RGD Reference Report - Regulation of cardiac bradykinin B1- and B2-receptor mRNA in experimental ischemic, diabetic, and pressure-overload-induced cardiomyopathy. - Rat Genome Database

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Regulation of cardiac bradykinin B1- and B2-receptor mRNA in experimental ischemic, diabetic, and pressure-overload-induced cardiomyopathy.

Authors: Spillmann, F  Altmann, C  Scheeler, M  Barbosa, M  Westermann, D  Schultheiss, HP  Walther, T  Tschope, C 
Citation: Spillmann F, etal., Int Immunopharmacol 2002 Dec;2(13-14):1823-32.
RGD ID: 704379
Pubmed: PMID:12489796   (View Abstract at PubMed)

Although kinins have been associated with the regulation of cardiovascular function in left ventricular hypertrophy (LVH) as a consequence of hypertension, myocardial infarction (MI), and/or diabetic cardiomyopathy, less is known about their receptor regulation under these conditions. We have therefore investigated the bradykinin B1-receptor (B1R) and B2-receptor (B2R) mRNA expression in rat models of MI, LVH and diabetes mellitus (DM). Sprague-Dawley rats (SD) were submitted to permanent ligation of the left descending coronary artery (LAD) to induce a MI, whereas DM was induced by a single injection of streptozotocin (STZ). LVH was induced after thoracic aortic banding (AB). Three weeks after MI, six weeks after STZ injection or six weeks after AB, left ventricular (LV) function was characterized using a Millar-tip catheter. Cardiac B1R- and B2R-mRNA expression were analyzed by specific RNase-protection assays (RPA). LV contractility (dP/dt max) was impaired by 40-48% in rats after induction of MI or DM compared to their controls. However, despite an enormous increase in LV end-diastolic pressure (LEVDP) to 310% after AB, LV contractility did not differ compared to the controls. These hemodynamic changes were accompanied by an up-regulation of cardiac B1R- (MI, 288%; STZ, 215%; AB, 4180%) and B2R-mRNA expression (MI, 122%; STZ, 288%; AB, 96%). Up-regulation of both BK-receptor (BKR) types in early stages of cardiac wound healing induced by ischemia and in chronic stages of cardiac remodeling induced by pressure-overload or by hyperglycemia indicates that kinins play a major role in the complex processes of cardiac tissue injury and repair.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Experimental Diabetes Mellitus  ISOBdkrb1 (Rattus norvegicus)704379; 704379mRNA:increased expression:heartRGD 
Experimental Diabetes Mellitus  ISOBdkrb2 (Rattus norvegicus)704379; 704379mRNA:increased expression:heartRGD 
Experimental Diabetes Mellitus  IEP 704379; 704379mRNA:increased expression:heartRGD 
Left Ventricular Hypertrophy  ISOBdkrb1 (Rattus norvegicus)704379; 704379mRNA:increased expression:heartRGD 
Left Ventricular Hypertrophy  ISOBdkrb2 (Rattus norvegicus)704379; 704379mRNA:increased expression:heartRGD 
Left Ventricular Hypertrophy  IEP 704379; 704379mRNA:increased expression:heartRGD 
myocardial infarction  ISOBdkrb1 (Rattus norvegicus)704379; 704379mRNA:increased expression:heartRGD 
myocardial infarction  ISOBdkrb2 (Rattus norvegicus)704379; 704379mRNA:increased expression:heartRGD 
myocardial infarction  IEP 704379; 704379mRNA:increased expression:heartRGD 

Objects Annotated

Genes (Rattus norvegicus)
Bdkrb1  (bradykinin receptor B1)
Bdkrb2  (bradykinin receptor B2)

Genes (Mus musculus)
Bdkrb1  (bradykinin receptor, beta 1)
Bdkrb2  (bradykinin receptor, beta 2)

Genes (Homo sapiens)
BDKRB1  (bradykinin receptor B1)
BDKRB2  (bradykinin receptor B2)


Additional Information