Modulation of endothelial cell KCa3.1 Channels during endothelium-derived hyperpolarizing factor signaling in mesenteric resistance arteries

Arterial hyperpolarization to acetylcholine (ACh) reflects coactivation of KCa3.1 (IKCa) channels and KCa2.3 (SKCa) channels in the endothelium that transfers through myoendothelial gap junctions and diffusible factor(s) to affect smooth muscle relaxation (endothelium-derived hyperpolarizing factor [EDHF] response). However, ACh can differentially activate KCa3.1 and KCa2.3 channels, and we investigated the mechanisms responsible in rat mesenteric arteries. KCa3.1 channel input to EDHF hyperpolarization was enhanced by reducing external [Ca2+]o but blocked either with forskolin to activate protein kinase A or by limiting smooth muscle [Ca2+]i increases stimulated by phenylephrine depolarization. Imaging [Ca2+]i within the endothelial cell projections forming myoendothelial gap junctions revealed increases in cytoplasmic [Ca2+]i during endothelial stimulation with ACh that were unaffected by simultaneous increases in muscle [Ca2+]i evoked by phenylephrine. If gap junctions were uncoupled, KCa3.1 channels became the predominant input to EDHF hyperpolarization, and relaxation was inhibited with ouabain, implicating a crucial link through Na+/K+-ATPase. There was no evidence for an equivalent link through KCa2.3 channels nor between these channels and the putative EDHF pathway involving natriuretic peptide receptor-C. Reconstruction of confocal z-stack images from pressurized arteries revealed KCa2.3 immunostain at endothelial cell borders, including endothelial cell projections, whereas KCa3.1 channels and Na+/K+-ATPase {alpha}2/{alpha}3 subunits were highly concentrated in endothelial cell projections and adjacent to myoendothelial gap junctions. Thus, extracellular [Ca2+]o appears to modify KCa3.1 channel activity through a protein kinase A-dependent mechanism independent of changes in endothelial [Ca2+]i. The resulting hyperpolarization links to arterial relaxation largely through Na+/K+-ATPase, possibly reflecting K+ acting as an EDHF. In contrast, KCa2.3 hyperpolarization appears mainly to affect relaxation through myoendothelial gap junctions. Overall, these data suggest that K+ and myoendothelial coupling evoke EDHF-mediated relaxation through distinct, definable pathways

Use of high-intensity data to define large river management units: A case study on the lower Waikato River, New Zealand

The importance of environmental heterogeneity in lotic ecosystems is well recognised in river management, and continues to underpin studies of hierarchical patch dynamics, geomorphology and landscape ecology. We evaluated how physical characteristics and water chemistry measurements at high spatiotemporal resolution define channel units of potential ecological importance along 134 km of the lower Waikato River in North Island, New Zealand. We used multivariate hierarchical clustering to classify river reaches in an a priori unstructured manner based on (i) high-frequency, along-river water quality measurements collected in four seasons and (ii) river channel morphology data resolved from aerial photos for 1-km long reaches. Patterns of channel character were shaped by the depth and lateral complexity of constituent river reaches, while water quality patterns were represented by differences in clarity, chlorophyll fluorescence and specific conductance driven by tributary inflows in the mid-section of the river and tidal cycles in the lower section. Management units defined by physical characteristics or water quality did not necessarily align with boundaries typically reflecting clinal processes (e.g. tidal influence) or geomorphic, network or anthropogenic discontinuities. The results highlight the dynamic spatial and temporal properties of large rivers and the need to define clear objectives when deriving spatial units for management and research. Given that actions and targets for physical channel and water quality management may differ, the spatial extent identified for each of these does not necessarily need to directly coincide, although both should be considered in decision making and experimental design

Heat transfer to a gas containing a cloud of particles

Heat transfer to gas containing particle clou

A Correlation between Galaxy Light Concentration and Supermassive Black Hole Mass

