Fluid, Ionic and Hormonal Changes Induced by High Salt Intake in Salt-Sensitive and Salt-Resistant Hypertensive Patients

Abstract

1. The aim of the study was to detect differences between salt-sensitive and salt-resistant hypertensive patients in the response of the renin—aldosterone axis, plasma noradrenaline and atrial natriuretic peptide to high salt intake. 2. Fifty essential hypertensive patients followed 2 weeks of a standard diet with 20 mmol of NaCl daily, supplemented by placebo tablets for the first 7 days and by NaCl tablets for the last 7 days, in a single-blind fashion. Salt sensitivity was defined as a significant rise (P < 0.05) in 24 h mean blood pressure obtained by ambulatory blood pressure monitoring from the low- to the high-salt period. Biochemical and hormonal measurements were performed on the last day of both periods. 3. Twenty-two (44%) patients fulfilled criteria of salt-sensitive hypertension, whereas the remaining 28 (56%) were considered salt-resistant. High salt intake promoted a significant decrease (P < 0.05) in plasma creatinine, potassium, glucose, cholesterol, low-density lipoprotein-cholesterol, triacylglycerols, uric acid and plasma renin activity, and a significant increase in plasma atrial natriuretic peptide and 24 h urinary calcium excretion. The direction of these changes did not differ between salt-sensitive and salt-resistant patients. Salt-resistant hypertensive patients exhibited a significant decrease in plasma aldosterone induced by high salt intake (from 446 ∓ 35 to 226 ± 35 pmol/l; P < 0.001), whereas this parameter was not significantly modified in salt-sensitive patients (from 485 ± 76 to 364 ± 83 pmol/l; P not significant). Salt-sensitive patients showed an increase in plasma noradrenaline after high salt intake (from 1.15 ± 0.11 to 1.56 ± 0.14 nmol/l; P < 0.05), whereas salt-resistant patients presented a decrease in this parameter (from 1.48 ± 0.08 to 1.12 ± 0.08 nmol/l; P < 0.05). The change in plasma noradrenaline was directly correlated with the change in mean blood pressure induced by high salt intake (r = 0.479; P = 0.003). 4. We conclude that the increase in blood pressure induced by high salt intake in salt-sensitive patients is associated with a stimulation of the sympathetic nervous system and a blunted decrease in plasma aldosterone. Conversely, changes in renal function, electrolyte excretion and plasma concentrations of atrial natriuretic peptide induced by high salt intake seem to be similar in both salt-sensitive and salt-resistant patients.

Single-Nucleotide Polymorphisms for Diagnosis of Salt-Sensitive Hypertension

“…This profile in SS patients is in keeping with decreased D 1 R-mediated inhibition of renal sodium transport and sodium and fluid retention in SS hypertension (13,15 ). However, our findings and those of others indicate that low specificity precludes the use of PRA concentrations as an effective way to distinguish SS from SR individuals (2,11,12 ).…”

Interaction of Angiotensin I-Converting Enzyme Insertion-Deletion Polymorphism and Daily Salt Intake Influences Hypertension in Japanese Men

“…Giner et al (24) and Poch et al (25) reported the same tendency in Spanish hypertensives, and further demonstrated that patients with the ID+II genotype had a significantly greater blood pressure rise during high salt diet load than patients with the DD genotype. This salt sensitivity is partially explained by blunted RAAS response to high salt intake (48). It can be speculated that the ID+II genotype may lead to a decreased response to high salt intake, and thus the effects of a high salt diet may not be suppressed as efficiently as in patients with the DD genotype.…”

Renin-Angiotensin System Genetic Polymorphisms and Salt Sensitivity in Essential Hypertension

“…9 Moreover, the RAS response to high salt intake is blunted in salt-sensitive subjects and is inversely correlated with the BP response. 10 Thus it is logical to suppose that salt-sensitive hypertensive patients may differ in genotypes encoding the different steps of the RAS cascade.…”

“…Low-renin hypertensives show an increased BP response to NaCl load, 9 and salt-sensitive individuals exhibit a blunted response of the RAS when they switch from low to high salt intake compared with salt-resistant subjects. 10 Moreover, plasma levels of ACE and angiotensinogen differ in subjects with different ACE and angiotensinogen genotypes. 11,12 The relation between ACE gene polymorphism and salt sensitivity has been tested in 2 Japanese hypertensive groups, with controversial results.…”