Abstract
Hydrogen sulfide (H2S) is a modulator of various physiological and pathological processes in the cardiovascular and nervous system and plays an important role in the regulation of gastrointestinal tract, liver and kidney function. The effect of the pleiotropic action of the tissue specific angiotensin-converting enzyme inhibitor (ACEI), ramipril, exceeds renin-angiotensin aldosterone system (RAAS) blockade and involves different biological mechanisms. The aim of the study is to assess the influence of ramipril on H2S production in mouse liver and kidneys. Thirty mice (CBA) of both sexes were given intraperitoneal injections of ramipril solutions--0.125 mg (5 mg/kg--group D1) and 0.25 mg (10 mg/kg--group D2) for 5 consecutive days at the same time of the day (10:30 am). The control group received physiological saline in portions of the same volume--0.2 ml. The measurements of the tissue concentration of H2S were performed using the modified spectrophotometric method of Siegel. There was a significant rise in the tissue concentration of H2S [microg/g] in livers of group D1 (2.70 +/- 0.02 vs 2.81 +/- 0.06; P = 0.03) and group D2 (2.70 +/- 0.02 vs 2.98 +/- 0.03; P < 0.001) and a significant decrease of H2S kidney tissue concentration in group D1 (3.35 +/- 0.06 vs 3.15 +/- 0.07; P = 0.02) and in group D2 (3.35 +/- 0.06 vs 2.89 +/- 0.03; P < 0.001). Our results show that ACEI ramipril affects hydrogen sulfide generation in mouse liver and kidneys.
Highlights
Hydrogen sulfide (H2S) is endogenously produced in enzymatic reactions in many tissues, especially in the nervous system, cardiovascular system, liver and kidney
In the kidney ramipril led to the decrease of H2S tissue concentration in the group D1 by 6.0% and in D2 by 13.8% (Table 1)
Hydrogen sulfide tissue concentration in mouse liver and kidney following the administration of 0.125 mg or 0.25 mg of ramipril
Summary
Hydrogen sulfide (H2S) is endogenously produced in enzymatic reactions in many tissues, especially in the nervous system, cardiovascular system, liver and kidney. The reninangiotensin aldosterone system (RAAS) is a hormonal cascade that functions in the homeostatic control of arterial pressure, tissue perfusion, extracellular volume, cell growth end proliferation, apoptosis, reactive oxygen species generation, inflammation and fibrogenesis. Deregulation of the RAAS plays an important role in the pathogenesis of cardiovascular and renal disorders and in the pathophysiology of liver diseases (LUBEL et al 2008; WOLF 2008). The effects of ramipril – a member of the angiotensin-converting enzyme inhibitors (ACEIs) family – exceeds the RAAS blockade. The impact of ACEIs on H2S generation in liver and kidney is unknown. The aim of the study is to assess the influence of ramipril administration on endogenous H2S concentration in mouse liver and kidney
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