Endothelial dysfunction in salt-sensitive essential hypertension

被引:134
作者
Bragulat, E [1 ]
de la Sierra, A [1 ]
Antonio, MT [1 ]
Coca, A [1 ]
机构
[1] Hosp Clin Barcelona, Inst Invest Biomed August Pi & Sunyer, Dept Internal Med, Hypertens Unit, E-08036 Barcelona, Spain
关键词
endothelium; salt sensitivity; hypertension; nitric oxide; dietary salt;
D O I
10.1161/01.HYP.37.2.444
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
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 N-G-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 mt 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 mu mol/d; P=0.033) compared with salt-resistant hypertensives (from 341+/-50 to 378+/-54 mu mol/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.
引用
收藏
页码:444 / 448
页数:5
相关论文
共 50 条
[41]   Salt-sensitive hypertension: mechanisms and effects of dietary and other lifestyle factors [J].
Pilic, Leta ;
Pedlar, Charles R. ;
Mavrommatis, Yiannis .
NUTRITION REVIEWS, 2016, 74 (10) :645-658
[42]   Assessment of Mitochondrial DNA Polymorphisms in Salt-Sensitive Hypertension in Dahl Salt-Sensitive Rats [J].
Chu-Shih Chen ;
Yumiko Hiura ;
Chun-Shen Shen ;
Naoharu Iwai .
Hypertension Research, 2008, 31 :107-115
[43]   Vascular abnormalities in salt-sensitive hypertension [J].
de la Sierra, A .
CURRENT HYPERTENSION REPORTS, 2003, 5 (02) :93-94
[44]   The role of the kidney in salt-sensitive hypertension [J].
Francesco Trepiccione ;
Miriam Zacchia ;
Giovambattista Capasso .
Clinical and Experimental Nephrology, 2012, 16 :68-72
[45]   Pathophysiology and genetics of salt-sensitive hypertension [J].
Maaliki, Dina ;
Itani, Maha M. ;
Itani, Hana A. .
FRONTIERS IN PHYSIOLOGY, 2022, 13
[46]   Assessment of mitochondrial DNA polymorphisms in salt-sensitive hypertension in Dahl salt-sensitive rats [J].
Chen, Chu-Shih ;
Hiura, Yumiko ;
Shen, Chun-Shen ;
Iwai, Naoharu .
HYPERTENSION RESEARCH, 2008, 31 (01) :107-115
[47]   Implication of ENaC in salt-sensitive hypertension [J].
Hummler, E .
JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY, 1999, 69 (1-6) :385-390
[48]   Vascular abnormalities in salt-sensitive hypertension [J].
Alejandro de la Sierra .
Current Hypertension Reports, 2003, 5 :93-94
[49]   Telmisartan improves endothelial dysfunction and renal autoregulation in Dahl salt-sensitive rats [J].
Satoh, Minoru ;
Haruna, Yoshisuke ;
Fujimoto, Sohachi ;
Sasaki, Tamaki ;
Kashihara, Naoki .
HYPERTENSION RESEARCH, 2010, 33 (02) :135-142
[50]   Telmisartan improves endothelial dysfunction and renal autoregulation in Dahl salt-sensitive rats [J].
Minoru Satoh ;
Yoshisuke Haruna ;
Sohachi Fujimoto ;
Tamaki Sasaki ;
Naoki Kashihara .
Hypertension Research, 2010, 33 :135-142