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ANGIOTENSIN II–NITRIC OXIDE INTERACTION IN GLOMERULAR ARTERIOLES
Author(s) -
Patzak Andreas,
Lai EnYin,
Persson Pontus B,
Persson A Erik G
Publication year - 2005
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2005.04203.x
Subject(s) - afferent arterioles , dilator , angiotensin ii , medicine , nitric oxide , endocrinology , efferent , chemistry , renin–angiotensin system , kidney , arteriole , microcirculation , receptor , blood pressure , afferent
SUMMARY 1. Resistance changes of the afferent and efferent arterioles determine blood flow and filtration rate in the kidney. The tone of both vessels results from the influence of nerves and humoral and paracrine factors, through a balance of constrictor and dilator systems. Angiotensin (Ang) II and nitric oxide (NO) are important factors determining vascular tone. 2. In the present review, we show that, in addition to the basal production of NO, a specific and significant AngII‐induced release of NO occurs in glomerular arterioles. Data from investigations of arteriolar contraction, as well as from fluorescence measurements of NO, in the presence of selective angiotensin AT 1 and AT 2 receptor antagonists indicate an AT 1 receptor‐stimulated release of NO in afferent arterioles. 3. The AngII‐induced liberation of NO could prevent glomerular arterioles from a marked constriction, particularly in situations of high AngII levels in the kidney.