Abstract
Hydrogen sulfide (H 2 S), a third gasotransmitter, has been confirmed as playing a major role in diverse biological processes such as vascular relaxation, insulin secretion, inflammation and apoptosis. Cystathionine β -Synthase (CBS) and cystathionine γ -lyase (CSE) are major biosynthetic enzymes of H 2 S. Much interest has been focused on H 2 S as a potent vasorelaxative substance, since CSE knockout mice developed hypertension. In the normal kidney, both CBS and CSE are expressed in the proximal tubules, but not in the glomeruli or distal tubules. Administration of the H 2 S donor sodium hydrosulfide (NaHS) increased peritubular capillary (PTC) diameter and blood flow. In the models of DN, we reported that hyperglycemia reduces the expression of eNOS in the glomeruli, thereby reducing NO production and inducing typical pathological glomerular lesions of DN. However, the precise roles of H 2 S in DN have not been fully identified. In a spontaneous diabetic model CSE expression was markedly reduced, whereas CBS expression was unaffected. Progressive DN showed vasoconstriction and a loss of blood flow in PTC that was ameliorated by the NaHS treatment. The biological profile of CSE resembles that of eNOS. These findings suggest that both H 2 S and NO might share the role of regulation of tubulointerstitial microcirculation. H 2 S could represent a target of treatment for ischemic injury in DN.
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