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Beneficial effects of diminished production of hydrogen sulfide or carbon monoxide on hypertension and renal injury induced by NO withdrawal
Author(s) -
Wesseling Sebastiaan,
Fledderus Joost O,
Verhaar Marianne C,
Joles Jaap A
Publication year - 2015
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/bph.12674
Subject(s) - medicine , kidney , hydrogen sulfide , nitric oxide , endocrinology , pharmacology , chemistry , sulfur , organic chemistry
Whether NO, carbon monoxide (CO) and hydrogen sulfide (H2 S) compensate for each other when one or more is depleted is unclear. Inhibiting NOS causes hypertension and kidney injury. Both global depletion of H2 S by cystathionine γ-lyase (CSE) gene deletion and low levels of exogenous H2 S cause hypertension. Inhibiting CO-producing enzyme haeme oxygenase-1 (HO-1) makes rodents hypersensitive to hypertensive stimuli. We hypothesized that combined inhibition of NOS and HO-1 exacerbates hypertension and renal injury, but how combined inhibition of NOS and CSE affect hypertension and renal injury was unclear.