Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
 free
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
 free
 free
Warning: file_get_contents(http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=19858408&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 445
 
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve
Pubget Overpricing |  
lüll
Ablation of transient receptor potential vanilloid 1 abolishes endothelin-induced increases in afferent renal nerve activity: mechanisms and functional significance Xie C; Wang DHHypertension 2009[Dec]; 54 (6): 1298-305Endothelin 1 (ET-1) and its receptors, ETA and ETB, play important roles in regulating renal function and blood pressure, and these components are expressed in sensory nerves. Activation of transient receptor potential vanilloid (TRPV) 1 channels expressed in sensory nerves innervating the renal pelvis enhances afferent renal nerve activity (ARNA), diuresis, and natriuresis. We tested the hypothesis that ET-1 increases ARNA via activation of ETB, whereas ETA counterbalances ETB in wild-type (WT) but not TRPV1-null mutant mice. ET-1 alone or with BQ123, an ETA antagonist, perfused into the left renal pelvis increased ipsilateral ARNA in WT but not in TRPV1-null mutant mice, and ARNA increases were greater in the latter. [Ala1, 3,11,15]-endothelin 1, an ETB agonist, increased ARNA that was greater than that induced by ET-1 in WT mice only. [Ala1, 3,11,15]-endothelin 1-induced increases in ARNA were abolished by chelerythrine, a protein kinase C inhibitor, but not by H89, a protein kinase A inhibitor. Chelerythrine, H89, and BQ788, an ETB antagonist, did not affect ARNA triggered by capsaicin in WT mice. Substance P release from the renal pelvis was increased by [Ala1, 3,11,15]-endothelin 1 in WT mice only, and the increase was abolished by chelerythrine but not by H89. Chelerythrine, H89, and BQ788 did not affect capsaicin-induced substance P release. Our data show that ET1 increases ARNA via activation of ETB, whereas ETA counterbalances ETB in WT but not in TRPV1-null mutant mice, suggesting that TRPV1 mediates ETB-dependent increases in ARNA, diuresis, and natriuresis possibly via the protein kinase C pathway.|Animals[MESH]|Antihypertensive Agents/pharmacology[MESH]|Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism[MESH]|Diuresis/physiology[MESH]|Endothelin A Receptor Antagonists[MESH]|Endothelin B Receptor Antagonists[MESH]|Endothelin-1/analogs & derivatives/*metabolism[MESH]|Hypertension, Renal/*physiopathology[MESH]|Isoquinolines/pharmacology[MESH]|Kidney/*innervation/physiology[MESH]|Male[MESH]|Mice[MESH]|Mice, Inbred C57BL[MESH]|Mice, Mutant Strains[MESH]|Natriuresis/physiology[MESH]|Neurons, Afferent/*physiology[MESH]|Oligopeptides/pharmacology[MESH]|Peptides, Cyclic/pharmacology[MESH]|Piperidines/pharmacology[MESH]|Protein Kinase C/metabolism[MESH]|Protein Kinase Inhibitors/pharmacology[MESH]|Receptor, Endothelin A/metabolism[MESH]|Receptor, Endothelin B/agonists/metabolism[MESH]|Substance P/metabolism[MESH]|Sulfonamides/pharmacology[MESH]|TRPV Cation Channels/agonists/*genetics/*metabolism[MESH] |
