Properties of spontaneous inward currents recorded in smooth muscle cells isolated from the rabbit portal vein

• Published in: The Journal of physiology Vol. 451; no. 1; pp. 525 - 537
• Main Authors: Wang, Q, Hogg, R C, Large, W A
• Format: Journal Article
• Language: English
• Published: Oxford The Physiological Society 01-06-1992; Blackwell
• Subjects: Animals; Biological and medical sciences; Blood vessels and receptors; Caffeine - pharmacology; Calcium - metabolism; characterization; Chlorides - metabolism; Electrophysiology; Female; Fundamental and applied biological sciences. Psychology; In Vitro Techniques; Male; membrane currents; Membrane Potentials - drug effects; Muscle, Smooth, Vascular - cytology; Muscle, Smooth, Vascular - drug effects; Muscle, Smooth, Vascular - metabolism; Norepinephrine - pharmacology; Portal Vein - cytology; Portal Vein - drug effects; Portal Vein - metabolism; Rabbits; smooth muscle; veins; Vertebrates: cardiovascular system; Electrophysiology; Rabbit; Smooth muscle; Patch clamp method; Ionic current; Lagomorpha; Vertebrata; Mammalia; Chlorides; Blood vessel; Isolated cell; Circulatory system; Portal vein; Inward current
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/jphysiol.1992.sp019177

1. Characteristics of spontaneous transient inward currents (STICs) which produced membrane depolarization were analysed with
the perforated patch technique in single smooth muscle cells isolated from the rabbit portal vein. 2. In K(+)-free solutions
the amplitude of STICs was linearly related to membrane potential and the reversal potential (Er) was -3.0 +/- 0.9 mV. Replacement
of external NaCl with NaI shifted Er to -40.0 +/- 1.0 mV. Substitution of external NaCl by NaSCN also moved Er to negative
values but replacement of sodium with Tris and choline did not change Er. It is concluded that STICs are generated by an increase
in chloride conductance. 3. STICs were abolished or reduced by the chloride channel antagonists anthracene-9-carboxylic acid
(1 mM) and 4-acetamido-4'-isothiocyanato-2,2'- stilbene-disulphonic acid (2 mM). 4. STICs were blocked by noradrenaline and
caffeine which deplete intracellular calcium stores. This effect was reversible and this result indicates that the primary
trigger for STICs is calcium released from intracellular stores and therefore STICs are calcium-activated chloride currents
(ICl(Ca)). 5. Removal of calcium from the bathing solution abolished STICs in six out of seven cells but STICs persisted in
Ca(2+)-free solution in one cell. When STICs were abolished in Ca(2+)-free external solution the size of the internal calcium
store, as estimated from the noradrenaline-induced ICl(Ca), was not altered. It appears that an influx of calcium is usually
necessary for STICs to be observed. 6. The frequency and amplitude of STICs were not altered by the voltage-dependent calcium
channel antagonist cadmium (1 mM). However, in some quiescent cells influx of calcium through voltage-dependent channels did
activate STICs. 7. It was concluded that in isolated portal vein cells STICs represent a Ca(2+)-activated chloride current
which leads to spontaneous depolarization of the membrane and may play an important physiological or pathophysiological role
to produce smooth muscle contraction.