PMID- 23389451
OWN - NLM
STAT- MEDLINE
DCOM- 20130523
LR  - 20181202
IS  - 1522-1466 (Electronic)
IS  - 1522-1466 (Linking)
VI  - 304
IP  - 7
DP  - 2013 Apr 1
TI  - Renal protective effects of alpha-calcitonin gene-related peptide in 
      deoxycorticosterone-salt hypertension.
PG  - F1000-8
LID - 10.1152/ajprenal.00434.2012 [doi]
AB  - Deoxycorticosterone salt (DOC-salt) hypertension-induced renal damage is enhanced 
      in alpha-calcitonin gene-related peptide (alpha-CGRP) knockout (KO) compared with 
      wild-type (WT) mice. However, since the alpha-CGRP KO mice have a 15-20 mmHg higher 
      baseline mean arterial pressure (MAP) than WT mice, they also have a higher MAP 
      than WT mice throughout the course of DOC-salt hypertension. To determine the 
      mechanism by which the absence of alpha-CGRP enhances hypertension-induced renal 
      damage, DOC-salt hypertension was induced in telemetry probe implanted alpha-CGRP KO 
      and WT mice. To equalize the blood pressure (BP) to that of DOC-salt WT mice, an 
      additional group of DOC-salt alpha-CGRP KO mice was given 0.025% hydralazine to 
      drink. The DOC-salt protocol increased the final MAP in alpha-CGRP KO mice to 155 +/- 6 
      mmHg and in WT mice to 140 +/- 5 mmHg. The MAP of the hydralazine-treated DOC-salt 
      alpha-CGRP KO mice was 139 +/- 6 mmHg. Urinary excretion of microalbumin and 
      isoprostane, a marker for oxidative stress, was increased, and creatinine 
      clearance was decreased in DOC-salt alpha-CGRP KO compared with DOC-salt WT mice. 
      Equalization of the MAP in DOC-salt alpha-CGRP KO to that of DOC-salt WT mice did not 
      significantly improve these parameters. Renal macrophage infiltration; desmin, a 
      marker of podocyte damage; and the inflammatory cytokines TNF-alpha and IFN-gamma and the 
      chemokines monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory 
      protein-1alpha (MIP-1alpha) were increased in DOC-salt alpha-CGRP KO mice and were not 
      reduced by hydralazine treatment. However, BP equalization did improve the renal 
      histopathological damage, as determined by light microscopy. Therefore, in 
      DOC-salt hypertension in mice, the mechanism(s) of the renal protective effects 
      of alpha-CGRP are both BP independent and BP dependent.
FAU - Li, Jianping
AU  - Li J
AD  - Department of Cell Biology and Anatomy, University of South Carolina School of 
      Medicine, Columbia, SC 29208, USA.
FAU - Carnevale, Kevin A
AU  - Carnevale KA
FAU - Dipette, Donald J
AU  - Dipette DJ
FAU - Supowit, Scott C
AU  - Supowit SC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130206
PL  - United States
TA  - Am J Physiol Renal Physiol
JT  - American journal of physiology. Renal physiology
JID - 100901990
RN  - 0 (Chemokines)
RN  - 0 (Cytokines)
RN  - 0 (Desmin)
RN  - 26NAK24LS8 (Hydralazine)
RN  - 40GP35YQ49 (Desoxycorticosterone)
RN  - JHB2QIZ69Z (Calcitonin Gene-Related Peptide)
SB  - IM
MH  - Animals
MH  - Arterial Pressure/drug effects
MH  - Calcitonin Gene-Related Peptide/genetics/*physiology
MH  - Chemokines/metabolism
MH  - Cytokines/metabolism
MH  - Desmin/biosynthesis
MH  - Desoxycorticosterone
MH  - Hydralazine/pharmacology
MH  - Hypertension/chemically induced/*physiopathology
MH  - Kidney/pathology/*physiology
MH  - Macrophages/immunology
MH  - Mice
MH  - Mice, Knockout
EDAT- 2013/02/08 06:00
MHDA- 2013/05/25 06:00
CRDT- 2013/02/08 06:00
PHST- 2013/02/08 06:00 [entrez]
PHST- 2013/02/08 06:00 [pubmed]
PHST- 2013/05/25 06:00 [medline]
AID - ajprenal.00434.2012 [pii]
AID - 10.1152/ajprenal.00434.2012 [doi]
PST - ppublish
SO  - Am J Physiol Renal Physiol. 2013 Apr 1;304(7):F1000-8. doi: 
      10.1152/ajprenal.00434.2012. Epub 2013 Feb 6.