Objective. To investigate whether angiotensin II receptor antagonist and endothelin receptor antagonist can improve the nitroglycerin (Nit) tolerance in vivo. Methods. Twenty-four rats were divided into 4 groups (n=6,each): Control group, Nitroglycerin (Nit) group, Nit＋ bosentan group and Nit＋ losartan group. Nitroglycerin tolerance was induced by 2-day treatment of nitroglycerin patch (0.05 mg/h). AngiotensinⅡ receptor antagonist losartan ( 10 mg· kg－ 1· d－ 1 ) and endothelin receptor antagonist bosentan ( 100 mg· kg－ 1· d－ 1 ) were given by gavage for 2 days respectively. Results. The least hypotensive response to sodium nitroprusside (SNP) was observed in Nit group . The effective percentages of hypotensive response to SNP were increased in both Nit＋ losartan group and Nit＋ bosentan group compared with Nit group [(31.95± 4.45 ) ％ vs (21.00± 3.69 ) ％ , P Conclusion. Endothelin receptor antagonist and angiotensin Ⅱ receptor antagonist could prevent against the Nit tolerance .

Objective. To investigate whether angiotensin II receptor antagonist and endothelin receptor antagonist can improve the nitroglycerin (Nit) tolerance in vivo. Methods. Twenty-four rats were divided into 4 groups (n=6,each): Control group, Nitroglycerin (Nit) group, Nit＋ bosentan group and Nit＋ losartan group. Nitroglycerin tolerance was induced by 2-day treatment of nitroglycerin patch (0.05 mg/h). AngiotensinⅡ receptor antagonist losartan ( 10 mg· kg－ 1· d－ 1 ) and endothelin receptor antagonist bosentan ( 100 mg· kg－ 1· d－ 1 ) were given by gavage for 2 days respectively. Results. The least hypotensive response to sodium nitroprusside (SNP) was observed in Nit group . The effective percentages of hypotensive response to SNP were increased in both Nit＋ losartan group and Nit＋ bosentan group compared with Nit group [(31.95± 4.45 ) ％ vs (21.00± 3.69 ) ％ , P Conclusion. Endothelin receptor antagonist and angiotensin Ⅱ receptor antagonist could prevent against the Nit tolerance .

Endothelin-1 ( ET-1 ) is not only a potent vasoconstrictor , but causes proliferation of many of the vascular cells involved in vascular remodelling .ETA receptors mediate vasoconstriction and cell proliferation , whereas ETB receptors are important for the clearance of ET-1, endothelial cell survival , the release of nitric oxide and prostacyclin , and the inhibition of endothelin-converting enzyme ( ECE )-1.ET is activated in pulmonary arterial hypertension ( PAH) , heart failure ( HF) and many other cardiovascular diseases .The most efficient way to antagonize the ET-1 system is the use of ET-1 receptor antagonists that can block either ETA-or ETA-and ETB-receptors, or ECE inhibition which blocks the conversion of big ET-1 to ET-1.In this brief review , we will try to summarize the progress of anti-endothelin therapy in the treatment of PAH and HF treatment therapies .

内皮素受体拮抗剂波森坦(Bosentan)对原发性高血压病人血压的影响