Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl
Preferences help
Polish version English version Language
enabled [disable] Abstract
Number of results

Results found: 5

Number of results on page
first rewind previous Page / 1 next fast forward last

Search results

Search:
in the keywords:  RENNIN-ANGIOTENSIN SYSTEM
help Sort By:

help Limit search:
first rewind previous Page / 1 next fast forward last
1

Renin-angiotensin system in the kidney physiology and pathology

100%
Lapinski R.
Postępy Higieny i Medycyny Doświadczalnej
|
2000
|
vol. 54
|
issue 5
639-656
EN
Clinical and experimental studies indicate that angiotensin II (A II) is involved in the process of tissue destruction in chronic renal diseases. Since the recognition of its potent vasoconstrictor action in the renal circulation. A II has several times come into the forefront in the scientists by revealing new biological actions which are apparently unrelated to any of its previously recognised actions. Many of these actions have now been extensively studied. Of interest, also, are its non-renal actions which are now known to be similarly rich in variety, due to extensive investigations on the central nervous and other organ systems.
2

Renin-angiotensin system and atherosclerosis

100%
Stajszczak M., Gminski J.
Postępy Higieny i Medycyny Doświadczalnej
|
1993
|
vol. 47
|
issue 6
475-485
3

Noninfalmatory acure renal failure.New pathogenetic aspects in the light of findings obtained in authopic and bioptic specimentstic

100%
Bohle A., Kokot F., Osswald H., Schubert B., Wehrmann M., Erley C., Risler^T., Risler T.
Postępy Higieny i Medycyny Doświadczalnej
|
1994
|
vol. 48
|
issue 2
109-125
4

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

75%
Stajszczak M., Gminski J.
Postępy Higieny i Medycyny Doświadczalnej
|
1997
|
vol. 51
|
issue 1
171-183
EN
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.
5

ACE-inhibitors and atherosclreosis

51%
Gminski J., Stajszczyk M.
Postępy Higieny i Medycyny Doświadczalnej
|
1996
|
vol. 50
|
issue 2
157-171
EN
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.
first rewind previous Page / 1 next fast forward last
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.