PMID- 8703708
OWN - NLM
STAT- MEDLINE
DCOM- 19960911
LR  - 20190905
IS  - 0931-041X (Print)
IS  - 0931-041X (Linking)
VI  - 10
IP  - 2
DP  - 1996 Apr
TI  - Decrease in endothelin-1 renal receptors during the 1st month of life in the rat.
PG  - 185-9
AB  - Endothelin-1 (Et1), like angiotensin II, is implicated in postnatal maturation 
      and development. The present study was designed to identify Et1 receptors and 
      subtype Et1 receptors present in rat kidney between 1 and 30 days of postnatal 
      life. On day 1, high-affinity and high-density Et1 binding sites were identified 
      in rat kidney. The dissociation constant and maximum binding for ET1 to membranes 
      from whole kidney were 0.073 +/- 0.05 nM and 1,345.9 +/- 73 fmol/mg protein, 
      respectively. On day 30, affinity and receptor density were markedly decreased. 
      The dissociation constant and maximum binding were 0.147 +/- 0.021 nM (P < 0.01) 
      and 633.2 +/- 56.4 fmol/mg protein (P < 0.001), respectively. Using BQ 123 
      (EtA-selective antagonist) and sarafotoxin S6c (EtB-selective agonist), the two 
      Et1 receptor subtypes EtA and EtB were identified in 1- and 30-day-old rat 
      kidney. BQ 123 selectively recognized EtA receptors with high affinity (2.9 +/- 
      0.44 on day 1 and 4.0 +/- 0.5 nM on day 30) and sarafotoxin S6c bound with higher 
      affinity EtB receptors (0.871 +/- 0.14 on day 1 and 0.717 +/- 0.12 nM on day 30). 
      Between birth and day 30, the EtA binding capacity was decreased (304 +/- 27 vs. 
      752 +/- 202 fmol/mg protein, P < 0.05), whereas EtB binding was not affected (514 
      +/- 87 vs. 656 +/- 171 fmol/mg protein, NS). The decrease in the total number of 
      Et1 receptors during the 1st month of life may be due to the concomitant decrease 
      in the number of EtA receptors. Increased Et1 receptor density in early postnatal 
      life suggests an influence of Et1 on immature kidney circulation and/or kidney 
      growth.
FAU - Abadie, L
AU  - Abadie L
AD  - Department of Physiology, CHU Necker-Enfants Malades, Paris, France.
FAU - Blazy, I
AU  - Blazy I
FAU - Roubert, P
AU  - Roubert P
FAU - Plas, P
AU  - Plas P
FAU - Charbit, M
AU  - Charbit M
FAU - Chabrier, P E
AU  - Chabrier PE
FAU - Dechaux, M
AU  - Dechaux M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Pediatr Nephrol
JT  - Pediatric nephrology (Berlin, Germany)
JID - 8708728
RN  - 0 (Endothelin Receptor Antagonists)
RN  - 0 (Endothelins)
RN  - 0 (Peptides, Cyclic)
RN  - 0 (Receptors, Endothelin)
RN  - 0 (Vasoconstrictor Agents)
RN  - 0 (Viper Venoms)
RN  - 0 (sarafotoxins s6)
RN  - S2A8YZM151 (cyclo(Trp-Asp-Pro-Val-Leu))
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Binding, Competitive
MH  - Cell Membrane/metabolism
MH  - Endothelin Receptor Antagonists
MH  - Endothelins/metabolism
MH  - Kidney/cytology/growth & development/*metabolism
MH  - Peptides, Cyclic/metabolism/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Endothelin/*metabolism
MH  - Vasoconstrictor Agents/metabolism/pharmacology
MH  - Viper Venoms/metabolism/pharmacology
EDAT- 1996/04/01 00:00
MHDA- 1996/04/01 00:01
CRDT- 1996/04/01 00:00
PHST- 1996/04/01 00:00 [pubmed]
PHST- 1996/04/01 00:01 [medline]
PHST- 1996/04/01 00:00 [entrez]
AID - 10.1007/BF00862072 [doi]
PST - ppublish
SO  - Pediatr Nephrol. 1996 Apr;10(2):185-9. doi: 10.1007/BF00862072.