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High inorganic phosphate diet augments the sympathetic response to exercise pressor reflex activation in rats
Author(s) -
Mizuno Masaki,
Crawford Scott,
Carnahan Cooper,
Mitchell Jere H,
Smith Scott A,
Vongpatanasin Wanpen
Publication year - 2016
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.30.1_supplement.1006.1
Subject(s) - endocrinology , medicine , reflex , stimulation , excretion , sympathetic nervous system , blood pressure , phosphate , chemistry , inorganic phosphate , contraction (grammar) , biochemistry
Inorganic phosphates are widely used in the food industry as preservatives, flavor enhancers, and color stabilizers. Evidence suggests high inorganic phosphate (Pi) diets induce hypertension in normal rats. Whether alterations in sympathetic function contribute to this manifestation of high blood pressure is unknown. Accordingly, we measured changes in renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) during stimulation of the muscle exercise pressor reflex (EPR) in decerebrated Sprague‐Dawley rats fed a normal (0.6%) or high (1.2%) Pi diet for 12 weeks. Compared to normal Pi diet‐fed rats, a high Pi diet significantly increased 24‐hour urine excretion of phosphate (12±1 vs. 77±5 mg/day, P<0.05 ) as well as resting MAP (94±5 vs. 120±5 mmHg, P<0.05 ). There were no differences in sodium and potassium excretion between groups. Comparing control rats to those fed a high Pi diet, contraction‐induced stimulation of the EPR evoked significantly greater increases in RSNA (Δ = 46±9 vs. 126±25 %, P<0.05 ) and MAP (Δ = 14±2 vs. 44±5 mmHg, P<0.05 ) in rats fed a 1.2% Pi diet. The data provide the first evidence that excess phosphorus intake induces sympathetic overactivity in response to EPR activation. This finding suggests that the high dietary Pi commonly observed in the normal American diet may lead to sympathetic dysfunction contributing to the pathogenesis of hypertension. Support or Funding Information Supported by NIH HL‐113738