kallidin has been researched along with Myocardial-Infarction* in 2 studies
1 review(s) available for kallidin and Myocardial-Infarction
Article | Year |
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[Vasoactive kinins in the physiology and pathology of the cardiovascular system].
Topics: Animals; Arteries; Arteriovenous Anastomosis; Blood Circulation; Blood Vessels; Bradykinin; Cardiovascular Diseases; Cardiovascular Physiological Phenomena; Coronary Disease; Dogs; Guinea Pigs; Heart; Hemodynamics; Humans; Hypertension; Kallidin; Kallikreins; Kidney; Kinins; Models, Chemical; Myocardial Infarction; Pancreas; Salivary Glands; Shock | 1969 |
1 other study(ies) available for kallidin and Myocardial-Infarction
Article | Year |
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[Relationship between the kininase- and angiotensin- converting activity under normal conditions and in experimental myocardial infarct].
In rat experiments the depressor and pressor responses to kinins and angiotensins recorded in the carotid artery were compared as to the different methods of their administration. With intravenous injection, the responses to bradykinin and kallidin were lower, and to angiotensin I--higher, than with their intra-aortic administration. The responses to angiotensin II remain identical under these conditions. The administration of all the preparations against the background of 2,3-dimercaptopropanol (unithiol) resulted in levelling of the responses irrespective of the mode of administration. In experimental myocardial infarction induced in rats by ligation of the coronary artery a reduction of the kinin-destructing and an increase of the angiotensin-converting activity was noted in the early postinfarction period. The response of the peripheral vessels to angiotensin, bradykinin and noradrenaline is decreased, while that to isoproterenol remain unchanged. The obtained results support the concept of the existence of the kininase and angiotensin-converting activity connected with a common biochemical factor of pulmonary circulation. Changes in the proportion of these functions under normal conditions and in cases of pathological states are interpreted as a particular regulation mechanism of the vascular tone and arterial pressure. Topics: Acute Disease; Angiotensin II; Animals; Aorta; Blood Pressure; Bradykinin; Carboxypeptidases; Injections, Intra-Arterial; Injections, Intravenous; Kallidin; Lysine Carboxypeptidase; Male; Myocardial Infarction; Peptidyl-Dipeptidase A; Rats; Unithiol | 1977 |