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Potassium as a renal vasodilator
Author(s) -
Magnusson Linda,
HolsteinRathlou NielsHenrik,
Salomonsson Max
Publication year - 2007
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.21.5.a501-c
Subject(s) - vasodilation , chemistry , medicine , endocrinology , ouabain , stimulation , renal circulation , renal blood flow , in vivo , kidney , sodium , biology , microbiology and biotechnology , organic chemistry
The aims of the present study were to investigate the mechanisms behind K + induced renal vasodilation in vivo, and whether extracellular K + could act as a mediator of the renal vascular response to endothelial activation by acethylcholine (ACh). Renal blood flow (RBF) was measured in vivo in anesthetized Sprague‐Dawley rats using an ultrasonic flow probe. Intrarenal infusion of K + (plasma concentration ~12 mM) significantly increased RBF transiently by 7.3 % (n = 22). This increase was totally blocked by preinfusion of Ba 2+ (plasma concentration ~25 μM, n = 10), which blocks inward rectifier K + (K ir ) channels. On the other hand, preinfusion of the Na + /K + ATPase inhibitor oubain (plasma concentration ~10 μM, n = 6) did not affect the K + induced renal vasodilation. The Ba 2+ and oubain infusions significantly lowered baseline RBF by 5.6 % (n = 23) and 2.6 % (n = 18), respectively. Intrarenal infusion of ACh (plasma concentration ~0.1 μM) significantly increased RBF by 13.9 % (n = 11). This response was unaffected by Ba 2+ or ouabain. The results indicate that the action of Kir channels and to a lesser extent Na+ /K + ATPase affects baseline RBF. The results also suggest that the K + induced vasodilation is mediated via stimulation of K ir channels and that K + is not mediating the ACh response. This study is supported by the Danish Medical Research Council and the Danish Heart Foundation.