We present evidence for a strong correlation between the concentration of bulges and the mass of their central supermassive black hole (M_bh) -- more concentrated bulges have more massive black holes. Using C_{r_e}(1/3) from Trujillo, Graham & Caon (2001b) as a measure of bulge concentration, we find that log (M_bh/M_sun) = 6.81(+/-0.95)C_{r_e}(1/3) + 5.03(+/-0.41). This correlation is shown to be marginally stronger (Spearman's r_s=0.91) than the relationship between the logarithm of the stellar velocity dispersion and log M_bh (Spearman's r_s=0.86), and has comparable, or less, scatter (0.31 dex in log M_bh), which decreases to 0.19 dex when we use only those galaxies whose supermassive black hole's radius of influence is resolved and remove one well understood outlying data point).Comment: 7 pages, 1 table, 2 figures. ApJ Letters, accepte

Characterisation of the vasodilation effects of DHA and EPA, n-3 PUFAs (fish oils), in rat aorta and mesenteric resistance arteries

Background and Purpose Increasing evidence suggests that the omega-3 polyunsaturated acids (n-3 PUFA), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), are beneficial to cardiovascular health, promoting relaxation of vascular smooth muscle cells and vasodilation. Numerous studies have attempted to study these responses, but to date there has not been a systematic characterisation of both DHA and EPA mediated vasodilation in conduit and resistance arteries. Therefore, we aimed to fully characterise the n-3 PUFA-induced vasodilation pathways in rat aorta and mesenteric artery. Methods Wire myography was used to measure the vasomotor responses of freshly dissected rat mesenteric artery and aorta. Arteries were pre-constricted with U46619 and cumulative concentrations of either DHA or EPA (10 nM-30 μM) were added. The mechanisms by which n-3 PUFA relaxed arteries were investigated using inhibitors of vasodilator pathways, which include: nitric oxide synthase (NOS; L-NAME), cycloxygenase (COX; indomethacin), cytochrome P450 epoxygenase (CYP450; clotrimazole); and calcium-activated potassium channels (KCa), SKCa (apamin), IKCa (TRAM-34) and BKCa (paxilline). Results Both DHA- and EPA-induced relaxations were partially inhibited following endothelium removal in rat mesenteric arteries. Similarly, in aorta EPA-induced relaxation was partially suppressed due to endothelium removal. CYP450 also contributed to EPA-induced relaxation in mesenteric artery. Inhibition of IKCa partially attenuated DHA-induced relaxation in aorta and mesenteric artery along with EPA-induced relaxation in mesenteric artery. Furthermore, this inhibition of DHA- and EPA-induced relaxation was increased following the additional blockade of BKCa in these arteries. Conclusions This study provides evidence of heterogeneity in the vasodilation mechanisms of DHA and EPA in different vascular beds. Our data also demonstrates that endothelium removal has little effect on relaxations produced by either PUFA. We demonstrate IKCa and BKCa are involved in DHA-induced relaxation in rat aorta and mesenteric artery; and EPA-induced relaxation in rat mesenteric artery only. CYP450 derived metabolites of EPA may also be involved in BKCa dependent relaxation. To our knowledge this is the first study indicating the involvement of IKCa in n-3 PUFA mediated relaxation

The Millennium Galaxy Catalogue: The connection between close pairs and asymmetry; implications for the galaxy merger rate

We compare the use of galaxy asymmetry and pair proximity for measuring galaxy merger fractions and rates for a volume limited sample of 3184 galaxies with -21 < M(B) -5 log h < -18 mag. and 0.010 < z < 0.123 drawn from the Millennium Galaxy Catalogue. Our findings are that: (i) Galaxies in close pairs are generally more asymmetric than isolated galaxies and the degree of asymmetry increases for closer pairs. At least 35% of close pairs (with projected separation of less than 20 h^{-1} kpc and velocity difference of less than 500 km s^{-1}) show significant asymmetry and are therefore likely to be physically bound. (ii) Among asymmetric galaxies, we find that at least 80% are either interacting systems or merger remnants. However, a significant fraction of galaxies initially identified as asymmetric are contaminated by nearby stars or are fragmented by the source extraction algorithm. Merger rates calculated via asymmetry indices need careful attention in order to remove the above sources of contamination, but are very reliable once this is carried out. (iii) Close pairs and asymmetries represent two complementary methods of measuring the merger rate. Galaxies in close pairs identify future mergers, occurring within the dynamical friction timescale, while asymmetries are sensitive to the immediate pre-merger phase and identify remnants. (iv) The merger fraction derived via the close pair fraction and asymmetries is about 2% for a merger rate of (5.2 +- 1.0) 10^{-4} h^3 Mpc^{-3} Gyr^{-1}. These results are marginally consistent with theoretical simulations (depending on the merger time-scale), but imply a flat evolution of the merger rate with redshift up to z ~1.Comment: 10 pages, 10 figures, emulateapj format. ApJ, accepte

