Acute dilatation to phytoestrogens and estrogen receptor subtypes expression in small arteries from women with coronary heart disease

2008 ◽  
Vol 196 (1) ◽  
pp. 49-58 ◽  
Author(s):  
Maria Natalia Cruz ◽  
Stefan Agewall ◽  
Karin Schenck-Gustafsson ◽  
Karolina Kublickiene
Keyword(s):  
Coronary Heart Disease ◽  
Estrogen Receptor ◽  
Heart Disease ◽  
Receptor Subtypes ◽  
Small Arteries

Stroke: cerebrovascular disease

2010 ◽  
pp. 4933-4948
Author(s):  
J van Gijn
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Cerebrovascular Disease ◽  
Case History ◽  
Cerebrovascular Diseases ◽  
Incidence Rates ◽  
Important Case ◽  
Small Arteries ◽  
Transient Ischaemic Attacks ◽  
Arterial Aneurysms

Case History—Four cases of headache. Cerebrovascular diseases include many pathological conditions but the principal categories are (1) infarction—through occlusion of major arteries, small arteries or venous sinuses; and (2) haemorrhage—most often through rupture of small arteries, arterial aneurysms or capillaries. Strokes are common, with annual incidence rates for subjects aged over 55 ranging from 420 to over 1000 per 100 000. They are the most important case of disability in developed Western nations and the second most frequent cause of death after coronary heart disease. About 80% of strokes are caused by cerebral infarcts, with the remainder due to haemorrhage, with 20% of these attributable to a bleeding cerebral aneurysm. The incidence of transient ischaemic attacks (TIAs) is about 50 per 100 000....

Stroke: Cerebrovascular disease

2020 ◽  
pp. 6010-6026
Author(s):  
J. van Gijn ◽  
Peter M. Rothwell
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Cerebrovascular Disease ◽  
Cerebrovascular Diseases ◽  
Incidence Rates ◽  
Annual Incidence ◽  
Important Case ◽  
Small Arteries ◽  
Transient Ischaemic Attacks ◽  
Arterial Aneurysms

Cerebrovascular diseases include many pathological conditions but the principal categories are (1) infarction—through occlusion of major arteries, small arteries or venous sinuses; and (2) haemorrhage—most often through rupture of small arteries, arterial aneurysms, or capillaries. Strokes are common, with annual incidence rates for subjects aged over 55 ranging from 420 to over 1,000 per 100,000. They are the most important case of disability in developed Western nations and the second most frequent cause of death after coronary heart disease. About 80% of strokes are caused by cerebral infarcts, with the remainder due to haemorrhage, with 20% of these attributable to a bleeding cerebral aneurysm. The annual incidence of transient ischaemic attacks (TIAs) is about 50–100 per 100,000.

Acute responses to phytoestrogens in small arteries from men with coronary heart disease

2006 ◽  
Vol 290 (5) ◽  
pp. H1969-H1975 ◽  
Author(s):  
Maria Natalia Cruz ◽  
Leonid Luksha ◽  
Henareh Logman ◽  
Lucilla Poston ◽  
Stefan Agewall ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Ex Vivo ◽  
Subcutaneous Fat ◽  
Estrogen Receptor Α ◽  
Response Curves ◽  
Small Arteries ◽  
Before And After ◽  
Established Coronary Heart Disease ◽  
Normal Men

