Effects of excitatory neurotransmitters on Ca2+ channel current in smooth muscle cells isolated from guinea‐pig urinary bladder

  title={Effects of excitatory neurotransmitters on Ca2+ channel current in smooth muscle cells isolated from guinea‐pig urinary bladder},
  author={Shinsuke Nakayama},
  journal={British Journal of Pharmacology},
  • S. Nakayama
  • Published 1 September 1993
  • Biology
  • British Journal of Pharmacology
1 A whole‐cell voltage clamp technique was used to examine the effects of purinoceptor and muscarinic receptor agonists on voltage‐sensitive Ca2+ channels in guinea‐pig isolated urinary bladder cells. 2 When the cell membrane was clamped at the holding potential, rapid application of ATP elicited a large inward current in normal solution containing 2.5 mm Ca2+, and reduced the subsequent Ca2+ channel current evoked by a depolarizing pulse (0 mV). Carbachol (CCh) elicited little membrane current… 

Long Ca2+ channel opening induced by large depolarization and Bay K 8644 in smooth muscle cells isolated from guinea‐pig detrusor

It is concluded that L‐type Ca2+ channels in guinea‐pig detrusor cells are open for much longer after large depolarizations consistent with their being two channel open states, and that Bay K 8644 prolongs the lifetime of both open states.

Muscarinic suppression of Ca2+ current in smooth muscle cells of the guinea‐pig urinary bladder

It appears that CCh suppresses ICa via two independent mechanisms: (1) Ca(2+)‐mediated inactivation of the Ca2+ channel, which is caused byCa2+ release from InsP3‐ and TG‐sensitive internal stores, and (2) a GTP‐binding protein‐mediated mechanism, which requires intracellular Ca2+.

The α1‐subunit of smooth muscle Ca2+ channel preserves multiple open states induced by depolarization

The sum of unitary channel currents revealed that the tail current seen after large conditioning depolarization had a slower deactivation time constant compared to that seen when the cell membrane was depolarized briefly with a test step, suggesting that large depolarizations transform the conformation of the Ca2+ channels to a second open state.

Possible contribution of long open state to noninactivating Ca2+ current in detrusor cells.

Differences in the voltage dependence of the development of the long open state in various smooth muscles, as well as differences in the equilibrium constant between open and inactivated states, could underlie the different patterns of contractile behavior that characterize smooth muscles.

Slow deactivation and U-shaped inactivation properties in cloned Ca[v]1.2b channels in Chinese hamster ovary cells

A kinetic scheme with one closed state, two open states ( O 1, O 2 ) and two inactivated states linked to the closed state and open state O 1 , respectively, protected from inactivation is drawn up, suggesting involvement of physical processes in the channel protein.



Evidence for multiple open states of the Ca2+ channels in smooth muscle cells isolated from the guinea‐pig detrusor.

The results suggest that the voltage‐dependent Ca2+ channels have at least two open states with different time constants, the tail current being the result of a long open channel state induced by large depolarizations.

Intracellular calcium ions modulate acetylcholine‐induced inward current in guinea‐pig ileum.

The results show that the activity of Ins, ACh is very sensitive to the intracellular Ca2+ concentration in the physiological range.

ATP‐induced Ca2+ release and Cl‐ current in cultured smooth muscle cells from pig aorta.

It is concluded that ATP causes a release of calcium from intracellular stores via a Cl‐ current, which can depolarize the cell membrane and thereby promote a voltage‐gated Ca2+ entry.

Effect of membrane potential on acetylcholine‐induced inward current in guinea‐pig ileum.

The results show that ACh‐induced depolarization is controlled by the membrane potential, which is explained by the voltage‐dependent gating of Ins, Ach.

Inactivation of the voltage‐dependent Ca2+ channel current in smooth muscle cells isolated from the guinea‐pig detrusor.

The inactivation and recovery of voltage‐dependent Ca2+ channel currents were examined by manipulating the membrane potential over a wide range and by changing the extracellular divalent cation concentrations.

Large conductance calcium‐activated non‐selective cation channel in smooth muscle cells isolated from rat portal vein.

It is concluded that portal vein smooth muscle cells possess Ca(2+)‐activated nonspecific channels which are highly permeable to Ca2+ ions.

Ca2+ influx through ATP‐gated channels increments [Ca2+]i and inactivates ICa in myocytes from guinea‐pig urinary bladder.

The results are in agreement with the hypothesis of ‘ICa inactivation by Ca2+’ and the ATP‐induced [Ca2+]i transients and the reduction of peak ICa recovered along a similar time course.

Ca2+ and voltage inactivate Ca2+ channels in guinea‐pig ventricular myocytes through independent mechanisms.

Voltage and Ca2+ ions inactivate the L‐type Ca 2+ channel through separate, independent mechanisms, and it is found that Ca(2+)‐dependent inactivation does not result in the immobilization of gating charge, and apparently closes the Ca2- permeation pathway through a mechanism that does not involve the voltage‐sensing region of the channel.

The properties of the ATP‐induced depolarization and current in single cells isolated from the guinea‐pig urinary bladder

The actions of exogenously applied ATP were investigated with the whole‐cell patch clamp method in single cells isolated from guinea‐pig urinary bladder with a modified concentration jump technique to find the possible role of ATP as the fast excitatory transmitter.

Acetylcholine activates non‐selective cation and chloride conductances in canine and guinea‐pig tracheal myocytes.

It is concluded that activation of muscarinic receptors in mammalian tracheal myocytes causes release of Ca2+ from intracellular stores and subsequent activation of Cl‐ and non‐selective cation conductances.