Endothelial Dysfunction in Salt Sensitive Hypertension
The aim of the study was to evaluate endothelial function in a group of essential hypertensive patients classified on the basis of their salt sensitivity. Forty hypertensive patients were placed on two 7-day periods of low (50 mmol/day) and high (250 mmol/day) salt intakes. Salt sensitivity was defined as a significant rise (p<0.05) in 24-hour mean blood pressure (MBP), from low to high salt intake, measured by ambulatory blood pressure monitoring. Endothelial function was determined by the increase in the forearm blood flow (FBF) (strain-gauge plethysmography) to intrabrachial infusion of increasing doses of acetylcholine and sodium nitroprusside, before and after the addition of the NO synthase inhibitor, L-NMMA. Nineteen hypertensive patients significantly increased MBP with high salt intake (from 105 ± 2.6 to 112.5 ± 2.5 mmHg)and were considered salt sensitive (SS). In contrast, 21 patients did not modify their MBP after high salt intake (from 102 ± 3 to 100 ± 3 mmHg) and were diagnosed as having salt resistant hypertension (SR). The vasodilation response to acetylcholine was significantly blunted (p=0.001) in SS patients (FBF rose from 4.5 ± 0.2 to 20.6 ± 1.4 mL/100mL of forearm tissue [FT] per minute) when compared to SR (FBF rose to 4.4 ± 0.3 to 28.4 ± 1.7 mL/100mL FT per minute). Maximal acetylcholine-dependent vasodilation was inversely correlated with the MBP increase with high salt intake (r=-0.47; p=0.003). Sodium nitroprusside-related vasodilation was similar in SS and SR patients (from 4.4 ± 0.1 to 22.4 ± 1.1 mL/100mL/min in SS and from 4.5 ± 0.2 to 23.9 ± 1.3 mL/100mL/min in SR; p=0.4). In SS patients, L-NMMA infusion cause a decrease in baseline FBF (4.5 ± 0.2 to 3.2 ± 0.1 mL/100mL/min, whereas the response to acetylcholine was not significatively affected (from 3.2 ± 0.1 to 18.1 ± 1.8 mL/100mL/min) In SR patients, L-NMMA infusion also decreases baseline FBF (from 4.3 ± 0.2 to 3.1 ± 0.1 mL/100mL/min) and the response to acetylcholine was impaired in this group(from 3.1 ± 0.1 to 20.5 ± 1.4 mL/100mL/min). We conclude that salt-sensitive hypertension is associated with a higher degree of endothelial dysfunction. This deficient vasodilation may be secondary to an alteration in the L-arginine-NO pathway.