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The anti‐hypertensive response to renal denervation in aged SHR is independent of changes in body sodium (856.1)
Author(s) -
Phelps Jeremiah,
Fink Gregory
Publication year - 2014
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.28.1_supplement.856.1
Subject(s) - sodium , blood pressure , denervation , furosemide , endocrinology , medicine , chemistry , diuretic , organic chemistry
Since interruption of kidney functions influenced by renal sympathetic nerve activity (RSNA) may cause the fall in blood pressure (BP) after renal denervation (RDX), then the chronic anti‐hypertensive effect of RDX should be larger when RSNA is higher. RSNA is inversely related to body sodium content, so we hypothesized that the BP response to RDX in rats would be agreater during sodium depletion than during sodium loading. In male retired breeder spontaneously hypertensive rats (SHR) on a 0.1% sodium chloride (NaCl) diet, RDX chronically reduced BP by 10.6±2.5 mmHg whereas sham‐operation decreased BP by only 0.2±0.7 mmHg (a net difference (∆) of ‐10.4 mmHg). Additional sodium depletion with chlorthalidone lowered BP modestly in both groups but did not accentuate the effect of RDX (∆ = ‐10.0 mmHg.). Similar findings were noted with more aggressive sodium depletion with furosemide (∆ = ‐7.5 mmHg). Furthermore, the BP response to RDX was not mitigated when rats were taken off drug treatment and placed on a 0.4% NaCl diet (∆ = ‐10.1 mmHg), or when additional sodium loading was achieved by adding 1% NaCl to the drinking water (∆ = ‐13.4 mmHg). Finally, the BP effect of RDX remained when the animals were returned to drinking water only (∆ = ‐15.5 mmHg). These data suggest that the magnitude of the sustained BP response to RDX in this experimental model is not directly related to body sodium content or the level of RSNA.