Atherogenesis, calcium and calcium antagonists

Henry, Philip D.

doi:10.1016/0002-9149(90)91256-6

Cited by 46 publications

(19 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Like most vasoconstrictors, serotonin acts by way of specific membrane receptors and uses extracellular calcium as a second messenger. In addition, calcium channel antagonists are valuable as antiatherosclerotic agents 20 as well as effective in the treatment of vasospastic syndromes. 2122 We therefore pursued the hypothesis that alterations in calcium permeability by arterial smooth muscle mediate changes in contractile responsiveness to serotonin in atherosclerotic vessels.…”

Section: Discussionmentioning

confidence: 99%

“…It is also likely that increased Ca 2+ influx contributes to many of the alterations in smooth muscle cell function such as cell proliferation, 23 increased vasoreactivity, 30 and increased collagen synthesis. Given the putative role of calcium channel blocking drugs in the prevention and/or regression of atherosclerosis, 20 it is likely that augmented calcium uptake and intracellular calcium levels in the unstimulated (ie, basal) state in arterial smooth muscle play an important role in the overall atherogenic process.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Alterations in basal and serotonin-stimulated calcium permeability and vasoconstriction in atherosclerotic aorta.

Stepp

Tulenko

1994

Arterioscler Thromb

View full text Add to dashboard Cite

Hypersensitivity to vasoactive stimuli, a common finding in atherosclerotic arteries, is thought to play an important role in the pathology of arterial and coronary vasospasm and may be a factor in myocardial ischemia and infarction. While this phenomenon is well documented, the underlying mechanism is unknown. The present study used isometric force measurements coupled with <5 Ca 2+ and Fura 2-AM techniques in aortic smooth muscle to probe transmembrane calcium movements and cytosolic calcium levels in an attempt to determine their relation to altered vasomotion in a rabbit model of dietary atherosclerosis. Following 10 weeks of cholesterol feeding (2%), basal (unstimulated) calcium influx was augmented 1.5-fold in atherosclerotic segments with no change in basal calcium efflux. Serotonin-stimulated calcium uptake was increased 1.9-fold in atherosclerotic segments and was accompanied by a fivefold increase in serotonin vasocon-

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Alterations in basal and serotonin-stimulated calcium permeability and vasoconstriction in atherosclerotic aorta.

Stepp

Tulenko

1994

Arterioscler Thromb

View full text Add to dashboard Cite

show abstract

“…In atherosclerosis, lesion formation depends upon calcium-regulated cellular processes, such as chemotaxis, adhesion, migration, proliferation, lipid uptake, and necrosis. As reported by Henry (1990), interventions acting on cell calcium uptake, including treatment with calcium-chelating agents lanthanum trichloride and calcium antagonists, may retard atherogenesis in fat-fed animals in the absence of hypolipidemic effects. Several randomized control clinical trials, including the International Nifedipine Trial of Antiatherosclerotic Therapy, Verapamil Hypertension Atherosclerosis Study, and Prospective Randomized Evaluation of the Vascular Effects of Norvasc Trial with amlodipine, have substantiated the inhibitory effect of calcium channel blockers on the progression of atherosclerosis (for reference, see Godfraind, 2004).…”

mentioning

confidence: 90%

Calcium Channel Blocker Inhibits Western-Type Diet-Evoked Atherosclerosis Development in ApoE-Deficient Mice

Kyselovič

Martinka²,

Batova³

et al. 2005

J Pharmacol Exp Ther

View full text Add to dashboard Cite

Calcium channel blockers slow the progression of atherosclerosis. The purpose of the present experiments was to examine the action of lacidipine in a condition that accelerates the development of atherosclerosis in order to test the hypothesis that the protective action of lacidipine in atherosclerosis is unrelated to the reduction of blood pressure. Male ApoE-deficient mice (6 weeks old) were exposed either to normal chow (ND) or to a Western-type diet (WD, adjusted calorie diet containing 42% from fat) for 8 weeks. Western-type diet induced a reduction of nitric oxide (NO)-mediated endothelium-dependent relaxation to acetylcholine (Max relaxation % ϭ 55.8 Ϯ 2 for ND and 46.6 Ϯ 2 for WD, n ϭ 8, p Ͻ 0.05). Dose-relaxation curves to S-nitroso-N-acetylpenicillamine (SNAP) NO donor were also significantly rightward-shifted (n ϭ 7, ANOVA, p Ͻ 0.01) in WD compared with ND arteries. Chronic treatment of WD mice with lacidipine (1 and 3 mg/kg/day) increased significantly the acetylcholine-evoked relaxation (to 76.6 Ϯ 3.5%, n ϭ 6, ANOVA, p Ͻ 0.001) and prevented the loss of responsiveness to SNAP in mice exposed to WD. Plasma renin activity and endothelin-1 plasma levels as well as thiobarbituric acidreactive substance levels in kidneys were significantly lower in WD mice treated with lacidipine than in untreated ones. In mice exposed to WD lacidipine reduced extension of atherosclerotic lesions, renal injury and increase in blood pressure. Experimental data indicate that inhibition of Western-type diet-evoked alterations is related to both antioxidant and vasoactive properties of lacidipine.

show abstract

“…Atherosclerosis, the leading cause of death in Western countries, is a multi-factorial disease involving the localized accumulation of lipids, collagen, elastin, and calcium, together with monocyte infiltration, endothelial injury, and smooth muscle cell proliferation and migration [1,2,3]. Many of these events are calcium-dependent and may be affected by calcium antagonists.…”

Section: Introductionmentioning

confidence: 99%

Tracking Coronary Calcification and Atherosclerotic Lesions in Patients with Stable Angina Pectoris Undergoing Nifedipine Therapy

Motro

Brouwer²,

Poole‐Wilson³

et al. 2006

Cardiology

View full text Add to dashboard Cite

Aims: The objective of the Coronary Calcification (CC) study was to determine in patients with chronic symptomatic coronary artery disease, if, in addition to standard therapy, nifedipine GITS, relative to placebo, would arrest or slow down the progression of calcium or the development of new atherosclerotic lesions in the coronary arteries. Methods and Results: The CC study was part of the ACTION trial. Multi-slice computerized tomography was used to measure and track the progression of CC. Five hundred and eighteen patients were included in this study. The changes in calcium score from baseline every 24 months, over a period of between 4.5 and 6 years, were similar in the nifedipine and placebotreatment groups (p = 0.8). Compared to placebo, more patients in the nifedipine group (71 vs. 60%) were free of new calcified atherosclerotic lesions during follow-up(p = 0.095). Conclusion: Nifedipine GITS was not effective in slowing down the progression of calcium in advanced atherosclerotic plaques in patients with stable angina pectoris. Although statistically not significant, Nifedipine demonstrated a trend in slowing down the development of new atherosclerotic lesions.

show abstract

Atherogenesis, calcium and calcium antagonists

Cited by 46 publications

References 36 publications

Alterations in basal and serotonin-stimulated calcium permeability and vasoconstriction in atherosclerotic aorta.

Alterations in basal and serotonin-stimulated calcium permeability and vasoconstriction in atherosclerotic aorta.

Calcium Channel Blocker Inhibits Western-Type Diet-Evoked Atherosclerosis Development in ApoE-Deficient Mice

Tracking Coronary Calcification and Atherosclerotic Lesions in Patients with Stable Angina Pectoris Undergoing Nifedipine Therapy

Contact Info

Product

Resources

About