A critical review of pharmacological significance of Hydrogen Sulfide in hypertension

In the family of gas transmitters, hydrogen sulfide (H(2)S) is yet not adequately researched. Known for its rotten egg smell and adverse effects on the brain, lungs, and kidneys for more than 300 years, the vasorelaxant effects of H(2)S on blood vessel was first observed in 1997. Since then, research continued to explore the possible therapeutic effects of H(2)S in hypertension, inflammation, pancreatitis, different types of shock, diabetes, and heart failure. However, a considerable amount of efforts are yet needed to elucidate the mechanisms involved in the therapeutic effects of H(2)S, such as nitric oxide-dependent or independent vasodilation in hypertension and regression of left ventricular hypertrophy. More than a decade of good repute among researchers, H(2)S research has certain results that need to be clarified or reevaluated. H(2)S produces its response by multiple modes of action, such as opening the ATP-sensitive potassium channel, angiotensin-converting enzyme inhibition, and calcium channel blockade. H(2)S is endogenously produced from two sulfur-containing amino acids L-cysteine and L-methionine by the two enzymes cystathionine γ lyase and cystathionine β synthase. Recently, the third enzyme, 3-mercaptopyruvate sulfur transferase, along with cysteine aminotransferase, which is similar to aspartate aminotransferase, has been found to produce H(2)S in the brain. The H(2)S has interested researchers, and a great deal of information is being generated every year. This review aims to provide an update on the developments in the research of H(2)S in hypertension amid the ambiguity in defining the exact role of H(2)S in hypertension because of insufficient number of research results on this area. This critical review on the role of H(2)S in hypertension will clarify the gray areas and highlight its future prospects.