Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.3.14 (ATP synthase)
 7,042 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to show whether the ACE inhibitor captopril is able to protect the heart against the deleterious effect of passive cigarette smoking on left ventricular mitochondria. Four groups of rabbits were investigated: control (C), passive smoking of three cigarettes twice daily/30 minutes (S), control + captopril (7.5 mg/kg body weight twice daily) (Cap), and smoking + captopril (SCap) as in group 2 and 3. Three weeks lasting passive smoking impaired oxidative phosphorylation, diminished cytochrome oxidase activity and increased the mitochondrial F1-ATPase protein concentration. Moreover, the level of coenzyme Q10 (CoQ10) and coenzyme Q9 were decreased. Simultaneous treatment with captopril prevented partly the decrease of CoQ10 level, deterioration of oxidative phosphorylation, diminution of cytochrome oxidase activity and enhancement of F1-ATPase level. We conclude that captopril protected the myocardium against the harmful effect of passive smoking in rabbits.
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PMID:Captopril increased mitochondrial coenzyme Q10 level, improved respiratory chain function and energy production in the left ventricle in rabbits with smoke mitochondrial cardiomyopathy. 1047 91

We studied the physiological role of flow through pulmonary arterioles in CO(2) gas exchange. We established human pulmonary arteriolar endothelial cells (HPAoEC). The cells demonstrated marked immunocytochemical staining of PECAM-1, VEGF R2, ACE-1, and CA type IV on their cell surface. Ten seconds shear stress stimulation caused the co-release of H(+) and ATP via the activation of F(1)/F(O) ATP synthase on the HPAoEC. F(1)/F(O) ATP synthase was immunocytochemically observed on the cell surface of non-permeabilized HPAoEC. In the shear stress-loaded HPAoEC culture media supernatant, ATPase activity increased in a time-dependent manner. The HPAoEC were strongly stained for NTPDase 1, which partially co-localized with purinergic P2Y1. The purinergic P2Y1 receptor agonist UTP (10(-6) M) significantly potentiated the shear stress-induced increase in ATPase activity in the culture medium supernatant. Ten seconds shear stress stimulation also produced stress strength-dependent CO(2) gas excretion from the HPAoEC, which was significantly reduced by the inhibition of F(1)/F(O) ATP synthase or CA IV on the endothelial cell (EC) surface. In conclusion, we have proposed a new concept of CO(2) exchange in the human lung, flow-mediated F(1)/F(O) ATP synthase-dependent H(+) secretion, resulting in the facilitation of a dehydration reaction involving HCO3(-) in plasma and the excretion of CO(2) gas from arteriolar ECs.
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PMID:Shear stress-mediated F1/FO ATP synthase-dependent CO2 gas excretion from human pulmonary arteriolar endothelial cells. 2176 65