1.Upper airway irritation and small airways hyperreactivity due to exposure to potassium aluminium tetrafluoride flux: an extended case report.
Hjortsberg U1, Orbaek P, Arborelius M Jr, Karlsson JE. Occup Environ Med. 1994 Oct;51(10):706-9.
OBJECTIVES: 22 workers, exposed to potassium aluminium tetrafluoride used as flux for soldering aluminium, were studied as clinical outpatients for symptoms of irritation of the nose, eye, skin, and airways.
2.Action of a NO donor on the excitation-contraction pathway activated by noradrenaline in rat superior mesenteric artery.
Ghisdal P1, Gomez JP, Morel N. J Physiol. 2000 Jan 1;522 Pt 1:83-96.
The aim of the present study was to investigate the actions of NO donors in ratsuperior mesenteric artery stimulated with noradrenaline by studying their effects on isometric tension, membrane potential (Vm), cytosolic calcium concentration ([Ca2+]cyt) and accumulation of inositol phosphates. In unstimulated arteries, SNAP (S-nitroso-N-acetylpenicillamine, 10 microM) hyperpolarised Vm by 3.0 +/- 0.5 mV (n = 9). In KCl-stimulated arteries, SNAP relaxed contraction without changing Vm and [Ca2+]cyt. In noradrenaline-stimulated arteries, SNAP relaxed tension, repolarised Vm and decreased [Ca2+]cyt with the same potency. Responses to SNAP were unaffected by the following K+ channel blockers: glibenclamide, 4-aminopyridine, apamin and charybdotoxin, and by increasing the KCl concentration to 25 mM. In SNAP-pretreated arteries, the production of inositol phosphates and the contraction stimulated by noradrenaline were inhibited similarly. The guanylate cyclase inhibitor ODQ abolished the increase in cyclic GMP content evoked by SNAP and inhibited the effects of SNAP on contraction, Vm and accumulation of inositol phosphates in noradrenaline-stimulated artery.
3.Rho-dependent kinase is involved in agonist-activated calcium entry in rat arteries.
Ghisdal P1, Vandenberg G, Morel N. J Physiol. 2003 Sep 15;551(Pt 3):855-67. Epub 2003 Jul 9.
The present study was aimed at investigating whether, besides its pivotal role in Ca(2+)-independent contraction of smooth muscle, Rho-kinase is involved in the mechanisms underlying the Ca2+ signal activated by noradrenaline in arteries. In rat aorta and mesenteric artery, the Rho-kinase inhibitor Y-27632 (10 microM) completely relaxed the contraction evoked by noradrenaline (1 microM) and simultaneously inhibited the Ca2+ signal by 54 +/- 1 % (mesenteric artery) and 71 +/- 15 % (aorta), and the cell membrane depolarisation by 56 +/- 11 % (mesenteric artery). A similar effect was observed in arteries contracted by AlF4-, while in KCl-contracted arteries, Y-27632 decreased tension without changing cytosolic Ca2+. The same effects were observed with another inhibitor of Rho-kinase (HA1077) but not with an inhibitor of protein kinase C (Ro-31-8220). Effects of Y-27632 were not prevented by incubating the artery in 25 mM KCl, with K+ channel blockers or with the Ca2+ channel blocker nimodipine.
4.Mode of regulation by G protein of the ATP-sensitive K+ channel in guinea-pig ventricular cell membrane.
Ito H1, Vereecke J, Carmeliet E. J Physiol. 1994 Jul 1;478 ( Pt 1):101-7.
1. The effect of G protein activation on the ATP-sensitive K+ (K+ATP) channel was examined in inside-out patches from guinea-pig ventricular myocytes. At low (0.3 mM) intracellular ATP concentration ([ATP]i) in the bathing solution, in the absence of agonists in the pipette, guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) or AlF4- applied to the intracellular side of the patch membrane gradually activated the K+ATP channel. The activation by GTP gamma S was irreversible, although high [ATP]i could completely close the channel. 2. In ATP-free media GTP gamma S did not increase further the activity of the fully active channel, and was unable to reactivate the channel in the non-operative state after rundown. [ATP]i-channel activity curves constructed before and after GTP gamma S application demonstrated that GTP gamma S shifts the half-inhibitory [ATP]i from 19.5 to 110 microM without changing the Hill coefficient. 3. When acetylcholine or adenosine was included in the pipette, intracellular GTP reversibly activated the K+ATP channel which was partially inhibited by [ATP]i.