Changes in components of kinin system and hemodynamics in acute myocardial infarction

Hashimoto, Keiichi; Hamamoto, Hideki; Honda, Yukiharu; Hirose, Masaru; Furukawa, Shinya; Kimura, Eiichi

doi:10.1016/0002-8703(78)90304-6

Cited by 70 publications

(28 citation statements)

References 12 publications

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“…Myocardial ischemia is accompanied by an enormous release of cardiac BK, which can be maintained for several weeks (29). Thus, according to its behavior described in cell lines after chronic stimulation, we expected a down-regulation of the B2R in this situation.…”

Section: Physiological Relevance Of B1r and B2r Up-regulation After Mmentioning

confidence: 86%

“…It has been shown that kinins are released directly from the myocardium during MI (27,28) and contribute to the impact of ischemic damage (29). Several car-dioprotective effects of BK have been found by various authors after induction of myocardial ischemia.…”

Section: Regulation Of B1r and B2r After Induction Of Myocardial Infamentioning

confidence: 99%

“…After myocardial infarction (MI), increased plasma levels of KLK, kininogen and BK were found (24)(25)(26)(27)(28), and the increase in plasma KLK levels was positively correlated with the early survival rate of post-MI patients (29). It has been shown that kinins are released directly from the myocardium during MI (27,28) and contribute to the impact of ischemic damage (29).…”

Section: Regulation Of B1r and B2r After Induction Of Myocardial Infamentioning

confidence: 99%

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Regulation of the kinin receptors after induction of myocardial infarction: a mini-review

Tschöpe

Heringer-Walther

Walther

2000

Braz J Med Biol Res

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It is well known that the responses to vasoactive kinin peptides are mediated through the activation of two receptors termed bradykinin receptor B1 (B1R) and B2 (B2R). The physiologically prominent B2R subtype has certainly been the subject of more intensive efforts in structure-function studies and physiological investigations. However, the B1R activated by a class of kinin metabolites has emerged as an important subject of investigation within the study of the kallikreinkinin system (KKS). Its inducible character under stress and tissue injury is therefore a field of major interest. Although the KKS has been associated with cardiovascular regulation since its discovery at the beginning of the last century, less is known about the B1R and B2R regulation in cardiovascular diseases like hypertension, myocardial infarction (MI) and their complications. This mini-review will summarize our findings on B1R and B2R regulation after induction of MI using a rat model. We will develop the hypothesis that differences in the expression of these receptors may be associated with a dual pathway of the KKS in the complex mechanisms of myocardial remodeling. Key wordsThe kallikrein-kinin system Kinins are biologically active peptides which exert a broad spectrum of physiological effects, including vasodilation, smooth muscle contraction and pain induction. Several kinin peptides have been identified in mammalian species: the nonapeptide bradykinin (BK) and the decapeptide Lys-bradykinin (kallidin) belong to the best investigated members of the kinin family. Kinins are formed by cleavage from precursor kininogens by kallikreins (KLK). They are rapidly degraded by several kininases, including kininase II which is identical to angiotensinconverting enzyme. Kinins exert their effect after stimulation of their cell surface receptors: BK B1 receptor (B1R) and B2 receptor (B2R). Whereas the B2R is responsive to the intact kinins, BK and kallidin, the B1R has a higher affinity for the carboxypeptidase metabolites of kinins, des-Arg 9 -BK and des-

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Section: Physiological Relevance Of B1r and B2r Up-regulation After Mmentioning

confidence: 86%

Section: Regulation Of B1r and B2r After Induction Of Myocardial Infamentioning

confidence: 99%

Section: Regulation Of B1r and B2r After Induction Of Myocardial Infamentioning

confidence: 99%

See 1 more Smart Citation

Regulation of the kinin receptors after induction of myocardial infarction: a mini-review

Tschöpe

Heringer-Walther

Walther

2000

Braz J Med Biol Res

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show abstract

“…This could have a cardioprotective effect (102,186,202); indeed, studies showed that intracoronary bradykinin infusion significantly limited infarct size, reduced ventricular arrhythmias, improved cardiac performance, and normalized myocardial metabolism (135,137,163). In angioplasty patients, balloon inflation for 1 minute (simulating ischemic preconditioning) increased coronary sinus kinins 50-fold (203).…”

Section: Role Of Kinins In Myocardial Ischemia and The Protective Effmentioning

confidence: 99%

The Kallikrein-Kinin System as a Regulator of Cardiovascular and Renal Function

Carretero¹,

Yang²,

Rhaleb³

2005

Hypertension

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“…37 Some experimental studies reported that ACE inhibition in the immediate post-MI period could reduce both infarct size 38 and myocardial damage. 39 However, our own experiments failed to demonstrate a reduction of infarct size, 40 and a subsequent large clinical trial indicated that ACE inhibition given intravenously immediately after MI was not beneficial.…”

Section: Angiotensin Ii-mediated Effectsmentioning

confidence: 99%

Corcoran Lecture. Angiotensin-converting enzyme inhibition and the heart.

Gavras

1994

Hypertension

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Changes in components of kinin system and hemodynamics in acute myocardial infarction

Cited by 70 publications

References 12 publications

Regulation of the kinin receptors after induction of myocardial infarction: a mini-review

Regulation of the kinin receptors after induction of myocardial infarction: a mini-review

The Kallikrein-Kinin System as a Regulator of Cardiovascular and Renal Function

Corcoran Lecture. Angiotensin-converting enzyme inhibition and the heart.

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