Blood pressure, sodium intake, insulin resistance, and urinary nitrate excretion

Citation
Fs. Facchini et al., Blood pressure, sodium intake, insulin resistance, and urinary nitrate excretion, HYPERTENSIO, 33(4), 1999, pp. 1008-1012
Citations number
32
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
HYPERTENSION
ISSN journal
0194911X → ACNP
Volume
33
Issue
4
Year of publication
1999
Pages
1008 - 1012
Database
ISI
SICI code
0194-911X(199904)33:4<1008:BPSIIR>2.0.ZU;2-9
Abstract
The objective of this study was to investigate the relationships among vari ous humoral factors thought to be involved in the regulation of blood press ure during high NaCl intake. Nineteen healthy subjects underwent sequential 5-day periods ingesting a low-sodium (25 mmol/d) or high-sodium (200 mmol/ d) diet. Insulin resistance was assessed by the steady-state plasma glucose concentration at the end of a 3-hour insulin suppression test. Insulin res istance correlated inversely with natriuresis (P = 0.04) and directly with increase in weight (P = 0.03). The increase in mean arterial pressure assoc iated with the high-sodium diet correlated directly with the gain in weight (P < 0.05) and inversely with the increase in urinary nitrate excretion (P < 0.0001). In a multiple regression model, more than 2/3 of the variance i n mean arterial pressure was accounted for by the gain in weight and change in urinary nitrate excretion. The steady-state plasma glucose concentratio ns obtained with the 2 diets were similar, indicating that insulin resistan ce was unaffected by sodium intake. During high sodium intake, plasma renin activity and aldosterone decreased and plasma atrial natriuretic peptide i ncreased; these changes did not correlate with the change in mean arterial pressure, insulin resistance, or change in urinary nitrate excretion. To th e extent that urinary nitrate excretion reflects activity of the endogenous nitric oxide system, these results suggest that the salt sensitivity of me an arterial pressure may be related to blunted generation of endogenous nit ric oxide. The results also demonstrate that insulin-resistant individuals have an impaired natriuretic response to high sodium intake.