Document Detail


Baroreflex impairment by low sodium diet in mild or moderate essential hypertension.
MedLine Citation:
PMID:  9052899     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Low sodium intake is the most widely used nonpharmacological approach to the treatment of hypertension. Although nonpharmacological treatment is by definition regarded as safe, the suggestion has been made that low sodium intake is not totally devoid of inconveniences, and animal data have shown it to be accompanied by an impairment of reflex blood pressure control and homeostasis. However, no data exist on this issue in humans. In mild essential hypertensive patients (age, 34.1+/-3.3 years [mean+/-SEM]), we measured beat-to-beat arterial blood pressure (finger photoplethysmographic device), heart rate (electrocardiogram), and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during baroreceptor stimulation and deactivation, induced by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. Measurements were performed at the end of three dietary periods, ie, after 8 days of regular sodium intake (210 mmol NaCl/d), low sodium intake (20 mmol NaCl/d) with unchanged potassium intake, and again regular sodium intake. Compared with the initial regular sodium diet, low sodium intake reduced urinary sodium excretion, whereas urinary potassium excretion was unchanged. Systolic blood pressure was significantly (P<.05), although slightly, reduced, whereas diastolic blood pressure was unaffected. Muscle sympathetic nerve activity was increased by 23.1+/-5.2% (P<.05). The increase was accompanied by a clear-cut impairment of the baroreceptor ability to modulate muscle sympathetic nerve activity, ie, by a 43.9+/-5.7% (P<.01) reduction in the sensitivity of the baroreceptor-muscle sympathetic nerve activity reflex compared with the control condition. Baroreceptor modulation of heart rate was also impaired, although to a smaller and less consistent extent. When regular sodium intake was restored, all the above-mentioned parameters and baroreflex responses returned to the values observed at the initial regular sodium diet. These data raise evidence that in humans sodium restriction may impair the arterial baroreflex. This may be responsible for the sympathetic activation occurring in this condition and for the impairment of blood pressure homeostasis.
Authors:
G Grassi; B M Cattaneo; G Seravalle; A Lanfranchi; G Bolla; G Mancia
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Publication Detail:
Type:  Clinical Trial; Comparative Study; Controlled Clinical Trial; Journal Article    
Journal Detail:
Title:  Hypertension     Volume:  29     ISSN:  0194-911X     ISO Abbreviation:  Hypertension     Publication Date:  1997 Mar 
Date Detail:
Created Date:  1997-03-26     Completed Date:  1997-03-26     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  802-7     Citation Subset:  IM    
Affiliation:
Cattedra di Medicina Interna, Ospedale S. Gerardo, Monza, Universita di Milano, Milan, Italy.
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MeSH Terms
Descriptor/Qualifier:
Adult
Antihypertensive Agents / pharmacology
Baroreflex / drug effects*
Blood Pressure / drug effects
Cardiotonic Agents / pharmacology
Dose-Response Relationship, Drug
Electrolytes / blood,  urine
Heart Rate / drug effects
Humans
Hypertension / diet therapy*
Male
Middle Aged
Nitroprusside / pharmacology
Phenylephrine / pharmacology
Renin / blood
Sodium, Dietary / administration & dosage,  adverse effects*,  therapeutic use*
Chemical
Reg. No./Substance:
0/Antihypertensive Agents; 0/Cardiotonic Agents; 0/Electrolytes; 0/Sodium, Dietary; 15078-28-1/Nitroprusside; 59-42-7/Phenylephrine; EC 3.4.23.15/Renin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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