| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1. Two types of effects of tetraethylammonium chloride (TEA) have been found in the smooth muscle cells of the rabbit main pulmonary artery. (a) With rapid onset of action TEA depolarizes the cell membrane, increases the membrane resistance, causes anomalous rectification and occasionally spike potentials in response to externally applied depolarizing current pulses and produces tonic contractions. (b) During prolonged (greater than 30 min) incubation in TEA phasic contractions develop progressively and the vascular strips respond to electrical stimulation with synchronized and powerful contractions. 2. There is a linear relationship between log concentration TEA and depolarization over the range of 10-100 mM-TEA. TEA (10 and 30 mM) raises the membrane resistance and decreases the core resistance. The latter effect appeared to develop more slowly than the former. 3. During short exposure to TEA part of the smooth muscle cells respond to depolarizing current pulses with spike potentials of variable amplitude and duration. These spikes are very sensitive to inhibition by verapamil or nickel chloride but are not affected by tetrodotoxin. The amplitude of electrotonic potentials, increased by TEA, is slightly further elevated by verapamil or nickle chloride. 4. TEA (10 mM) increases the mechanical response to low and intermediate potassium concentrations but has no effect on maximal contractions to high potassium. The slope of the line relating log potassium concentration to membrane potential is decreased by TEA. 5. TEA (10 mM) shifts the concentration response curve for the contractile effect of noradrenaline to the left and increases the maximum of noradrenaline-induced contractions. In the presence of TEA, noradrenaline reduces the membrane potential to markedly lower values than under control conditions. 6. It is concluded that the rapidly occurring effects of TEA on the vascular smooth muscle cells of the rabbit main pulmonary artery are a decrease in potassium and an increase in calcium conductance. The latter effect may be related to a blockade of potassium channels; however, we cannot rule out the possibility that TEA affects calcium conductance independent of its presumed action on potassium channels. The slowly developing effects of TEA may be ascribed to the formation of gap junctions and/or (less likely) to an intracellular accumulation of TEA.
This article has been cited by other articles:
|
|
 |
|
  L. Fernandes, Z. B. Fortes, D. Nigro, R. C. A. Tostes, R. A. S. Santos, and M. H. Catelli de Carvalho Potentiation of Bradykinin by Angiotensin-(1-7) on Arterioles of Spontaneously Hypertensive Rats Studied In Vivo Hypertension, February 1, 2001; 37(2): 703 - 709. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. V. Remillard, M.-A. Lupien, V. Crepeau, and N. Leblanc Role of Ca2+- and swelling-activated Cl- channels in {alpha}1-adrenoceptor-mediated tone in pressurized rabbit mesenteric arterioles Cardiovasc Res, June 1, 2000; 46(3): 557 - 568. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. F. V. Dantas, M. Urban, D. Spray, M. H. Catelli de Carvalho, and R. d. C. A. T. Passaglia Increased Acetylcholine-Induced Vasodilation in Pregnant Rats : A Role for Gap Junctional Communication Hypertension, October 1, 1999; 34(4): 937 - 942. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y.-C. Lo, J.-R. Wu, S.-N. Wu, and I.-J. Chen Glyceryl Nonivamide: A Capsaicin Derivative with Cardiac Calcitonin Gene-Related Peptide Releasing, K+ Channel Opening and Vasorelaxant Properties J. Pharmacol. Exp. Ther., April 1, 1997; 281(1): 253 - 260. [Abstract] [Full Text]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
