(Hypertension. 2001;37:444.)
© 2001 American Heart Association, Inc.
Scientific Contributions |
Endothelial Dysfunction in Salt-Sensitive Essential Hypertension
From the Hypertension Unit, Department of Internal Medicine, Institut d’Investigacions Biomèdiques August Pi i Sunyer, Hospital Clínic, Barcelona, Spain.
Correspondence to Alejandro de la Sierra, MD, Hypertension Unit, Department of Internal Medicine, Hospital Clínic Barcelona, Villarroel 170, 08036-Barcelona, Spain. E-mail asierra{at}clinic.ub.es
The aim of this study was to evaluate endothelium-dependent and -independent vasodilation, as well as endothelium biochemical markers, in a group of essential hypertensive patients classified on the basis of salt sensitivity. Changes in forearm blood flow in response to acetylcholine, sodium nitroprusside, and NG-monomethyl-L-arginine (L-NMMA) infusion were determined by means of strain-gauge plethysmography. Moreover, plasma and urinary concentrations of nitrates, cGMP, and endothelin were measured during low (50 mmol/d) and high (250 mmol/d) salt intake. Salt-sensitive hypertension was diagnosed in 26 patients who exhibited a significant increase in 24-hour mean blood pressure assessed by ambulatory blood pressure monitoring after 1 week of high salt intake. Nineteen patients were considered salt resistant. Compared with salt-resistant hypertensives, salt-sensitive patients presented a significant lower (P=0.005) maximal acetylcholine-induced vasodilation (21±6.3 versus 28±7.5 mL · 100 mL-1 · tissue · min-1). On the contrary, maximal sodium nitroprusside–induced vasodilation did not significantly differ between groups (22.4±4.5 versus 23.9±5.3 mL · 100 mL-1 · tissue · min-1). The decrease in maximal acetylcholine-induced vasodilation promoted by the coadministration of L-NMMA was significantly more pronounced in salt-resistant compared with salt-sensitive patients (P=0.003). Finally, high salt intake promoted a significant decrease in 24-hour urinary nitrate excretion in salt-sensitive patients (from 443±54 to 312±54 µmol/d; P=0.033) compared with salt-resistant hypertensives (from 341±50 to 378±54 µmol/d). We conclude that salt-sensitive hypertension is associated with endothelial dysfunction characterized by a defective endothelium-dependent vasodilation. Impairment of the L-arginine–nitric oxide pathway may be responsible for this abnormal endothelial response.
Key Words: endothelium • salt sensitivity • hypertension • nitric oxide • dietary salt
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