Abstract 527: Natriuretic Effect Mediated by the Renal Medullary α7 Nicotinic Acetylcholine Receptor
Although there are extensive studies on the regulation of renal sodium excretion by adrenergic pathway, the role of cholinergic pathway in the renal sodium excretion is largely unknown. The present study characterized the expression of α7 nicotinic acetylcholine receptor (nAChR) in the kidneys and determined the functional role of this nAChR subtype in urinary sodium excretion in Sprague Dawley rats. RT-PCR and Western blot analyses showed that α7 nAChR was present in the kidneys. Immunohistochemistry analysis demonstrated that the strongest immunostaining of α7 nAChR was observed in the distal tubules and collecting ducts in the kidneys. Infusion of an α7 nAChR agonist PNU-282987 (2.7 μM, 10 μl/min) into the renal medulla dramatically increased the urine volume (from 15.4 ± 2.1 to 42.5 ± 3.9 μl/min/g kwt) and sodium excretion (from 1.26 ± 0.18 to 4.15 ± 0.60 μmole/min/g kwt), which was blocked by an α7 nAChR antagonist methyllycaconitine (MLA, 5 μM, 10 μl/min), in anesthetized rats. Infusion of PNU-282987 did not cause any change in renal medullary blood flow as measured by Laser Doppler flowmeter. In addition, intra-renal medullary infusion of MLA (5 μM, 10 μl/min) significantly inhibited the volume expansion-induced increase of urine volume and sodium excretion by 25%. These data suggest that activation of renal medullary α7 nAChR produces a natriuretic effect through its tubular action in rats. (Supported by NIH grant HL89563 and HL106042)
Author Disclosures: W. Wang: None. W. Han: None. Q. Zhu: None. I. Damaj: None. P. Li: None. N. Li: None.
- © 2014 by American Heart Association, Inc.