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The adrenergic regulation of proximal tubular Na + /H + exchanger 3 in the rat
Author(s) -
Healy V.,
Thompson C.,
Johns E. J.
Publication year - 2014
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/apha.12181
Subject(s) - natriuresis , medicine , endocrinology , chemistry , reabsorption , stimulation , diuresis , prazosin , denervation , phenylephrine , kidney , tubular fluid , antagonist , receptor , blood pressure
Aim This study in the anaesthetized rat investigated how renal sympathetic nerve activity and catecholamine release influenced NHE 3 abundance and activity in proximal tubular brush border membranes using both in vivo and in vitro approaches. Methods Renal excretory function and brush border NHE 3 abundance and activity were measured in rat kidneys which underwent renal denervation, renal nerve electrical stimulation and renal infusion of phenylephrine and the NHE 3 inhibitor S1661. NHE 3 activity and cell surface abundance were also measured in primary cultures of proximal tubular cells treated with noradrenaline and prazosin. Results Acute renal denervation caused a natriuresis and diuresis, which occurred with a reduction in NHE 3 abundance and activity in the brush border membranes. By contrast, low‐level electrical stimulation of the renal innervation causing an antinatriuresis and antidiuresis increased NHE 3 activity in the brush border membranes. Intrarenal infusion of phenylephrine caused an antinatriuresis and antidiuresis, while blockade of NHE 3 activity, using local infusion of the blocker S1661, caused a natriuresis and diuresis. Exposure of primary cultures of proximal tubular cells to noradrenaline increased brush border NHE 3 abundance and activity which was blocked by prior exposure to prazosin, indicating it as an α 1 ‐adrenoceptor‐mediated mechanism. Conclusion Together, these findings demonstrate that the renal sympathetic nerves not only have a direct action to modulate tubular sodium reabsorption via stimulation of the NHE transporter, but also have an indirect effect, whereby NHE 3 abundance is increased within the brush border membrane, thereby increasing the capacity for fluid reabsorption.