title: Aldosterone and Salt Loading Independently Exacerbate the Exercise Pressor Reflex in Rats.
abstract: The sympathetic and pressor responses to exercise are exaggerated in hypertension. Evidence suggests that an overactive exercise pressor reflex (EPR) contributes to this abnormal responsiveness. The mechanisms underlying this EPR overactivity are poorly understood. An increasing body of evidence suggests that aldosterone and excessive salt intake play a role in regulating resting sympathetic activity and blood pressure in hypertension. Therefore, each is a good candidate for the generation of EPR dysfunction in this disease. The purpose of this study was to examine whether excessive salt intake and chronic administration of aldosterone potentiate EPR function. Changes in mean arterial pressure and renal sympathetic nerve activity induced by EPR stimulation were examined in vehicle and aldosterone-treated (4 weeks via osmotic mini-pump) Sprague-Dawley rats given either water or saline (elevated salt load) to drink. When compared with vehicle/water-treated rats, stimulation of the EPR by muscle contraction evoked significantly greater increases in mean arterial pressure in vehicle/saline, aldosterone/water, and aldosterone/saline-treated animals (14±3, 29±3, 37±6, and 44±7 mm Hg/kg, respectively; P<0.01). A similar renal sympathetic nerve activity response profile was likewise produced (39±11%, 87±15%, 110±20%, and 151±25%/kg, respectively; P<0.01). The pressor and sympathetic responses to the individual activation of the mechanically and chemically sensitive components of the EPR were also augmented by both saline and aldosterone. These data provide the first direct evidence that both aldosterone and high salt intake elicit EPR overactivity. As such, each represents a potential mechanism by which sympathetic activity and blood pressure are augmented during exercise in hypertension.
authors.affiliation: From the Departments of Health Care Sciences (M.M., S.A.S.) and Internal Medicine (M.M., R.M.D., J.H.M., S.A.S., W.V.) and Hypertension Section, Cardiology Division (W.V.), University of Texas Southwestern Medical Center, Dallas; and Department of Internal Medicine, University of Michigan Medical School, Ann Arbor (R.J.A.).
authors.forename: Masaki
authors.initials: M
authors.lastname: Mizuno
authors.affiliation: From the Departments of Health Care Sciences (M.M., S.A.S.) and Internal Medicine (M.M., R.M.D., J.H.M., S.A.S., W.V.) and Hypertension Section, Cardiology Division (W.V.), University of Texas Southwestern Medical Center, Dallas; and Department of Internal Medicine, University of Michigan Medical School, Ann Arbor (R.J.A.).
authors.forename: Ryan M
authors.initials: RM
authors.lastname: Downey
authors.affiliation: From the Departments of Health Care Sciences (M.M., S.A.S.) and Internal Medicine (M.M., R.M.D., J.H.M., S.A.S., W.V.) and Hypertension Section, Cardiology Division (W.V.), University of Texas Southwestern Medical Center, Dallas; and Department of Internal Medicine, University of Michigan Medical School, Ann Arbor (R.J.A.).
authors.forename: Jere H
authors.initials: JH
authors.lastname: Mitchell
authors.affiliation: From the Departments of Health Care Sciences (M.M., S.A.S.) and Internal Medicine (M.M., R.M.D., J.H.M., S.A.S., W.V.) and Hypertension Section, Cardiology Division (W.V.), University of Texas Southwestern Medical Center, Dallas; and Department of Internal Medicine, University of Michigan Medical School, Ann Arbor (R.J.A.).
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Auchus
authors.affiliation: From the Departments of Health Care Sciences (M.M., S.A.S.) and Internal Medicine (M.M., R.M.D., J.H.M., S.A.S., W.V.) and Hypertension Section, Cardiology Division (W.V.), University of Texas Southwestern Medical Center, Dallas; and Department of Internal Medicine, University of Michigan Medical School, Ann Arbor (R.J.A.).
authors.forename: Scott A
authors.initials: SA
authors.lastname: Smith
authors.affiliation: From the Departments of Health Care Sciences (M.M., S.A.S.) and Internal Medicine (M.M., R.M.D., J.H.M., S.A.S., W.V.) and Hypertension Section, Cardiology Division (W.V.), University of Texas Southwestern Medical Center, Dallas; and Department of Internal Medicine, University of Michigan Medical School, Ann Arbor (R.J.A.). wanpen.vongpatanasin@utsouthwestern.edu.
authors.forename: Wanpen
authors.initials: W
authors.lastname: Vongpatanasin
mesh_terms: D000450:Aldosterone / Q000494:pharmacology*; D000818:Animals; D017704:Baroreflex / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects*; D006339:Heart Rate / Q000187:drug effects; D007668:Kidney / Q000187:drug effects; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D010805:Physical Conditioning, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D012018:Reflex / Q000187:drug effects*; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage*; D013564:Sympathetic Nervous System / Q000187:drug effects*
chemical_list: D017673:Sodium Chloride, Dietary; D000450:Aldosterone
keywords: aldosterone; exercise; hypertension; salt; sympathetic nervous system