Myocardial bradykinin B2-receptor expression at different time points after induction of myocardial infarction

Tschöpe, Carsten; Heringer-Walther, Silvia; Koch, Matthias; Spillmann, Frank; Wendorf, Michael; Hauke, Dorian; Bäder, Michael; Schultheiß, H.-P.; Walther, Thomas

doi:10.1097/00004872-200018020-00014

Cited by 49 publications

(32 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In agreement with others, we found a basal B2R expression in the left ventricle (LV) as well as in the right ventricle (RV) of the heart in non-operated rats (32,33). No regulation of B2R expression has been found in time-matched sham-operated rats, indicating that the operation itself did not induce any B2R regulation (33).…”

Section: Regulation Of the B2r After Induction Of MIsupporting

confidence: 92%

“…Surprisingly, we found an up-regulation of B2R expression starting as early as 6 h after MI induction with a peak at 24 h which was maintained in the LV for at least 6 days (33,34) (Figure 1). This up-regulation also correlated with an increase in the protein level of the B2R in the scar of the LV at least 6 days after MI induction, further indicating a role of the B2R during the early stages of tissue repair after MI (33).…”

Section: Regulation Of the B2r After Induction Of MImentioning

confidence: 66%

“…No regulation of B2R expression has been found in time-matched sham-operated rats, indicating that the operation itself did not induce any B2R regulation (33). Surprisingly, we found an up-regulation of B2R expression starting as early as 6 h after MI induction with a peak at 24 h which was maintained in the LV for at least 6 days (33,34) (Figure 1).…”

Section: Regulation Of the B2r After Induction Of MImentioning

confidence: 67%

“…Furthermore, an increase in B2R up-regulation was also found in the RV, as well as in the interventricular septum, which are remote from infarct site (33).…”

Section: Regulation Of the B2r After Induction Of MImentioning

confidence: 84%

See 3 more Smart Citations

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

Tschöpe

Heringer-Walther

Walther

2000

Braz J Med Biol Res

View full text Add to dashboard Cite

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-

show abstract

Section: Regulation Of the B2r After Induction Of MIsupporting

confidence: 92%

Section: Regulation Of the B2r After Induction Of MImentioning

confidence: 66%

Section: Regulation Of the B2r After Induction Of MImentioning

confidence: 67%

“…Furthermore, an increase in B2R up-regulation was also found in the RV, as well as in the interventricular septum, which are remote from infarct site (33).…”

Section: Regulation Of the B2r After Induction Of MImentioning

confidence: 84%

See 2 more Smart Citations

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

Tschöpe

Heringer-Walther

Walther

2000

Braz J Med Biol Res

View full text Add to dashboard Cite

show abstract

“…MI was induced by permanent ligation of the left anterior descending coronary artery. 10 Hemodynamics were measured 6 hours, 6 days, and 3 weeks after MI with a Millar-tip catheter. Details are given in the online additions.…”

Section: Rat MI Modelmentioning

confidence: 99%

Induction of Coxsackievirus-Adenovirus–Receptor Expression During Myocardial Tissue Formation and Remodeling

et al. 2003

View full text Add to dashboard Cite

Background— The coxsackievirus-adenovirus receptor (CAR) was cloned as a receptor for both viruses, but its primary biological functions and regulatory mechanisms are unknown. CAR was low in healthy adult myocardium, whereas strong CAR reexpression was observed in human dilated cardiomyopathy. The molecular mechanisms of CAR induction in cardiomyocytes are unknown. Methods and Results— We report on CAR regulation during development, CAR induction after myocardial infarction, and cell-to-cell contact–dependent CAR regulation in the rat. The high CAR expression during development in various organs decreased up to 190-fold after birth. After infarction resulting in severe cardiac dysfunction (dP/dt max , −53%; dP/dt min , −58%; left ventricular pressure, −45%), CAR was induced locally in cardiomyocytes of the infarct zone, where it was also expressed by capillary-like CD31 + structures and CD18 + interstitial cells, whereas it remained confined to subendothelial layers of arterioles and venules. In cultured cardiomyocytes, endothelin-1, cardiotrophin-1, leukemia-inhibiting factor, and cyclic stretch had no effect on CAR, whereas at high versus low cell density, CAR was suppressed up to 10-fold ( P =0.006). Conditioned media from low- or high-density cardiomyocytes or cardiofibroblasts had no effect. Conclusions— The locally confined CAR upregulation after infarction makes induction by various humoral factors unlikely, because cardiac dysfunction results in high activities of sympathetic and renin-angiotensin systems and cytokines. The cell culture experiments identify a cell-to-cell contact–dependent mechanism of CAR regulation. Further characterization of the signals linking cell-to-cell interactions to CAR gene expression may provide insight into mechanisms and functional consequences of the generalized CAR induction in dilated cardiomyopathy, and of its local induction after myocardial infarction.

show abstract

Imprinting of the Murine Mas Protooncogene Is Restricted to Its Antisense RNA

Alenina

Bäder

Walther

2002

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

Myocardial bradykinin B2-receptor expression at different time points after induction of myocardial infarction

Abstract: We conclude that myocardial ischaemia triggers B2-receptor up-regulation in both the infarcted and non-infarcted areas of the heart.

Cited by 49 publications

References 24 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

Induction of Coxsackievirus-Adenovirus–Receptor Expression During Myocardial Tissue Formation and Remodeling

Imprinting of the Murine Mas Protooncogene Is Restricted to Its Antisense RNA

Contact Info

Product

Resources

About