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Amlodipine affects endogenous hydrogen sulfide tissue concentrations in different mouse organs
Bogdan Wiliński1, Jerzy Wiliński, Eugeniusz Somogyi
1Zakład Biologii Rozwoju Człowieka, Wydział Nauk o Zdrowiu, Uniwersytet Jagielloński Collegium Medicum, Kraków, Poland. bowil@interia.pl
Folia Medica Cracoviensia
|August 16, 2012
Summary
Calcium channel blockers like amlodipine impact hydrogen sulfide (H2S) levels in mice. Amlodipine administration significantly reduced H2S in the brain and liver, with varied effects in the heart and kidneys.
Area of Science:
- Pharmacology
- Biochemistry
- Cardiovascular Research
Background:
- Endogenous hydrogen sulfide (H2S) plays a crucial role in physiological processes.
- The interaction between calcium channel blockers (CCBs) and H2S biology remains largely unexplored.
- Understanding these interactions is vital for cardiovascular health and drug development.
Purpose of the Study:
- To investigate the effects of amlodipine, a common CCB, on endogenous H2S concentrations in various mouse tissues.
- To determine if amlodipine influences H2S levels in a dose-dependent manner.
Main Methods:
- CBA strain mice were administered amlodipine (3 mg/kg or 10 mg/kg) intraperitoneally or physiological saline (control).
- Free H2S tissue concentrations were measured using a modified Siegel spectrophotometric method.
- H2S levels were analyzed in brain, liver, heart, and kidney tissues.
Main Results:
- Amlodipine administration led to a significant decrease in H2S levels in the brain and liver across both dosage groups.
- A lower dose of amlodipine increased H2S concentrations in the heart and kidneys.
- A higher dose of amlodipine decreased H2S accumulation in the heart and kidneys.
Conclusions:
- Amlodipine demonstrably interferes with endogenous H2S biology.
- The drug affects tissue-specific H2S concentrations, with dose-dependent effects observed in cardiac and renal tissues.
- These findings highlight a novel interaction between CCBs and H2S metabolism with potential clinical implications.

