title: Dietary salt intake exaggerates sympathetic reflexes and increases blood pressure variability in normotensive rats.
abstract: Previous studies have reported that chronic increases in dietary salt intake enhance sympathetic nerve activity and arterial blood pressure (ABP) responses evoked from brain stem nuclei of normotensive, salt-resistant rats. The purpose of the present study was to determine whether this sensitization results in exaggerated sympathetic nerve activity and ABP responses during activation of various cardiovascular reflexes and also increases ABP variability. Male Sprague-Dawley rats were fed 0.1% NaCl chow (low), 0.5% NaCl chow (medium), 4.0% NaCl chow (high) for 14 to 17 days. Then, the animals were prepared for recordings of lumbar, renal, and splanchnic sympathetic nerve activity and ABP. The level of dietary salt intake directly correlated with the magnitude of sympathetic nerve activity and ABP responses to electrical stimulation of sciatic afferents or intracerebroventricular infusion of 0.6 mol/L or 1.0 mol/L NaCl. Similarly, there was a direct correlation between the level of dietary salt intake and the sympathoinhibitory responses produced by acute volume expansion and stimulation of the aortic depressor nerve or cervical vagal afferents. In contrast, dietary salt intake did not affect the sympathetic and ABP responses to chemoreflex activation produced by hypoxia or hypercapnia. Chronic lesion of the anteroventral third ventricle region eliminated the ability of dietary salt intake to modulate these cardiovascular reflexes. Finally, rats chronically instrumented with telemetry units indicate that increased dietary salt intake elevated blood pressure variability but not mean ABP. These findings indicate that dietary salt intake works through the forebrain hypothalamus to modulate various centrally mediated cardiovascular reflexes and increase blood pressure variability.
authors.affiliation: From the Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey.
authors.forename: Sarah S
authors.initials: SS
authors.lastname: Simmonds
authors.affiliation: From the Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey.
authors.forename: Jennifer
authors.initials: J
authors.lastname: Lay
authors.affiliation: From the Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey. sstocker@hmc.psu.edu.
authors.forename: Sean D
authors.initials: SD
authors.lastname: Stocker
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D001933:Brain Stem / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D008297:Male; D023421:Models, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D012018:Reflex / Q000187:drug effects* / Q000502:physiology; D017673:Sodium Chloride, Dietary / Q000494:pharmacology*; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000502:physiology; D020542:Third Ventricle / Q000187:drug effects / Q000502:physiology
chemical_list: D017673:Sodium Chloride, Dietary
keywords: blood pressure; brain; hypernatremia; sodium; sympathetic nervous system