Potassium transport in isolated guinea pig ileum

1960 ◽  
Vol 198 (1) ◽  
pp. 94-98 ◽  
Author(s):  
Leon Hurwitz
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Surrounding Medium ◽  
Radioactive Tracer ◽  
Muscle Membrane ◽  
Guinea Pig Ileum ◽  
Potassium Efflux ◽  
Smooth Muscle Membrane ◽  
Potassium Influx ◽  
Ion Species

A study was carried out to characterize the transport of potassium ions across the smooth muscle membrane of the isolated guinea pig ileum. The relative magnitudes of unidirectional ion fluxes were followed by employing the radioactive tracer K42. In unstimulated tissues both the efflux and influx of potassium were found to be proportional to the total quantities of exchangeable ion present in the tissue and in the surrounding medium respectively. The addition of approximately 7.5 x 10–6 m pilocarpine, a concentration which produced a maximal contraction of longitudinal smooth muscle, increased potassium efflux about 100–150%, whereas potassium influx was markedly impeded. Cocaine (about 9 x 10–4 m) blocked the enhancement of potassium efflux induced by pilocarpine, but did not alter potassium efflux in the untreated tissue. The data suggest that the movements of potassium in excited smooth muscle fibers reflect, to a large extent, a permeability change either to sodium ions or some other ion species which exert a depolarizing influence on the cell membrane.

BaCl2-induced contractions in the guinea pig ileum longitudinal muscle: role of presynaptic release of neurotransmitters and Ca2+ translocation in the postsynaptic membrane

1981 ◽  
Vol 59 (6) ◽  
pp. 541-547 ◽  
Author(s):  
John G. Clement
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Longitudinal Muscle ◽  
Postsynaptic Membrane ◽  
Muscle Membrane ◽  
Guinea Pig Ileum ◽  
Presynaptic Neuron ◽  
Smooth Muscle Membrane ◽  
Release Of Acetylcholine ◽  
The Right

Early studies indicated that the BaCl2-induced contractions in the guinea pig ileum longitudinal muscle strip (GPI-LMS) were, in part, neuronal in origin. However, recent studies have suggested that BaCl2-induced contractions were produced by an action directly on the smooth muscle membrane. The purpose of this study was to investigate the mechanism of the BaCl2 contractions in the GPI-LMS. Botulinum toxin (5 × 105 MLD/mL), which blocks the electrically induced release of acetylcholine (ACh), hemicholinium-3 (HC-3; 110 μM), which blocks ACh synthesis, tetrodotoxin (TTX; 60 nM), which blocks Na+ channels, black widow spider venom, which depletes the presynaptic neuron of neurotransmitter, and atropine (2.9 μM), a potent muscarinic antagonist, had no effect on the BaCl2 contractions. Desensitization of the GPI-LMS to substance P did not affect the BaCl2 contraction. In Ca2+-free buffer the BaCl2 dose–response curve was shifted to the right. In Ca2+-free solution the time to 50% inhibition of the contractile response to ACh (73 nM) and BaCl2 (1.16 mM) was 3.7 and 125 min, respectively. The D 600 IC50 for ACh and BaCl2 contractions was 220 and 130 nM, respectively. In Ca2+-free buffer either EGTA (0.53 mM) or D 600 (1 μM) were potent inhibitors of BaCl2 contractions. These results suggest that in the GPI-LMS the BaCl2 response is not mediated by a release of ACh (or substance P) because inhibitors of ACh release, synthesis, and receptors do not affect the responses. Also, the BaCl2 contraction is not due to activation of Na+ channels because TTX is without effect. The BaCl2-induced contraction appears to be mainly due to the movement of membrane bound Ca2+ through D 600 sensitive Ca2+ channels with extracellular Ca2+ and possible passage of Ba2+ ions intracellularly playing relatively minor roles.

Cyclopiazonic acid decreases spontaneous transient depolarizations in guinea pig mesenteric lymphatic vessels in endothelium-dependent and -independent manners

2004 ◽  
Vol 286 (6) ◽  
pp. H2287-H2295 ◽  
Author(s):  
Ilia Ferrusi ◽  
Jun Zhao ◽  
Dirk van Helden ◽  
Pierre-Yves von der Weid
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Lymphatic Vessels ◽  
Cyclopiazonic Acid ◽  
Muscle Membrane ◽  
Pacemaker Activity ◽  
Smooth Muscle Membrane ◽  
Intracellular Ca