Implications for the origin of dwarf early-type galaxies: a detailed look at the isolated rotating dwarf early-type galaxy CG 611, with ramifications for the Fundamental Plane's (S_K)^2 kinematic scaling and the spin-ellipticity diagram

Selected from a sample of nine, isolated, dwarf early-type galaxies (ETGs) having the same range of kinematic properties as dwarf ETGs in clusters, we use CG 611 (LEDA 2108986) to address the Nature versus Nurture debate regarding the formation of dwarf ETGs. The presence of faint disk structures and rotation within some cluster dwarf ETGs has often been heralded as evidence that they were once late-type spiral or dwarf irregular galaxies prior to experiencing a cluster-induced transformation into an ETG. However, CG 611 also contains significant stellar rotation (~20 km/s) over its inner half light radius, R_(e,maj)=0.71 kpc, and its stellar structure and kinematics resemble those of cluster ETGs. In addition to hosting a faint young nuclear spiral within a possible intermediate-scale stellar disk, CG 611 has accreted an intermediate-scale, counter-rotating gas disk. It is therefore apparent that dwarf ETGs can be built by accretion events, as opposed to disk-stripping scenarios. We go on to discuss how both dwarf and ordinary ETGs with intermediate-scale disks, whether under (de)construction or not, are not fully represented by the kinematic scaling S_0.5=sqrt{ 0.5(V_rot)^2 + sigma^2 }, and we also introduce a modified spin-ellipticity diagram, lambda(R)-epsilon(R), with the potential to track galaxies with such disks.Comment: 15 pages (includes 9 figures and an extensive 2+ page reference list

Regulation of KCa2.3 andendothelium-dependent hyperpolarization (EDH) in the rat middle cerebral artery: the role of lipoxygenase metabolites and isoprostanes

Background and Purpose. In rat middle cerebral arteries, endothelium-dependent hyperpolarization (EDH) is mediated by activation of calcium-activated potassium(KCa) channels specifically KCa2.3 and KCa3.1. Lipoxygenase (LOX) products function as endothelium-derived hyperpolarizing factors (EDHFs) in rabbit arteries by stimulating KCa2.3. We investigated if LOX products contribute to EDH in rat cerebral arteries. Methods. Arachidonic acid (AA) metabolites produced in middle cerebral arteries were measured using HPLC and LC/MS. Vascular tension and membrane potential responses to SLIGRL were simultaneously recorded using wire myography and intracellular microelectrodes. Results. SLIGRL, an agonist at PAR2 receptors, caused EDH that was inhibited by a combination of KCa2.3 and KCa3.1 blockade. Non-selective LOX-inhibition reduced EDH, whereas inhibition of 12-LOX had no effect. Soluble epoxide hydrolase (sEH) inhibition enhanced the KCa2.3 component of EDH. Following NO synthase (NOS) inhibition, the KCa2.3 component of EDH was absent. Using HPLC, middle cerebral arteries metabolized 14C-AA to 15- and 12-LOX products under control conditions. With NOS inhibition, there was little change in LOX metabolites, but increased F-type isoprostanes. 8-iso-PGF2α inhibited the KCa2.3 component of EDH. Conclusions. LOX metabolites mediate EDH in rat middle cerebral arteries. Inhibition of sEH increases the KCa2.3 component of EDH. Following NOS inhibition,loss of KCa2.3 function is independent of changes in LOX production or sEH inhibition but due to increased isoprostane production and subsequent stimulation of TP receptors. These findings have important implications in diseases associated with loss of NO signaling such as stroke; where inhibition of sEH and/or isoprostane formation may of benefit