PMID- 28193784
OWN - NLM
STAT- MEDLINE
DCOM- 20180622
LR  - 20210109
IS  - 2051-817X (Electronic)
IS  - 2051-817X (Linking)
VI  - 5
IP  - 3
DP  - 2017 Feb
TI  - Impaired myogenic response of the afferent arteriole contributes to the increased 
      susceptibility to renal disease in Milan normotensive rats.
LID - 10.14814/phy2.13089 [doi]
LID - e13089
AB  - Milan normotensive (MNS) rats are more susceptible to the development of renal 
      disease than Milan hypertensive (MHS) rats, but the genes and pathways involved 
      are unknown. This study compared the myogenic response of isolated perfused 
      afferent arterioles (Af-Art) and autoregulation of renal blood flow (RBF) and 
      glomerular capillary pressure (Pgc) in 6-9-week-old MNS and MHS rats. The 
      diameter of the Af-Art of MHS rats decreased significantly from 14.3 +/- 0.5 to 
      11.5 +/- 0.6 mum when perfusion pressure was elevated from 60 to 120 mmHg. In 
      contrast, the diameter of Af-Art of MNS rats did not decrease. RBF was well 
      autoregulated in MHS rats, but it increased by 26% in MNS rats. Pgc rose by 
      11 mmHg when renal perfusion pressure (RPP) was increased from 100 to 140 mmHg in 
      MNS but not in MHS rats. Protein excretion increased from 10 +/- 1 to 
      245 +/- 36 mg/day in MNS rats as they aged from 3 to 11 months but it did not 
      increase in MHS rats. We also compared the development of proteinuria in MNS and 
      MHS rats following the induction of diabetes with streptozotocin. Protein 
      excretion rose from 16 +/- 3 to 234 +/- 43 mg/day in MNS rats, but it remained 
      unaltered in MHS rats. These data indicate that the myogenic response of the 
      Af-art is impaired in MNS rats and increased transmission of pressure to the 
      glomerulus may contribute to renal injury in MNS rats similar to what is seen in 
      fawn-hooded hypertensive and Dahl salt-sensitive rats.
CI  - (c) 2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on 
      behalf of The Physiological Society and the American Physiological Society.
FAU - Ge, Ying
AU  - Ge Y
AD  - Department of Pharmacology and Toxicology, University of Mississippi Medical 
      Center, Jackson, Mississippi.
FAU - Fan, Fan
AU  - Fan F
AD  - Department of Pharmacology and Toxicology, University of Mississippi Medical 
      Center, Jackson, Mississippi.
FAU - Didion, Sean P
AU  - Didion SP
AD  - Department of Pharmacology and Toxicology, University of Mississippi Medical 
      Center, Jackson, Mississippi.
FAU - Roman, Richard J
AU  - Roman RJ
AD  - Department of Pharmacology and Toxicology, University of Mississippi Medical 
      Center, Jackson, Mississippi rroman@umc.edu.
LA  - eng
GR  - P20 GM104357/GM/NIGMS NIH HHS/United States
GR  - R01 DK104184/DK/NIDDK NIH HHS/United States
GR  - R21 AG050049/AG/NIA NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Physiol Rep
JT  - Physiological reports
JID - 101607800
SB  - IM
MH  - Animals
MH  - Arterioles/*physiopathology
MH  - Diabetes Mellitus, Experimental/metabolism
MH  - Disease Models, Animal
MH  - *Homeostasis
MH  - Hypertension/metabolism/pathology/*physiopathology
MH  - Kidney/blood supply/metabolism/pathology
MH  - Kidney Diseases/metabolism/pathology/*physiopathology
MH  - Male
MH  - Proteinuria/metabolism
MH  - Rats
PMC - PMC5309574
OTO - NOTNLM
OT  - Chronic kidney disease
OT  - diabetic nephropathy
OT  - glomerulus
OT  - renal hemodynamics
EDAT- 2017/02/15 06:00
MHDA- 2018/06/23 06:00
PMCR- 2017/02/13
CRDT- 2017/02/15 06:00
PHST- 2016/09/30 00:00 [received]
PHST- 2016/11/25 00:00 [revised]
PHST- 2016/12/01 00:00 [accepted]
PHST- 2017/02/15 06:00 [entrez]
PHST- 2017/02/15 06:00 [pubmed]
PHST- 2018/06/23 06:00 [medline]
PHST- 2017/02/13 00:00 [pmc-release]
AID - 5/3/e13089 [pii]
AID - PHY213089 [pii]
AID - 10.14814/phy2.13089 [doi]
PST - ppublish
SO  - Physiol Rep. 2017 Feb;5(3):e13089. doi: 10.14814/phy2.13089.