Angiotensin II stimulates nitric oxide release in glomerular arterioles via AT1 receptors, providing a counter-regulatory mechanism to prevent excessive vasoconstriction.
Should not change RAAS inhibitor practice; leaves open translation of glomerular AT1-NO counter-regulation to human disease.
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.
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Patzak et al. (2005) studied this question.
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