The aim of this study was to investigate acute vasodilator responses to phytoestrogens and selective estrogen receptor-α (ERα) agonist in isolated small arteries from men with established coronary heart disease (CHD) and with a history of myocardial infarction versus healthy male control subjects. As to methodology, small arteries obtained from subcutaneous fat biopsies and mounted on a wire myograph were preconstricted with norepinephrine, and dilator responses to increasing nanomolar-micromolar concentrations of the phytoestrogens resveratrol and genistein (predominantly ERβ agonists) and to propyl-[1H]-pyrazole-1,3,5-triyl-trisplenol (PPT, a selective ERα agonist) were determined. These were compared with responses to reference compound 17β-estradiol (17β-E2). Concentration-response curves were constructed before and after nitric oxide (NO) synthase inhibition with Nω-nitro-l-arginine methyl ester. As a result, relaxation induced by the investigated compounds was similar in men with CHD and control men, but in both groups PPT and genistein-induced relaxation was greater than that of resveratrol and 17β-E2. NO contributed to both phytoestrogens and PPT-induced relaxation but not to 17β-E2 responses in arteries from control men. This NO-mediated component of relaxation was absent in arteries from men with established CHD. In conclusion, phytoestrogens, at concentrations achievable by ingestion of phytoestrogen-rich food products, evoke dilatation ex vivo of small peripheral arteries from normal men and those with established CHD. The contribution of NO to dilatory responses by these compounds is pertinent to arteries from control males, whereas other NO-independent dilatory mechanism(s) are involved in arteries from CHD.

The PlA Polymorphism of Glycoprotein IIIa Functions as a Modifier for the Effect of Estrogen on Platelet Aggregation

2001 ◽  
Vol 125 (1) ◽  
pp. 112-115
Author(s):  
Konstantinos D. Boudoulas ◽  
Glen E. Cooke ◽  
Christine M. Roos ◽  
Paul F. Bray ◽  
Pascal J. Goldschmidt-Clermont
Keyword(s):  
Coronary Heart Disease ◽  
Estrogen Receptor ◽  
Heart Disease ◽  
Hormone Replacement Therapy ◽  
Platelet Aggregation ◽  
Replacement Therapy ◽  
Hormone Replacement ◽  
Adenosine Diphosphate ◽  
Inhibitory Effect ◽  
Aggregation Of Platelets

Abstract Background.—Although estrogen has been shown to contribute to retardation of the development of coronary heart disease in premenopausal women, the efficacy of hormone replacement therapy for coronary heart disease prevention in women with established coronary heart disease remains controversial. Hence, additional research is needed to clarify the effects of hormone replacement therapy on the cardiovascular and clotting systems. We investigated the effect of estrogen on platelet aggregation induced by standard agonists (epinephrine and adenosine diphosphate), with and without the platelet antagonist aspirin. Furthermore, we analyzed our data according to the presence or absence of a prevalent polymorphism of the glycoprotein (GP) IIIa subunit of the platelet fibrinogen receptor GPIIb-IIIa, PlA2. Methods and Results.—The effect of estrogen on aggregation of platelets was studied in healthy men (n = 20, 10 PlA1/A1 and 10 PlA1/A2) and premenopausal healthy women (n = 10, 5 PlA1/A1 and 5 PlA1/A2). The PlA1/A1 and PlA1/A2 individuals were matched for age and race. Platelet response to agonists was investigated in the presence of (1) estrogen (10−11 to 10−8 mol/L), (2) aspirin (0.056 to 56 μmol/L), (3) estrogen plus aspirin, and (4) estrogen plus ICI 182 780 (ICI, 10−9 mol/L, an inhibitor of the estrogen receptor). We found that physiologic concentrations of estrogen strongly and significantly inhibited the aggregation of PlA1/A2 platelets (P ;lt .005 for epinephrine and P ;lt .05 for adenosine diphosphate, induced aggregation, respectively) in both men and women. Concentrations of estrogen that were 1000-fold greater were required to observe the same level of inhibition with PlA1/A1 platelets. In the presence of aspirin, estrogen failed to provide additional inhibitory effect on aggregation of both PlA1/A1 and PlA1/A2 platelets. The estrogen-specific inhibitor ICI blocked the effect of estrogen on aggregation, suggesting that this effect is mediated by the estrogen receptor. Conclusions.—Estrogen inhibits the aggregation of platelets, but such inhibition is highly dependent on the presence or absence of the PlA2 polymorphism of GPIIIa. However, in the presence of aspirin, the inhibitory effect of estrogen on aggregation was no longer detectable.

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