Tags

Type your tag names separated by a space and hit enter

Dietary salt intake exaggerates sympathetic reflexes and increases blood pressure variability in normotensive rats.
Hypertension. 2014 Sep; 64(3):583-9.H

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+Show Affiliations

From the Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey.From the Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey.From the Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey. sstocker@hmc.psu.edu.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24914195

Citation

Simmonds, Sarah S., et al. "Dietary Salt Intake Exaggerates Sympathetic Reflexes and Increases Blood Pressure Variability in Normotensive Rats." Hypertension (Dallas, Tex. : 1979), vol. 64, no. 3, 2014, pp. 583-9.
Simmonds SS, Lay J, Stocker SD. Dietary salt intake exaggerates sympathetic reflexes and increases blood pressure variability in normotensive rats. Hypertension. 2014;64(3):583-9.
Simmonds, S. S., Lay, J., & Stocker, S. D. (2014). Dietary salt intake exaggerates sympathetic reflexes and increases blood pressure variability in normotensive rats. Hypertension (Dallas, Tex. : 1979), 64(3), 583-9. https://doi.org/10.1161/HYPERTENSIONAHA.114.03250
Simmonds SS, Lay J, Stocker SD. Dietary Salt Intake Exaggerates Sympathetic Reflexes and Increases Blood Pressure Variability in Normotensive Rats. Hypertension. 2014;64(3):583-9. PubMed PMID: 24914195.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dietary salt intake exaggerates sympathetic reflexes and increases blood pressure variability in normotensive rats. AU - Simmonds,Sarah S, AU - Lay,Jennifer, AU - Stocker,Sean D, Y1 - 2014/06/09/ PY - 2014/6/11/entrez PY - 2014/6/11/pubmed PY - 2014/10/17/medline KW - blood pressure KW - brain KW - hypernatremia KW - sodium KW - sympathetic nervous system SP - 583 EP - 9 JF - Hypertension (Dallas, Tex. : 1979) JO - Hypertension VL - 64 IS - 3 N2 - 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. SN - 1524-4563 UR - https://www.unboundmedicine.com/medline/citation/24914195/Dietary_salt_intake_exaggerates_sympathetic_reflexes_and_increases_blood_pressure_variability_in_normotensive_rats_ L2 - http://www.ahajournals.org/doi/full/10.1161/HYPERTENSIONAHA.114.03250?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -