Endothelial function and atherosclerosis

Biegelsen, Elizabeth S.; Loscalzo, Joseph

doi:10.1097/00019501-199906000-00006

Cited by 80 publications

(46 citation statements)

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“…A recent study demonstrated that in hypercholesterolemic patients statin combined with ACE inhibitor showed significantly more improvement of endotheliumdependent vasodilation than ACE inhibitor alone. 39 Because ACE inhibitors reduce BP by potentiating endotheliummediated vasodilatation and by reducing peripheral vascular tone, 40 interactions between the effect of the statins and the vasorelaxant effect of the ACE inhibitor may underlie the mechanism by which statins modulate BP. Previous studies have also demonstrated that LDL-C induces upregulation of the expression of the AT1 receptor in vascular smooth muscle cells and increased activity of angiotensin II, 41,42 and that statins reverse the elevated BP response to angiotensin II infusion and downregulate AT1 receptor density.…”

Section: Discussionmentioning

confidence: 99%

Pravastatin Decreases Blood Pressure in Hypertensive and Hypercholesterolemic Patients Receiving Antihypertensive Treatment

Kawano

Yano

2006

Circ J

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any patients with hypertension have concomitant hypercholesterolemia [1][2][3] and it has been reported that reductions in cholesterol levels correlate with lower diastolic blood pressure (DBP). 4 Further, experimental and clinical studies have demonstrated a strong correlation between high plasma cholesterol levels and impaired endothelium-dependent vascular relaxation. [5][6][7] These findings suggest that hypercholesterolemia may contribute to increased vascular reactivity and thereby contribute to systemic hypertension.Several studies have reported that administration of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (ie, statins) can result in reductions in blood pressure (BP) as well as cholesterol. Statins reduced BP and prevented hypertension-induced glomerular injury in Dahl salt-sensitive rats and spontaneously hypertensive rats, [8][9][10][11] and statin treatment alone decreased BP in patients with hypercholesterolemia and untreated hypertension. 12,13 Three studies have reported that concomitant treatment with statins and antihypertensive drugs resulted in better BP control in Western patients with hypertension. [14][15][16] Only 1 study has reported that pravastatin had an additional depressor effect in Japanese patients taking antihypertensive drugs, 17 so the precise BP-lowering effects of statins in Japanese patients remains unclear. Therefore, in the present study designed to assess the different BP-lowering effects of statins and anti-hypertensive drugs, the effect of pravastatin on BP and cholesterol levels was compared between Japanese hypertensive patients who were already receiving antihypertensive treatment and normotensive patients not on antihypertensive treatment. MethodsThe clinical data of 82 patients with hypercholesterolemia (low-density lipoprotein cholesterol (LDL-C) >140 mg/dl) (39 men, 43 women; age range, 40-77 years; mean age, 62±9 years) before and after 3 months of treatment with pravastatin (10 mg/day orally) from January 1990 to December 1995 were retrospectively analyzed. Of these patients 44 had hypertension (HT group) and had been on antihypertensive treatment for at least 1 year; the remaining 38 patients were normotensive (NT group). Patients in the HT group were further subdivided into those with uncontrolled BP (systolic BP (SBP) ≥140 mmHg or DBP ≥90 mmHg) and those with controlled BP (SBP <140 mmHg and SBP <90 mmHg). Patients with diabetes, liver or disease, chronic pancreatitis, cancer, or major cardiovascular complication (myocardial infarction or unstable angina within the past 6 months, or congestive heart failure) were excluded from the study in order to evaluate the direct effect of pravastatin on hypertension with hypercholesterolemia. Those with a diagnosis of secondary hypertension were excluded after standard routine clinical and laboratory examinations. Patients on antihypertensive treatment continued with the same antihypertensive regimen before and after the 3 months of treatment with pravastatin. Background Previous studies have...

