Drugs online research references
Life Sci. 1997;61(7):PL67-73.
Bradykinin, lemakalim and sodium nitroprusside relax the mouse trachea in vitro by different mechanisms.
Li L, Vaali K, Paakkari I, Vapaatalo H.
Institute of Biomedicine, Department of Pharmacology and Toxicology, University of Helsinki, Finland.
The role of K+ channels in the relaxations induced by bradykinin, lemakalim, an activator of ATP-sensitive K+ channels and sodium nitroprusside (SNP), a nitric oxide (NO) donor was examined in the isolated mouse trachea precontracted by methacholine (1 microM). 4-aminopyridine (4-AP, 0.1-2 mM), an inhibitor of 4-AP sensitive delayed rectifier channels, did not alter relaxations induced by bradykinin, lemakalim or SNP. Glibenclamide and glipizide (10-33 microM), inhibitors of ATP-sensitive K+ channels, inhibited relaxation to lemakalim without affecting responses to bradykinin and SNP. Charybdotoxin (10-100 nM) and iberiotoxin (10-100 nM), inhibitors of large conductance Ca2+-activated K+ channels, failed to inhibit relaxation to bradykinin, lemakalim or SNP. Apamin (0.1-1 microM), an inhibitor of small conductance Ca2+-activated K+ channels, did not alter responses to bradykinin, lemakalim and SNP. The results implicate that the mechanism of relaxation induced by bradykinin and SNP is different from that of lemakalim. Relaxation of the isolated mouse trachea by lemakalim appears to be mediated by ATP-sensitive K+ channels. Bradykinin and SNP induced relaxations are not mediated via Ca2+-activated K+ channels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9252250&dopt=Abstract
Br J Clin Pharmacol. 1997 Sep;44(3):292-4.
Forearm endothelium-dependent vascular responses and the potassium-ATP channel.
McAuley D, McGurk C, Nugent AG, Hanratty C, Maguire S, Johnston GD.
Department of Therapeutics and Pharmacology, Queen's University of Belfast, Northern Ireland.
AIMS: Vasodilation to acetylcholine is mediated at least in part by endothelium-derived hyperpolarising factor (EDHF) which causes membrane hyperpolarisation by activating potassium channels. It is however uncertain which potassium channel mediates this effect. The aim of this study was to determine the role of the potassium-ATP (K(+)-ATP) channel in mediating endothelium-dependent vascular responses to acetylcholine. METHODS: In 10 healthy volunteers acetylcholine, an endothelium-dependent vasodilator, and sodium nitroprusside as a control assessing endothelium-independent vasodilatation were infused into the non-dominant brachial artery. Forearm blood flow (FBF) in response to each dose was measured by strain-gauge venous occlusion plethysmography. The K(+)-ATP channel blocker glipizide (2.5 mg) was then administered orally. After 45 min the infusions with FBF measurements were repeated. RESULTS: Acetylcholine (P < 0.01) and sodium nitroprusside (P < 0.01) both caused an increase in FBF. There was no significant difference in vascular responses to acetylcholine (P > 0.05) or sodium nitroprusside (P > 0.05) following K(+)-ATP channel blockade. CONCLUSIONS: The K(+)-ATP channel does not modulate forearm arteriolar endothelium-dependent responses in healthy volunteers and therefore does not play a role in membrane hyperpolarisation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9296326&dopt=Abstract
Eur J Pharmacol. 1997 Aug 20;333(1):105-11.
Two populations of smooth muscle cells in the guinea-pig gastric antrum.
Duridanova DB, Gagov HS, Boev KK.
Department of Membrane Ion Channels, Institute of Biophysics, Bulgarian Academy of Sciences, Sofia.
K+ outward currents (I[K]) expressed by guinea-pig antral smooth muscle cells were studied using the whole-cell voltage-clamp technique. In about 88% of cells depolarization steps applied from Vh = -70 mV activated a fast transient component (I[K(to)]) with voltage-dependent characteristics, and a noninactivating component with slow activation kinetics (I[K(sl)]). Both components were carried by K+ ions. Apamin (10 nM to 1 microM) selectively depressed I(K[to]) in a concentration-dependent manner. I(K(sl)) was blocked by 1 mM tetraethylammonium or 0.1 microM charybdotoxin. 10 mM tetraethylammonium abolished both components of I(K). Nicardipine (1 microM) did not affect the voltage- and time-dependent characteristics of the net I(K), but reduced the current density of I(K[sl]) from 22.36+/-1.38 microA/cm2 to 13.06+/-0.92 microA/cm2 at +40 mV. In about 12% of the cells depolarization-evoked I(K) could be separated as two pharmacologically distinguishable components: a glipizide-sensitive current (forming about 70% of the net I[K]) and a charybdotoxin-sensitive current (30% of the net I[K]). Nicardipine (1 microM) affected neither the amplitude nor the time-course of I(K) of this cell population. The depletion of intracellular Ca2+ stores by thapsigargin (1 microM) or ryanodine (1 microM) led to a 50-200% increase of I(K[sl]) in the majority of cells and to an about 30% increase of the net I(K) in 12% of cells. The data obtained suggest the existence of at least two populations of cells in guinea-pig antral smooth muscle. Twelve percent of cells seem to be responsible for the generation of slow wave potentials, while 88% of cells most probably respond passively to the electrotonically spread depolarization.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9311668&dopt=Abstract
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