Abstract

This paper reviews the evidence that salt sensitivity of blood pressure is related both to the anion ingested with sodium as well as to other components of the diet.

In several experimental models of salt-sensitive hypertension and in humans, blood pressure is not increased by a high sodium intake provided with anions other than chloride. Salt-induced increase of blood pressure depends on the concomitant ingestion of both sodium and chloride.

Both epidemiologic and clinical evidence suggest that sodium chloride-induced increases of blood pressure are augmented by diets deficient in potassium or calcium. In experimental animals, a high intake of simple carbohydrates also augments sodium chloride sensitivity of blood pressure.

These observations indicate that the effect of dietary sodium on blood pressure is modulated by other components of the diet.

PMID: 9022570 [PubMed - indexed for MEDLINE]

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Abstract

It is clear that salt is known to be a health hazard from the ancient times. Sodium intake, which was minimal during evolution, increased significantly with the civilization. The rise in prevalence of hypertension in populations with increased consumption of salt suggested a casual relationship. However, several of these studies showed conflicting results.

Many investigators agree that salt-sensitive persons often have a family history of hypertension. Such individuals possess a sodium transport inhibitor in the arterial smooth muscle cells, which affects their sodium handling (as compared to other persons).

However, many of the putative defects related to sodium can be dissociated from blood pressure and sodium consumption status. It is possible that calcium defects of deficiency of potassium and magnesium follow hypertension and sodium status. For example, the pressure response to sodium chloride may be dissociated from sodium, which may be secondary to adverse effects of chloride on calcium homeostasis. Clinical studies also indicate that the role of sodium is controversial in hypertension.

Sodium restriction can benefit salt-sensitive persons and might not otherwise. However, most authorities believe that moderation of salt intake to a relevant extent is justifiable.

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Abstract

Dietary combination of high salt with low potassium (HSLK) exacerbates hypertension development in Dahl salt-sensitive (S) rats, and produces a mild degree of hypertension in otherwise salt-resistant (R) rats. Increased blood pressure in both strains is associated with increased urinary excretion of calcium and magnesium. The objective of this study was to determine the effect of blood pressure on body balance of these ions in Dahl rats on HSLK diet. Two groups of S and two groups of R weanlings were all placed on HSLK diet (NaCl=8%, K=0.2%) for eight weeks. One group of each strain was subjected to chemical sympathectomy with 6-hydroxydopamine (6-OHDA) to counteract hypertension development. Urinary norepinephrine was used to determine efficacy of 6-OHDA treatment. Systolic blood pressures of conscious animals were measured daily throughout the study. The last three days on the diet were used to determine total dietary intake and urinary as well as fecal excretion of sodium, calcium and magnesium. At the end of the study, extracellular fluid volume, serum aldosterone and parathyroid hormone were analyzed. Final systolic blood pressures in the 4 groups were as follows: S=235+/-9 mmHg (n=9); R=155+/-3 mmHg (n=8); 6-OHDA S=151+/-6 mm Hg (n=8); 6-OHDA R=117+/-6 mm Hg. Chemical sympathectomy decreased blood pressure in both S and R rats. There was no indication of sodium accumulation in S rats. Associated with reduced parathyroid hormone levels the S strain had significantly less positive balance for calcium than the R strain, primarily due to increased urinary excretion. A less positive balance for magnesium was also observed, due mainly to relatively reduced intestinal absorption of the ion. We conclude that the HSLK diet is associated with inappropriate activation of the sympathetic nervous system and increased arterial pressure in both strains. In addition, since divalent cations may influence blood pressure, we suggest that the observed abnormalities in calcium and magnesium metabolism might independently promote hypertension development in the S strain.

Clin Exp Hypertens. 1995 Aug;17(6):989-1008.

Potassium depletion and salt-sensitive hypertension in Dahl rats: effect on calcium, magnesium, and phosphate excretions.

Wu X, Ackermann U, Sonnenberg H.

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