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Patch-clamp techniques, digital-imaging fluorescence microscopy, polymerase chain reaction and immunoblotting were employed in the investigation of potassium channels and their role in regulating cytoplasmic ionized calcium concentration in pulmonary arterial smooth muscle cells (PASMC). Results reveal that several genes encode these potassium channels. These channels have important functions in maintaining the membrane potential and intracellular calcium concentration in PASMC. The results of characterization studies for the various potassium channels are presented.

Tissue preparations of rodent pulmonary artery (PA) smooth muscle cells (SMCs) were analyzed to determine the role of K+ channel activity on NO-induced pulmonary vasodilation. Administration of sodium nitroprusside and nitric oxide in rodent PA SMC rings precontracted with extracellular K+ produced significant relaxation. Furthermore, NO-induced relaxation of PA rings depend on a K+ driving force that was established by transmembrane K+ gradient and by the activation of voltage-gated K+ and Ca2+-activated K+ channels.

Primary cultured rat pulmonary artery smooth muscle (PASMC) cells were analyzed after the administration of exogenous NO to determine the role of the vasodilator on PASMC cytostolic Ca2+ concentration. Serotonin (5-HT)-induced elevations in cytostolic Ca2+ and Ca2+ influx was inhibited by NO infusions in PASMC cultures. Furthermore, 5-HT stimulated the release of Ca2+ from 1,4,5-triphosphate-sensitive PASMC sarcoplasmic reticulum and sarcolemmal Ca2+ channels.

Blocking of oxidative phosphorylation by carbonyl cyanide p-trifluoromethoxyphenyl-hydrazone (FCCP) increases Ca2+-activated K+ (K(sub Ca)) channel current and decreases voltage-gated K+ (K(sub v)) current in pulmonary artery myocytes. A reduction in oxidative ATP synthesis appears to be involved in the decrease of the K(sub v) currents. FCCP increases the K(sub Ca) current by increasing intracellular Ca release. FCCP uncouples mitochondrial respiration from ATP formation.

Study on the role of glycolytic inhibition in the intracellular Ca2+ in the single pulmonary arterial smooth muscle cells (PASMC) showed that from both Ca2+ influx through the verapamil-sensitive voltage-gated Ca2+ channel and Ca2+ release from the CPA-sensitive intracellular Ca2+ stores results in the increase in 2-DG. It is also suggested that hypoxia- and 2-DG-induced share a common pathway leading to vasoconstriction in PASMC.

Analysis of the influence of cytochrome P-450 inhibitors on voltage-gated K+ (Kv) channel current (Ikv) and membrane potential Em by whole cell patch-clamp experiments to examine whether P-450 contributes to Kv channel regulation reveals that P-450 inhibitors reversibly suppress steady-state Kv channel current and cause pulmonary artery cell depolarization. The P-450 system may connect the change in cellular redox state and pulmonary vascular tone modulation through its effect on Kv channel current.

Increased concentrations of cystolic Ca2+ initiates hypoxia induced pulmonary vasoconstriction (HPV). Hypoxia-inhibited voltage-gated K+ channels in pulmonary artery (PA) myocytes lead to opening of voltage gated Ca2+ channels that increase the concentration of (Ca2+)i and start HPV. Hypoxia and 2-deoxy-D-glucose (2-DOG) exhibit similar selectivity on DA cells, which suggests a single mechanism for both processes.

Electrophysiological characteristics of vascular smooth muscles isolated from rat pulmonary and mesenteric arteries can be altered considerably in culture. However, fresh cultures have most of the electrophysiologic properties of the native cells andcan therefore serve as a useful model system in the investigation of vascular smooth muscles electrophysiology. One of the electrophysiologic characteristic that is modified in culturing the myocytes is the transient inward ionic current.

Whole cell patch-clamp analysis was employed in the investigation of the outward flux of potassium ions in culturedmyocytes isolated from the pulmonary and the mesenteric arteries of rat to investigate the mechanism of hypoxia-induced vasoconstriction. Results reveal that hypoxia inhibits the outward potassium current in cultures taken from the pulmonary artery. This leads to membrane depolarization which promotes calcium influx initiating contraction leading to vasoconstriction.

Analyzes the results of a study on the characterization of biophysical and pharmacological properties of CIa2 currents in a rat's pulmonary artery (PA) smooth muscle cells. How the study was conducted; Information on what vascular smooth muscle cells are; What is meant by membrane depolarization; Conclusions based from the results of the study conducted.

Determines whether inhibition of oxidative phosphorylation, that is, decreased oxidative ATP production, is involved in the regulation K+ channel activity that contributes to the regulation of resting Em and [Ca2+]i in pulmonary artery (PA) myocytes. Effect of p-trifluoromethoxphenylhydrazone (FCC) on IK in PA myocytes; Nature of FCCP-induced increase.

Abstract: We present an atomistic study on the phase stability, site preference and lattice constants of the rare earth intermetallics Lu2Fe17−x T x (T=Cr, Mn, Ru). The calculated preferential occupation site of ternary element T is found to be the 4f site. The order of site preference is given as 4f, 12k, 12j and 6g for Lu2Fe17−x T x . The calculated lattice parameters are corresponding to the experimental results. We have calculated the magnetic moments of Lu2Fe17−x T x compounds. Results show that the calculated total magnetic moment of Lu2Fe17 compound is M=37.34μB/f.u. In addition, the total and partial phonon densities of states are evaluated first for these complicated structures. [Copyright &y& Elsevier]

Abstract: A systemic study of the structural properties of the rare-earth intermetallics Lu2(Fe, T)17 (T = Mn, Ru) and their hydrides has been performed by a series of interatomic pair potentials. The site preference of T atoms at Fe sites is evaluated and the order is given as 4f, 12k, 12j and 6g for Lu2(Fe, T)17. The interstitial H atoms only occupy 6h interstitial sites in Lu2(Fe, T)17. The calculated lattice constants agree with a report in the literature. We have calculated the magnetic moments of Lu2(Fe, T)17 compounds. Results showed that the calculated total magnetic moment of Lu2Fe17 compound is M = 37.34 μB/f.u. Furthermore, the total and partial phonon densities of states are evaluated first for Lu2(Fe, T)17 and their hydrides with the hexagonal Th2Ni17-type structure. [Copyright &y& Elsevier]