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Interaction between Ang1–7 (‘ Mas’) and AT1 receptors in regulating renal sodium and water excretion
Author(s) -
o neill julie anna,
Johns Edward J
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1105.2
Subject(s) - losartan , angiotensin ii receptor type 1 , fractional excretion of sodium , chemistry , endocrinology , medicine , diuretic , excretion , receptor , natriuresis , angiotensin ii , sodium , kidney , angiotensin receptor , organic chemistry
Ang (1–7) has natriuretic and diuretic actions at the kidney but the underlying mechanisms are unclear. This study aimed to determine if Ang (1–7) induced increases in sodium and water excretion were solely dependant upon intrarenal (IR) Mas receptor activation or whether Ang II induced IR AT1 receptor stimulation was required. Male Wistar rats (n= 6–7) were anaesthetized (chloralose/urethane) and prepared for mean arterial pressure (MAP) and left renal function measurement and IR infusion of saline and drugs. Data ±SEM were subjected to a Students t‐test and significance set at (P<0.05). MAP was 101±3mmHg, Fractional Sodium Excretion (FENa) was 1.5±0.3% and Urine Volume was 52.4± 14.3μL/min/Kg. Ang (1–7) had no effect on MAP but increased FENa by 206% and UV by 150% (both P<0.05). In the presence of either ‘Mas’ receptor (A‐779) or AT1 receptor (Losartan) antagonists, Ang (1–7) only increased FENa by 21% and 19% respectively and UV by 16% and 6% respectively, significantly less than in the absence of both antagonists. These data indicate that there is an interaction between IR ‘Mas’ and AT1 receptors which appears to be necessary to fully mediate the actions of Ang (1–7).