Guinea pig mesenteric lymphatic vessels exhibit vasomotion through a pacemaker mechanism that involves intracellular Ca2+ release and resultant spontaneous transient depolarizations (STDs) of the smooth muscle membrane potential. This study presents a detailed characterization of the effects of cyclopiazonic acid (CPA) on this pacemaker activity. Microelectrode recordings from smooth muscle in vessel segments revealed that application of CPA (1–10 μM) caused a hyperpolarization accompanied by a decrease in the frequency and amplitude of STDs. The CPA-induced hyperpolarization was abolished after destruction of the endothelium and in the presence of NG-nitro-l-arginine (100 μM) or 1 H-[1,2,4]oxadiazolol-[4,3- a]quinoxaline-1-one (10 μM), which suggests a contribution of endothelium-derived nitric oxide (EDNO) in this response. In the absence of EDNO-induced effects, CPA decreased the frequency and amplitude of STDs recorded before and in the presence of the thromboxane A2 mimetic U-46619, norepinephrine, or thimerosal. CPA abolished U-46619-induced vasomotion as determined by measurement of constriction-associated intracellular Ca2+ concentration using the ratiometric Ca2+ indicator fura-2. The endothelial actions of CPA were compared with those of ACh, which is known to cause EDNO release in this preparation. Although CPA and ACh both increased endothelial intracellular Ca2+ concentration and depolarized the membrane potential, the kinetics of action for both parameters were markedly slower for CPA than ACh. These results suggest that CPA first hyperpolarizes the lymphatic smooth muscle and decreases STD frequency and amplitude through endothelial release of EDNO, and second, consistent with the action of CPA to inhibit sarcoplasmic reticulum Ca2+-ATPase and deplete Ca2+ stores, it further reduces STD activity. Inhibition of the lymphatic smooth muscle pacemaker mechanism is thought to abolish agonist-induced vasomotion.

K transport and mechanical responses of isolated longitudinal smooth muscle from guinea pig ileum

1961 ◽  
Vol 200 (4) ◽  
pp. 789-793 ◽  
Author(s):  
George B. Weiss ◽  
Robert E. Coalson ◽  
Leon Hurwitz
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Contractile Response ◽  
Muscle Tone ◽  
Muscle Layer ◽  
Smooth Muscle Contraction ◽  
Potassium Ion ◽  
Guinea Pig Ileum ◽  
Potassium Efflux ◽  
Longitudinal Smooth Muscle

The longitudinal smooth muscle layer of the guinea pig ileum was isolated in order to investigate its contractile responses and unidirectional K42 fluxes. Pilocarpine (7.5 x 10–6 m), acetylcholine (6.6 x 10–6 m), and a modified Tyrode's solution in which potassium ion was substituted for almost all the sodium ion were employed as excitatory agents. Cocaine (8.5 x 10–4 m) and a calcium-free Tyrode's solution served as inhibitory agents. Smooth muscle tone and potassium efflux of this relatively pure tissue were both increased by all three excitatory substances. Moreover, acetylcholine and pilocarpine produced a decrease in the influx of potassium ion. Bathing the tissue in a calcium-free medium for 1 hour before introducing pilocarpine to the muscle bath eliminated the contractile response that this drug ordinarily produces, but did not diminish appreciably the increase in K42 efflux. These observations are qualitatively similar to results previously obtained in analogous experiments on isolated whole ileum. In addition, cocaine (8.5 x 10–4 m) was found to block the contractile response and about three-quarters of the enhanced K42 efflux elicited by the isotonic potassium solution. It is presumed that cocaine acting at the membrane impedes ion fluxes important for smooth muscle contraction.

Changes in electrical properties of guinea pig smooth muscle membrane by experimental bladder outflow obstruction

1992 ◽  
Vol 262 (5) ◽  
pp. F885-F891 ◽  
Author(s):  
N. Seki ◽  
O. M. Karim ◽  
J. L. Mostwin
Keyword(s):  
Smooth Muscle ◽  
Electrical Properties ◽  
Guinea Pig ◽  
Electrical Activity ◽  
Membrane Depolarization ◽  
Muscle Membrane ◽  
Free Solution ◽  
Outflow Obstruction ◽  
Bladder Outflow Obstruction ◽  
Smooth Muscle Membrane

The changes in membrane electrical properties of guinea pig bladder smooth muscle following experimental bladder outflow obstruction were studied by means of an intracellular microelectrode technique. The results of this study can be summarized as follows. 1) Bladder outflow obstruction resulted in a threefold increase in bladder weight after 4-8 wk. 2) The resting membrane potential was unchanged with obstruction; however, the obstructed smooth muscle membrane was more quiescent, with less spontaneous electrical activity compared with control tissue. 3) The membrane constants, space constant and time constant, were both reduced in the obstructed bladders. 4) There was no detectable difference in membrane depolarization induced by high extracellular K+ solution between control and obstructed bladders. 5) Both the membrane depolarization induced by K(+)-free solution or ouabain-containing Krebs solution and ouabain-sensitive membrane hyperpolarization by K(+)-containing solution after application of K(+)-free solution were significantly increased in the obstructed bladders. 6) Low extracellular Cl- solution evoked greater membrane depolarization in obstructed bladders. These results suggest that bladder outflow obstruction results in suppression of the cell-to-cell transfer of electrical activity and activation of a membrane electrogenic Na(+)-K+ pump mechanism in guinea pig detrusor.

Sign in / Sign up

Export Citation Format

Share Document