Myocardial Hypertrophy: The Effect of Sodium and the Role of Sympathetic Nervous System Activity
Autor: | Leonard G. Meggs, Alvin I. Goodman, Jackie Ben-Ari, Donald Gammon |
---|---|
Rok vydání: | 1988 |
Předmět: |
Male
medicine.medical_specialty Sympathetic nervous system Sympathetic Nervous System Neuroeffector Sodium medicine.medical_treatment Alpha (ethology) chemistry.chemical_element Blood Pressure Cardiomegaly Baroreflex Iodine Radioisotopes Norepinephrine Internal medicine Internal Medicine medicine Animals Desoxycorticosterone Saline business.industry Myocardium Rats Inbred Strains Sodium Dietary Organ Size Receptors Adrenergic alpha Rats medicine.anatomical_structure Endocrinology chemistry Hypertension business Homeostasis medicine.drug |
Zdroj: | American Journal of Hypertension. 1:11-15 |
ISSN: | 1941-7225 0895-7061 |
DOI: | 10.1093/ajh/1.1.11 |
Popis: | Dietary sodium and the myocardial alpha 1-receptor have been implicated in the hypertrophic response of myocardial tissue. Alterations in sodium homeostasis have been demonstrated to influence sympathetic nervous function, centrally and peripherally. In this investigation, we have examined the effect of dietary sodium on the development of myocardial hypertrophy; and the role of sympathetic neuroeffector mechanisms in the hypertrophic response. Studies were performed in three groups of uninephrectomized rats: A-regular diet; B-1% saline/regular diet; C-1% Saline/doca/regular diet. Groups A and B did not develop systemic hypertension (SHT). Saline treatment increased heart weight and the density of surface alpha 1-receptors; myocardial norepinephrine (NE) was reduced. Group C developed SHT. Heart weight was greatest in Group C; and myocardial NE was severely depleted. Downregulation of myocardial alpha 1-receptors, a finding consistent with the hyperadrenergic state, was observed in Group C. Our results suggest dietary sodium may modulate hypertrophic response in myocardial tissue, by altering sympathetic neuroeffector mechanisms. |
Databáze: | OpenAIRE |
Externí odkaz: |