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Section: Discussionmentioning

confidence: 99%

Pravastatin Decreases Blood Pressure in Hypertensive and Hypercholesterolemic Patients Receiving Antihypertensive Treatment

Kawano

Yano

2006

Circ J

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“…38 The pathophysiological consequences of hypoxemia and reoxygenation could lead to vascular inflammation and remodeling, similar to atherosclerosis. [38][39][40] OSA increases sympathetic activity via complex mechanisms. Hypoxemia stimulates peripheral arterial chemoreceptors in the carotid bodies, triggering increased reflex sympathetic activity.…”

Section: Hypoxemia and Reoxygenationmentioning

confidence: 99%

Cardiac function and hypertension in patients with obstructive sleep apnea

Bertolami¹,

Gonzaga²,

Amodeo³

2014

RRCC

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Cardiovascular disease is one of the major causes of death worldwide. Among its risk factors, obstructive sleep apnea (OSA) is a common but still underestimated condition. OSA often coexists and interacts with obesity, sharing multiple pathophysiological mechanisms and subsequent cardiovascular risk factors, such as type 2 diabetes, dyslipidemia, systemic inflammation, and in particular hypertension. There is also evidence suggesting an increased risk of arrhythmia, heart failure, renal failure, acute myocardial infarction, stroke, and death. OSA is characterized by recurrent episodes of partial (hypopnea) or complete interruption (apnea) of breathing during sleep due to airway collapse in the pharyngeal region. The main mechanisms linking OSA to impaired cardiovascular function are secondary to hypoxemia and reoxygenation, arousals, and negative intrathoracic pressure. Consequently, the sympathetic nervous and the renin-angiotensin-aldosterone systems may be overestimulated, and blood pressure increased. Resistance to treatment for hypertension represents a growing issue, and given that OSA has been recognized as the major secondary cause of resistant hypertension, clinical investigation for apnea is mandatory in this population. Standard diagnosis includes polysomnography, and treatment for OSA should include control of risk factors for cardiovascular disease, including obesity. So far, continuous positive airway pressure is the treatment of choice for OSA, impacting positively on blood pressure goals; however, the impact on long-term follow-up and on cardiovascular disease should be better assessed.

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“…Middle coat contains mainly myocytes and elastic fibers (in elastic arteries) and is separated from intima and adventitia by internal and external elastic membranes. Blood vascular endothelial surface functions as a regulatory organ that supports vasomotor tone and anti-thrombotic system by regulating adhesion of platelets; it also regulates blood fluidity by discharging anticoagulants and fibrinolytic factors [6,17]. [26].…”

Section: Endothelium As a Regulatory Organmentioning

confidence: 99%

Role of Central Hemodynamic Parameters, Intimal Medial Thickness and Endothelial Dysfunction in Children With Renal Arterial Hypertension

Костюшина¹,

Komarova²,

Mazo³

et al. 2013

Pediatr. farmakol.

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Role of central hemodynamic parameters, intimal medial thickness and endothelial dysfunction in children with renal arterial hypertension Author affiliation:Kostyushina Irina Sergeevna, pediatrician of the medical rehabilitation department for children with nephrological-urological diseases, obesity and metabolic diseases at the research institute of preventive pediatrics and medical rehabilitation of the RAMS SCCH Address: 2, Lomonosovskiy Av., Moscow, 119991, tel.: +7 (499) (Pediatric pharmacology. 2013; 10 (3): 32-37)

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Endothelial function and atherosclerosis

Cited by 80 publications

References 0 publications

Pravastatin Decreases Blood Pressure in Hypertensive and Hypercholesterolemic Patients Receiving Antihypertensive Treatment

Pravastatin Decreases Blood Pressure in Hypertensive and Hypercholesterolemic Patients Receiving Antihypertensive Treatment

Cardiac function and hypertension in patients with obstructive sleep apnea

Role of Central Hemodynamic Parameters, Intimal Medial Thickness and Endothelial Dysfunction in Children With Renal Arterial Hypertension

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