Effects of sodium salts on pressor reactivity in salt-sensitive men.

Abstract

Blood pressure in patients with essential hypertension is raised by sodium chloride but not by nonchloride sodium salts. Although a high sodium chloride diet is known to augment the pressor response to norepinephrine and angiotensin II, the effect of nonchloride sodium salts on pressor responsiveness has not been studied so far. To examine whether sodium chloride and nonchloride sodium salts evoke different pressor responses to these agonists, we performed graded norepinephrine and angiotensin II infusions in salt-sensitive (u=7) and salt-resistant (it=8) normotensive subjects. The subjects were given a low salt diet (20 mmol/day) for 3 weeks, to which a supplement of 200 mmol sodium per day, provided as either sodium chloride or sodium citrate, or a placebo was added for 1 week each. We found that, although sodium chloride raised mean arterial blood pressure in the salt-sensitive subjects (p<0.005), sodium citrate did not However, under both sodium salts pressor response to norepinephrine and angiotensin II was significantly greater than under placebo (p<0.02). Furthermore, with both sodium salts, pressor response in the salt-sensitive subjects was greater than in the salt-resistant subjects (p<0.01). This study thus demonstrates that, although blood pressure in salt-sensitive individuals is raised by sodium chloride only, both sodium chloride and sodium citrate evoke similar increases in pressor response to norepinephrine and angiotensin H. Since pressor response increased with both sodium salts but resting blood pressure increased only with sodium chloride, enhanced pressor responsiveness alone cannot account for the sodium chloride-induced rise in resting blood pressure. (Hypertension 1992;l<h541-548) KEY WORDS • salt-sensitive hypertension • sodium chloride • catecholamines • vascular reactivity • renin-angiotensin-aldosterone system A enhanced pressor response to endogenous vasoactive substances including norepinephrine and angiotensin II has been found in patients with essential hypertension 1 -12 and in genetically predisposed normotensive subjects, 111314 and this response has been assumed to play a major role in the pathogenesis of essential hypertension. A high dietary sodium chloride intake increases the pressor response to both norepinephrine 15 and angiotensin II, 16 and this could contribute to the salt-induced blood pressure rise in salt-sensitive individuals. Although the blood pressureraising effect of salt has previously been thought to be mediated by the sodium ion alone, increasing evidence indicates that it depends on the administration of both sodium and chloride (see Reference 17 for review). Thus, in patients with essential hypertension, a blood pressure rise was induced by the administration of sodium chloride as a supplement to a low salt diet but not by comparable amounts of sodium provided as either the bicarbonate, 18 -19 citrate, 20 or phosphate 21 salt. Whether this difference between the blood pressure effects of sodium chloride and nonchloride sodium salts is due to their evoki...

The influence of the ACE (I/D) polymorphism on systemic and renal vascular responses to angiotensins in normotensive, normoalbuminuric Type 1 diabetes mellitus

“…Our data show that the magnitude of the AngI and AngII responses was larger during liberal sodium intake as an independent variable in the multiple regression analysis. This is in accord with similar findings in normal subjects, and has been attributed to up-regulation of the sensitivity of AngII receptors during high sodium intake [25,26,27]. On multivariate analysis we found that sodium intake also modified the effect of ACE genotype on AngI response, independent from AngII response.…”

Hemodynamic and Autonomic Response to Different Salt Intakes in Normotensive Individuals

“…However, we also showed that during low‐salt diet the SS‐Index is positively associated with cardiac output and arterial compliance and negatively associated with SVR and characteristic impedance, suggesting a residual positive salt balance in SS subjects during salt depletion and giving support to Guyton's physiology. We may also hypothesize a role played by altered modulations of the renin–angiotensin–aldosterone system or of the sympathetic nervous system, reported to occur in hypertensive SS individuals 3, 27. However, studies in normotensive humans revealed that an increased dietary salt intake (5–7 days of high‐salt regimen) induces a profound reduction in vascular nitric oxide bioavailability, which limits endothelium‐dependent vasodilation 28, 29.…”

Effects of Vitamin C on High Blood Pressure Induced by Salt in Spontaneously Hypertensive Rats

“…Moreover, the simultaneous absorption of halogen ions like Cl-or I-with Na+ has been shown to potentiate hypertension (20). For the prevention and medical treatment of hypertension, it has been generally accepted that limiting the dietary salt intake in daily life is important (25). On the other hand, a relationship between hypertension and vitamin C has been recently discovered.…”

“…It has recently been proposed that the difference in the sensitivity to salt is caused by multiple genetic patterns (24). It has been studied whether or not Na+ or Cl-ions are mainly responsible for high blood pressure (25). There have been two different discussions regarding the effects of salt and vitamin C on the increment or sup pression of high blood pressure.…”