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5 Postępy Higieny i Medycyny Doświadczalnej

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Renin-angiotensin system and atherosclerosis

100%

Stajszczak M. , Gminski J.

nr 6

475-485

Mechanism of antiatherosclerotic action of ACE-inhibitors

100%

Stajszczak M. , Gminski J.

nr 6

635-647

Blockade of the renin-angiotensin system reduces the development of the atherosclerotic process after vascular injury and in hyperlipidemic animals. ACE-inhibitors inhibit vascular smooth muscle cells migration and proliferation, macrophage-foam cell accumulation and preserve the antiaggregatory and antithrombotic function of the endothelium in atherosclerotic vessels. In addition to the inhibition of angiotensin II synthesis, reduced degradation of kinins and improvement of insulin action after ACE-inhibition may be responsible for observed actions. ACE-inhibitors may have also influence on lipids metabolism, including low density lipoproten oxidation. Despite this, ACE-inhibitors failed to prevent restenosis after coronary angioplasty in humans. One reason for the lack of ACE-inhibitors effect in human restenosis might depend on the activation of the alternative angiotensin II-generating system in human arteries after vascular injury.

Genetic polymorphism in rennin - angiotensin system and its association cardiovascular diseases

100%

Stajszczak M. , Gminski J.

tom 51

nr 1

171-183

Myocardial infarction and stroke are the major cause of death in developed countries and are the clinical manifestation of atherosclerosis and hypertension. Both the environmental factors and genetic predisposition have an influence on the pathogenesis of these diseases. Despite we know lots of environmental risk factors and we made important advances in the prevention and treatment of mentioned diseases, our knowledge about the pathogenic linkage between genetic predisposition and cardiovascular diseases is still very little. Activation of the renin-angiotensin system has been proposed as a very important step in the pathogenesis of hypertension and atherosclerosis. In spite of vasoconstrictor activity, angiotensin II can stimulate migration and proliferation of vascular smooth muscle cells, macrophage-foam cells formation, adhesion and agregation of platelets and fibrinolytic system inhibition. Angiotensin convertin enzyme inhibitors reduce the development of the atherosclerotic process after vascular injury and in hyperlipidemic animals. Blockade of renin-angiotensin system seems to be also effective in secondary prevention of myocardial infarction in men. In sum, the genetic variations inside the renin-angiotensin system which may affect the function of its components might have an influence on genetic predisposition to cardiovascular diseases. The paper deals with the current state of knowledge on association between polymorphic variations in renin gene, angiotensinogen gene, angiotensin converting enzyme gene and AT1 receptor gene and primary hypertension, ischeamic heart disease and myocardial infarction.

Heparin and atherosclerosis

100%

Stajszczak M. , Gminski J.

Postępy Higieny i Medycyny Doświadczalnej

1994

tom 48

nr 3

275-290

Heparin is a highly sulfated glycosaminoglycan with many functions such as antilipemic and antithrombotic.In spite os these activities heparin is able to inhibit vacsular smooth muscle cells proliferation and mmigration what seems to be very important event in the pathogenesis of atherosclerosos.The molecular mechanism of the action of heparin on smooth muscle cells is not yet understood.Heparin inhibits growth factors binding to their receptors,oncogenes expressionand has influence on the extracellular matrix protein deposition in the artery wall.

ACE-inhibitors and atherosclreosis

100%

Gminski J. , Stajszczyk M.

tom 50

nr 2

157-171

The activation of the renin-angiotensin system has been proposed as a very important step in the pathogenesis of atherosclerosis. Accordingly, ACE-inhibitors and angiotensin II receptors antagonists showed their ability to reduce the atherosclerotic process in animals. Inhibition of renin-angiotensin system reduces the development of atherosclerotic lesion either in cholesterol-fed animals and in animals after vascular injury. The precise mechanism for this action may depend on the inhibition of other than hypertensive property of angiotensin II.