Hydrogen sulfide (H2S) is the third member of gasotransmitter family together with nitric oxide and carbon monoxide. H2S is involved in the regulation of blood pressure by controlling vascular tone, sympathetic nervous system activity and renal sodium excretion. Moderate age-dependent hypertension and endothelial dysfunction develop in mice with knockout of cystathionine γ-lyase (CSE), the enzyme involved in H2S production in the cardiovascular system. Decreased H2S concentration as well as the expression and activities of H2S-producing enzymes have been observed in most commonly used animal models of hypertension such as spontaneously hypertensive rats, Dahl salt-sensitive rats, chronic administration of NO synthase inhibitors, angiotensin II infusion and two-kidney-one-clip hypertension, the model of renovascular hypertension. Administration of H2S donors decreases blood pressure in these models but has no major effects on blood pressure in normotensive animals. H2S donors not only reduce blood pressure but also end-organ injury such as vascular and myocardial hypertrophy and remodeling, hypertension-associated kidney injury or erectile dysfunction. H2S level and signaling are modulated by some antihypertensive medications as well as natural products with antihypertensive activity such as garlic polysulfides or plant-derived isothiocyanates as well as non-pharmacological interventions. Modifying H2S signaling is the potential novel therapeutic approach for the management of hypertension, however, more experimental clinical studies about the role of H2S in hypertension are required.
Keywords: Hydrogen sulfide; Hypertension; Kidney injury; Myocardial hypertrophy; Vascular tone.
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