RGD Reference Report - Expression and function of bradykinin B1 and B2 receptors in normal and inflamed rat urinary bladder urothelium. - Rat Genome Database

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

Expression and function of bradykinin B1 and B2 receptors in normal and inflamed rat urinary bladder urothelium.

Authors: Chopra, B  Barrick, SR  Meyers, S  Beckel, JM  Zeidel, ML  Ford, AP  De Groat, WC  Birder, LA 
Citation: Chopra B, etal., J Physiol. 2005 Feb 1;562(Pt 3):859-71. Epub 2004 Dec 2.
RGD ID: 1625040
Pubmed: PMID:15576455   (View Abstract at PubMed)
PMCID: PMC1665539   (View Article at PubMed Central)
DOI: DOI:10.1113/jphysiol.2004.071159   (Journal Full-text)

The bladder urothelium exhibits dynamic sensory properties that adapt to changes in the local environment. These studies investigated the localization and function of bradykinin receptor subtypes B1 and B2 in the normal and inflamed (cyclophosphamide (CYP)-induced cystitis) bladder urothelium and their contribution to lower urinary tract function in the rat. Our findings indicate that the bradykinin 2 receptor (B2R) but not the bradykinin 1 receptor (B1R) is expressed in control bladder urothelium. B2R immunoreactivity was localized throughout the bladder, including the urothelium and detrusor smooth muscle. Bradykinin-evoked activation of this receptor elevated intracellular calcium (EC(50) = 8.4 nM) in a concentration-related manner and evoked ATP release from control cultured rat urothelial cells. In contrast, B1R mRNA was not detected in control rat urinary bladder; however, following acute (24 h) and chronic (8 day) CYP-induced cystitis in the rat, B1R mRNA was detected throughout the bladder. Functional B1Rs were demonstrated by evoking ATP release and increases in [Ca(2+)](i) in CYP (24 h)-treated cultured rat urothelial cells with a selective B1 receptor agonist (des-Arg(9)-bradykinin). Cystometry performed on control anaesthetized rats revealed that intravesical instillation of bradykinin activated the micturition pathway. Attenuation of this response by the P2 receptor antagonist PPADS suggests that bradykinin-induced micturition facilitation may be due in part to increased purinergic responsiveness. CYP (24 h)-treated rats demonstrated bladder hyperactivity that was significantly reduced by intravesical administration of either B1 (des-Arg(10)-Hoe-140) or B2 (Hoe-140) receptor antagonists. These studies demonstrate that urothelial expression of bradykinin receptors is plastic and is altered by pathology.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
BDKRB1Humanoveractive bladder syndrome  ISOBdkrb1 (Rattus norvegicus) RGD 
Bdkrb1Ratoveractive bladder syndrome  IMP  RGD 
Bdkrb1Mouseoveractive bladder syndrome  ISOBdkrb1 (Rattus norvegicus) RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Bdkrb2Ratpositive regulation of cytosolic calcium ion concentration  IMP  RGD 
Bdkrb1Ratpositive regulation of release of sequestered calcium ion into cytosol  IDA in urinary bladder urotheliumRGD 

Objects Annotated

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

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

Genes (Homo sapiens)
BDKRB1  (bradykinin receptor B1)


Additional Information