Photoemission study of itinerant ferromagnet Cr1-δ Te

The electronic structures of the itinerant ferromagnets Cr1-δTe (δ=0.05, 0.25, and 0.375) have been studied by photoemission spectroscopy. The valence-band spectra are compared with the density of states given by band-structure calculations. In spite of the itinerant nature of the d electrons, disagreement between the photoemission spectra and the band-structure calculations exists in the magnitude of the d-band exchange splitting and the spectral weight at the Fermi level and 2-4 eV below it: The occupied d band for δ=0.05 is shifted away from the Fermi level; the observed spectral weight at the Fermi level is significantly suppressed compared with the band-structure calculations for δ=0.05 and 0.375, where the nominal d-electron numbers are close to integers 4 and 3, respectively. Configuration-interaction cluster-model calculations have been made for δ=0.05 and 0.375 to explain the spectral weight distribution in the high-binding-energy (2-4 eV) region in terms of electron-correlation effects. The d-d on-site Coulomb energy is estimated to be significant, U∼2 eV, and nearly equal to or smaller than the charge-transfer energy Δ∼2-3 eV

Role of Ca(2+)-activated K(+) channels in acetylcholine-induced dilatation of the basilar artery in vivo

1. We tested the hypothesis that activation of large conductance calcium-activated potassium channels is involved in dilator responses of the basilar artery to acetylcholine in vivo. Using a cranial window in anaesthetized rats, we examined responses of the basilar artery to acetylcholine. 2. Topical application of acetylcholine (10(−6) and 10(−5) M) increased diameter of the basilar artery from 238±7 μm to 268±7 and 288±7 μm, respectively (P<0.05 vs. baseline diameter). Iberiotoxin (10(−8) M), an inhibitor of large conductance calcium-activated potassium channels, did not affect baseline diameter of the basilar artery. In the presence of 10(−8) M iberiotoxin, 10(−6) and 10(−5) M acetylcholine increased diameter of the basilar artery from 239±7 μm to 246±7 and 261±7 μm, respectively. Thus, iberiotoxin attenuated acetylcholine-induced dilatation of the basilar artery (P<0.05). 3. Sodium nitroprusside (10(−7) and 10(−6) M) increased diameter of the basilar artery from 242±9 μm to 310±12 and 374±13 μm, respectively (P<0.05 vs. baseline diameter). In the presence of iberiotoxin (10(−8) M), sodium nitroprusside (10(−7) and 10(−6) M) increased diameter of the basilar artery from 243±6 μm to 259±9 and 311±12 μm, respectively. Thus, iberiotoxin attenuated dilator responses of the basilar artery to sodium nitroprusside (P<0.05). 4. Iberiotoxin partly inhibited dilator responses of the basilar artery to forskolin, a direct activator of adenylate cyclase, but did not affect vasodilatation produced by levcromakalim, a potassium channel opener. 5. These results suggest that dilator responses of the basilar artery to acetylcholine and sodium nitroprusside are mediated, in part, by activation of large conductance calcium-activated potassium channels. Because both acetylcholine and sodium nitroprusside have been shown to activate guanylate cyclase via nitric oxide, activation of large conductance calcium-activated potassium channels may be one of the major mechanisms by which cyclic GMP causes dilatation of the basilar artery in vivo