High dietary phosphate intake induces hypertension and augments exercise pressor reflex function in rats

Masaki Mizuno; Jere H Mitchell; Scott Crawford; Chou-Long Huang; Naim Maalouf; Ming-Chang Hu; Orson W Moe; Scott A Smith; Wanpen Vongpatanasin

doi:10.1152/ajpregu.00124.2016

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High dietary phosphate intake induces hypertension and augments exercise pressor reflex function in rats

Journal article

Open access

Peer reviewed

High dietary phosphate intake induces hypertension and augments exercise pressor reflex function in rats

Masaki Mizuno, Jere H Mitchell, Scott Crawford, Chou-Long Huang, Naim Maalouf, Ming-Chang Hu, Orson W Moe, Scott A Smith and Wanpen Vongpatanasin

American journal of physiology. Regulatory, integrative and comparative physiology, Vol.311(1), pp.R39-R48

07/01/2016

DOI: 10.1152/ajpregu.00124.2016

PMCID: PMC4967233

PMID: 27170660

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Abstract

An increasing number of studies have linked high dietary phosphate (Pi) intake to hypertension. It is well established that the rise in sympathetic nerve activity (SNA) and blood pressure (BP) during physical exertion is exaggerated in many forms of hypertension, which are primarily mediated by an overactive skeletal muscle exercise pressor reflex (EPR). However, it remains unknown whether high dietary Pi intake potentiates the EPR-mediated SNA and BP response to exercise. Accordingly, we measured renal SNA (RSNA) and mean BP (MBP) in normotensive Sprague-Dawley rats fed a normal Pi diet (0.6%, n = 13) or high Pi diet (1.2%, n = 13) for 3 mo. As previously reported, we found that resting BP was significantly increased by 1.2% Pi diet in both conscious and anesthetized animals. Activation of the EPR by electrically induced hindlimb contraction triggered greater increases in ΔRSNA and ΔMBP in the 1.2% compared with 0.6% Pi group (126 ± 25 vs. 42 ± 9%; 44 ± 5 vs. 14 ± 2 mmHg, respectively, P < 0.01). Activation of the muscle mechanoreflex, a component of the EPR, by passively stretching hindlimb muscle also evoked greater increases in ΔRSNA and ΔMBP in the 1.2% compared with 0.6% Pi group (109 ± 27 vs. 24 ± 7%, 38 ± 7 vs. 8 ± 2 mmHg, respectively, P < 0.01). A similar response was produced by hindlimb intra-arterial capsaicin administration to stimulate the metaboreflex arm of the EPR. Thus, our data demonstrate a novel action of dietary Pi loading in augmenting EPR function through overactivation of both the muscle mechanoreflex and metaboreflex.

Kidney - drug effects

Capsaicin - pharmacology

Sympathetic Nervous System - drug effects

Rats

Physical Exertion - drug effects

Rats, Sprague-Dawley

Baroreflex - drug effects

Heart Rate - drug effects

Animals

Diet

Muscle Contraction - drug effects

Hypertension - chemically induced

Muscle, Skeletal - drug effects

Phosphates - blood

Hindlimb - drug effects

Kidney - innervation

Blood Pressure - drug effects

Phosphates - toxicity

Details

Title: Subtitle: High dietary phosphate intake induces hypertension and augments exercise pressor reflex function in rats
Creators: Masaki Mizuno - Department of Health Care Sciences, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas; Cardiology Division, University of Texas Southwestern Medical Center, Dallas, Texas
Jere H Mitchell - Cardiology Division, University of Texas Southwestern Medical Center, Dallas, Texas
Scott Crawford - Department of Health Care Sciences, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas
Chou-Long Huang - Nephrology Division, University of Texas Southwestern Medical Center, Dallas, Texas; Charles and Jane Pak Center of Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas
Naim Maalouf - Mineral Metabolism Division, University of Texas Southwestern Medical Center, Dallas, Texas; and Charles and Jane Pak Center of Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas
Ming-Chang Hu - Mineral Metabolism Division, University of Texas Southwestern Medical Center, Dallas, Texas; and Charles and Jane Pak Center of Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas
Orson W Moe - Nephrology Division, University of Texas Southwestern Medical Center, Dallas, Texas; Charles and Jane Pak Center of Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas
Scott A Smith - Department of Health Care Sciences, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas; Cardiology Division, University of Texas Southwestern Medical Center, Dallas, Texas
Wanpen Vongpatanasin - Cardiology Division, University of Texas Southwestern Medical Center, Dallas, Texas; Hypertension Section, University of Texas Southwestern Medical Center, Dallas, Texas; Charles and Jane Pak Center of Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas wanpen.vongpatanasin@utsouthwestern.edu
Resource Type: Journal article
Publication Details: American journal of physiology. Regulatory, integrative and comparative physiology, Vol.311(1), pp.R39-R48
DOI: 10.1152/ajpregu.00124.2016
PMID: 27170660
PMCID: PMC4967233
NLM abbreviation: Am J Physiol Regul Integr Comp Physiol
ISSN: 0363-6119
eISSN: 1522-1490
Grant note: R01 DK100605 / NIDDK NIH HHS R01 DK092461 / NIDDK NIH HHS P30 DK079328 / NIDDK NIH HHS
Language: English
Date published: 07/01/2016
Academic Unit: Nephrology; Internal Medicine
Record Identifier: 9984094318302771

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