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Modulation by locally produced luminal angiotensin II of proximal tubular sodium reabsorption via an AT 1 receptor
Author(s) -
Hiranyachattada Siriphun,
Harris Peter J.
Publication year - 1996
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1996.tb15717.x
Subject(s) - losartan , angiotensin ii , medicine , endocrinology , chemistry , reabsorption , angiotensin ii receptor type 1 , tubular fluid , renin–angiotensin system , renal sodium reabsorption , sodium , convoluted tubule , receptor , kidney , biology , blood pressure , organic chemistry
The concentration of angiotensin II reported in proximal tubular fluid in anaesthetized rats is considerably higher than in plasma, indicating secretion of this peptide into the tubular lumen. Shrinking split‐drop micropuncture was used to examine the effect of endogenous angiotensin on sodium and water absorption in the proximal convoluted tubule. Addition of losartan, a nonpeptide AT 1 receptor blocker, to intratubular fluid increased fluid uptake by 15.7 ± 3.9% (10 −5 m ) and 24.7 ± 9.4% (10 −4 m ) whereas the AT 2 inhibitor, PD123319 had no effect. We conclude that angiotensin II is secreted into proximal tubular fluid and, in the anaesthetized rat, is maintained at a concentration that inhibits sodium and water transport via AT 1 receptors.