Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Successful organ transplantation depends on adequate preservation of cellular function. We tested the effect of four commonly used donor organ preservation fluids on the ability of cultured bovine pulmonary artery endothelial cells to release endothelium-derived relaxing factor (EDRF). Columns of endothelial cells grown on microcarrier beads were exposed to either University of Wisconsin (Belzer's) solution, Marshall's preservation fluid, Euro-Collins solution, or a blood-based preservation fluid at 4 degrees C for 6 hours, and then to Krebs-Henseleit buffer at 37 degrees C for 1 hour. They were then stimulated with boluses of bradykinin, and the EDRF released was detected by bioassay. The release of EDRF from endothelial cells previously exposed to a preservation fluid was compared with the release of EDRF from control columns of cells perfused throughout at 37 degrees C with Krebs-Henseleit buffer. Previous exposure to any of the three non-blood-based preservation fluids did not attenuate bradykinin-stimulated EDRF release. By contrast, previous perfusion with the blood-based solution completely inhibited EDRF release (p less than 0.01, ANOVA), an effect attributable to the acidity of the solution. Donor organ preservation fluids differ in their effect on endothelial cell function, and this has important implications for lung and for other organ transplantation.
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PMID:Donor organ preservation fluids differ in their effect on endothelial cell function. 175 67

The effects of 1-[(S)-3-acetylthio-2-methylpropanoyl]-L-prolyl-L-phenylalanine (alacepril, DU-1219) an antihypertensive compound with angiotensin converting enzyme inhibitory activity, and its metabolite, desacetyl-alacepril (DU-1227), on the cardiovascular and autonomic nervous systems and on the blood were compared with those of captopril in the experimental animals. Alacepril and DU-1227 at the i.v. dose of 10 mg/kg gradually lowered the diastolic blood pressure in pentobarbital anesthetized dogs. Captopril showed similar effects. However, the former two compounds showed triphasic effects on the carotid blood flow, i.e., transient increase immediately after the injection, second increase 2 min later, and gradual decrease 20-30 min later. The second increase by DU-1227 was more potent than that by alacepril. Alacepril, DU-1227 and captopril did not affect the pressor responses induced by norepinephrine in anesthetized cats. The contractions of the nictitating membrane in cats induced by electrical stimulation of the cervical sympathetic nerve or epinephrine were depressed with high doses of these three compounds. Captopril potentiated the contractions induced by bradykinin in isolated guinea-pig ileum, while alacepril and DU-1227 were without effect. These three compounds neither affected the resting tension of isolated ileum in guinea-pigs and rabbits nor the contractions induced by acetylcholine, histamine, serotonin and nicotine of isolated guinea-pig ileum. Alacepril at the oral dose of 60 mg/kg decreased the total acidity in pylorus ligated rats, and at higher doses depressed the intestinal charcoal meal passage in mice. Alacepril at comparatively low doses decreased the urine volume with slight reduction of Na+ and K+ excretions in saline-loaded rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:General pharmacology of the novel angiotensin converting enzyme inhibitor alacepril. 1st communication: Effects on cardiovascular, visceral and renal functions and on blood. 351 77

After removal of parotid glands in 104 white rats, the gastric acidity increased and excretion of neutral red occurred. Simultaneously the kallikrein activity and kallikreinogen concentration as well as concentration of kininogen became enhanced whereas the bradykinin of plasma decreased. The data suggest that the mechanism of activation of the stomach secretory and excretory functions after removal of parotid glands involves inactivation of the blood kallikrein system.
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PMID:[Dynamics of the secretory and excretory functions of the stomach and activity of the kallikrein-kinin system following removal of the parotid glands]. 678 48

Sensory neurons that innervate the heart sense ischemia and mediate angina. To use patch-clamp methods to study ion channels on these cells, we fluorescently labeled cardiac sensory neurons (CSNs) in rats so that they could later be identified in dissociated primary culture of either nodose or dorsal root ganglia (DRG). Currents evoked by a variety of different agonists imply the importance of lowered pH (</=7.0) in signaling ischemia. Acidic pH evoked extremely large depolarizing current in almost all cardiac afferent neurons from the DRG (CDRGNs). In contrast, only about half of the unlabeled DRG neurons responded to acid, and their current amplitudes were much less than that in CDRGNs. In all respects tested--kinetics, selectivity, and pharmacology--the acid-evoked current was similar to that of previously described native and cloned acid-sensing ion channels. Cardiac afferents from the nodose ganglia differed from CDRGNs in having smaller acid-evoked currents but clearly larger currents evoked by ATP. Serotonin, acetylcholine, bradykinin, and adenosine elicited currents in fewer CSNs than did ATP or lowered pH, and the currents were relatively small. Capsaicin, an activator of small nociceptive sensory neurons that innervate skin, evoked only small and rare currents in CDRGNs. The extremely large amplitude and prevalent expression of acid-evoked current in CSNs imply a critical role for acidity in sensation associated with myocardial ischemia.
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PMID:Acid-evoked currents in cardiac sensory neurons: A possible mediator of myocardial ischemic sensation. 1022 39

The gas phase H/D exchange reactions of bradykinin (M + 3H)3+ ions with D2O and DI were monitored in a quadrupole ion trap mass spectrometer. The H/D exchange kinetics of both chemical probes (D2O and DI) indicate the presence of two noninterconverting reactive gas phase ion populations of bradykinin (M + 3H)3+ at room temperature. The H/D exchange involving DI, however, generally proceeds faster than that involving D2O. The rate observations described here can be rationalized on the basis of the "relay mechanism" (see Campbell et al. J. Am. Chem. Soc. 1995, 117, 12840-12854) recently proposed to account for H/D exchange between D2O and gaseous protonated polypeptides. The higher exchange rate with DI is believed to arise primarily as a result of its lower gas-phase acidity relative to that of D2O and, secondarily, as a result of the longer bond length of DI relative to that of OD in D2O.
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PMID:Gas phase H/D exchange kinetics: DI versus D2O. 1068 70

Transient receptor potential vanilloid type channels (TRPVs) are expressed in several cell types in human and animal lungs. Increasing evidence has demonstrated important roles of these cation channels, particularly TRPV1 and TRPV4, in the regulation of airway function. These TRPVs can be activated by a number of endogenous substances (hydrogen ion, certain lipoxygenase products, etc.) and changes in physiological conditions (e.g., temperature, osmolarity, etc.). Activation of these channels can evoke Ca(2+) influx and excitation of the neuron. TRPV1 channels are generally expressed in non-myelinated afferents innervating the airways and lungs, which also contain sensory neuropeptides such as tachykinins. Upon stimulation, these sensory nerves elicit centrally-mediated reflex responses as well as local release of tachykinins, and result in cough, airway irritation, reflex bronchoconstriction and neurogenic inflammation in the airways. Recent studies clearly demonstrated that the excitability of TRPV1 channels is up-regulated by certain autacoids (e.g., prostaglandin E(2), bradykinin) released during airway inflammatory reaction. Under these conditions, the TRPV1 can be activated by a slight increase in airway temperature or tissue acidity. Indirect evidence also suggests that TRPV channels may play a part in the pathogenesis of certain respiratory diseases such as asthma and chronic cough. Therefore, the potential use of TRPV antagonists as a novel therapy for these diseases certainly merits further investigation.
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PMID:Role of TRPV receptors in respiratory diseases. 1734 45