scholarly journals Electrical properties of the smooth muscle membrane of the guinea-pig vas deferens

1966 ◽  
Vol 186 (1) ◽  
pp. 27-41 ◽  
Author(s):  
Y. Hashimoto ◽  
Mollie E. Holman ◽  
J. Tille
Keyword(s):  
Smooth Muscle ◽  
Electrical Properties ◽  
Guinea Pig ◽  
Vas Deferens ◽  
Muscle Membrane ◽  
Smooth Muscle Membrane

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.

scholarly journals A CHOLINERGIC COMPONENT IN THE INNERVATION OF THE LONGITUDINAL SMOOTH MUSCLE OF THE GUINEA PIG VAS DEFERENS

1969 ◽  
Vol 41 (2) ◽  
pp. 462-476 ◽  
Author(s):  
Peter M. Robinson
Keyword(s):  
Smooth Muscle ◽  
Plasma Membrane ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Plasma Membranes ◽  
Vas Deferens ◽  
Muscle Cells ◽  
Muscle Membrane ◽  
Smooth Muscle Tissue ◽  
Longitudinal Smooth Muscle

Acetylcholinesterase (AChE) has been detected on the plasma membrane of about 25% of the axons in the longitudinal smooth muscle tissue of guinea pig vas deferens. These axons are presumably cholinergic. No enzyme was detected in the remaining 75% of axons. These axons are presumably adrenergic. The plasma membrane of the Schwann cells associated with the cholinergic axons also stained for AChE. Some axon bundles contained only cholinergic or adrenergic axons while others contained both types of axon. When a cholinergic axon approached within 1100 A of a smooth muscle cell, there was a patch of AChE activity on the muscle membrane adjacent to the axon. It is suggested that these approaches are the points of effective transmission from cholinergic axons to smooth muscle cells. Butyrylcholinesterase activity was detected on the plasma membranes of all axons and smooth muscle cells in this tissue.

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.

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