorelaxant effect of testosterone. Furthermore, testosterone and cholesterol inhibited either basal and BAY-stimulated ICa,L in A7r5 cells and they have no effects on IK. In summary, our results demonstrate that cholesterol and testosterone relax rat aorta by inhibiting LTCC. This effect of testosterone is not mediated by the classic hormone receptor or by potassium channel activation. These results suggest that the vasodilator mechanism of cholesterol and testosterone is the same.

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Effects of hypertension on hypercholesterolemia-induced changes in contraction of rabbit aorta and carotid artery

Cited by 2 publications

References 32 publications

Different responses of fluvastatin to cholesterol‐induced oxidative modifications in rabbits: evidence for preventive effect against DNA damage

Different responses of fluvastatin to cholesterol‐induced oxidative modifications in rabbits: evidence for preventive effect against DNA damage

Testosterone and Cholesterol Vasodilation of Rat Aorta Involves L-Type Calcium Channel Inhibition

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