Neuromuscular transmission and smooth muscle membrane properties in the guinea-pig ear artery

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.

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Vasodilatation and smooth muscle membrane potential changes in arterioles from the guinea-pig small intestine.

The Journal of Physiology ◽

10.1113/jphysiol.1995.sp020548 ◽

1995 ◽

Vol 482 (3) ◽

pp. 661-667 ◽

Cited By ~ 21

Author(s):

N Kotecha ◽

T O Neild

Keyword(s):

Smooth Muscle ◽

Small Intestine ◽

Membrane Potential ◽

Guinea Pig ◽

Muscle Membrane ◽

Smooth Muscle Membrane

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Potassium transport in isolated guinea pig ileum

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1960.198.1.94 ◽

1960 ◽

Vol 198 (1) ◽

pp. 94-98 ◽

Cited By ~ 12

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.

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

AJP Renal Physiology ◽

10.1152/ajprenal.1992.262.5.f885 ◽

1992 ◽

Vol 262 (5) ◽

pp. F885-F891 ◽

Cited By ~ 10

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.

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