Hydrogen sulfide defends against the cardiovascular risk of Nw-nitro-L-argininemethyl ester-induced hypertension in rats via the nitric oxide/endothelial nitric oxide synthase pathway.

Wenqiang JI; Shangyu Liu; Jing Dai; Tao Yang; Xiangming Jiang; Xiaocui Duan; Yuming WU

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Hydrogen sulfide defends against the cardiovascular risk of Nw-nitro-L-argininemethyl ester-induced hypertension in rats via the nitric oxide/endothelial nitric oxide synthase pathway.

Author: Wenqiang JI ¹ ; Shangyu LIU ² ; Jing DAI ³ ; Tao YANG ¹ ; Xiangming JIANG ¹ ; Xiaocui DUAN ² ; Yuming WU ⁴
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1. Department of Emergency, First Hospital of Hebei Medical University, Shijiazhuang, Hebei 050030, China.
2. Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang, Hebei 050017, China.
3. Department of Cadres Health Care, Third Hospital of Shijiazhuang, Shijiazhuang, Hebei 050011, China.
4. Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang, Hebei 050017, China. Email: wuyum@yahoo.com.
Publication Type:Journal Article
MeSH: Animals; Cardiovascular Diseases; metabolism; prevention & control; Hydrogen Sulfide; therapeutic use; Hypertension; chemically induced; drug therapy; Liver; drug effects; metabolism; Male; NG-Nitroarginine Methyl Ester; toxicity; Nitric Oxide; metabolism; Nitric Oxide Synthase Type III; metabolism; Rats; Rats, Sprague-Dawley; Signal Transduction; drug effects
From: Chinese Medical Journal 2014;127(21):3751-3757
CountryChina
Language:English
Abstract:
BACKGROUNDDyslipidemia caused by liver injury is a significant risk factor for cardiovascular complications. Previous studies have shown that hydrogen sulfide (H2S) protects against multiple cardiovascular disease states in a similar manner as nitric oxide (NO), and NO/endothelial nitric oxide synthase (eNOS) pathway is the key route of NO production. The purpose of this study was to investigate whether H2S can ameliorate the high blood pressure and plasma lipid profile in Nw-nitro-L-argininemethyl ester (L-NAME)-induced hypertensive rats by NO/eNOS pathway.
METHODSThirty-six 4-week old Sprague-Dawley (SD) male rats were randomly assigned to 6 groups (n = 6): control group, L-NAME group, control + glibenclamide group, control + NaHS group, L-NAME + NaHS group, and L-NAME + NaHS + glibenclamide group. Measurements were made of plasma triglycerides (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL), total cholesterol (CHO), glutamic-pyruvic transaminase (ALT) levels after 5 weeks. Then measurements of NO level and proteins expression of eNOS, P-eNOS, AKT, P-AKT were made in liver tissue.
RESULTSAfter 5 weeks of L-NAME treatment, the blood pressure, plasma TG ((1.22±0.12) mmol/L in L-NAME group vs. (0.68±0.09) mmol/L in control group; P < 0.05) and LDL ((0.54±0.04) mmol/L in L-NAME group vs. (0.28±0.02) mmol/L in control group; P < 0.05) concentration were significantly increased, and the plasma HDL ((0.26±0.02) mmol/L in L-NAME group vs. (0.69±0.07) mmol/L in control group; P < 0.05) concentration significantly decreased. Meanwhile the rats treated with L-NAME exhibit dysfunctional eNOS, diminished NO levels ((1.36±0.09) mmol/g protein in L-NAME group vs. (2.34±0.06) mmol/g protein in control group; P < 0.05) and pathological changes of the liver. H2S therapy can markedly decrease the blood pressure ((37.25±4.46) mmHg at the fifth week; P < 0.05), and ameliorate the plasma TG ((0.59±0.06) mmHg), LDL ((0.32±0.04) mmHg), and HDL ((0.46±0.03) mmHg) concentration in L-NAME + NaHS group (all P < 0.05). H2S therapy can also restore eNOS function and NO bioavailability and attenuate the pathological changes in the liver in L-NAME-induced hypertensive rats.
CONCLUSIONH2S protects the L-NAME-induced hypertensive rats against liver injury via NO/ eNOS pathway, therefore decreases the cardiovascular risk.