Function of a truncated dihydropyridine receptor as both voltage sensor and calcium channel (2024)

FAQs

What is the function of the dihydropyridine receptor? ›

Abstract. The dihydropyridine receptor (DHPR), normally a voltage-dependent calcium channel, functions in skeletal muscle essentially as a voltage sensor, triggering intracellular calcium release for excitation-contraction coupling.

Physiological Function. In muscle excitation–contraction (E–C) coupling, the activation of CaV1. 1 voltage-gated calcium channels (dihydropyridine receptor channels) opens RY-1 channels and triggers Ca⁺⁺ release from the SR Endo (1985) Meissner (1994).

Abstract. Dihydropyridine receptors (DHPRs), which are voltage-gated Ca²⁺ channels, and ryanodine receptors (RyRs), which are intracellular Ca²⁺ release channels, are expressed in diverse cell types, including skeletal and cardiac muscle.

Dihydropyridine receptors are primarily functional L-type calcium channels in rabbit ventricular myocytes. Circ Res. 1991 Oct;69(4):1139-45. doi: 10.1161/01.

Calcium channel blockers come in two main types. Dihydropyridines (pronounced dy-hy-dro-py-rid-eens). These target blood vessels and cause them to relax, which is why they're so effective in treating high blood pressure (the exception is nimodipine, which treats subarachnoid hemorrhage).

It represents one of the most important groups of calcium-channel modulating agents and has experienced widespread use in the treatment of cardiovascular disease which includes antihypertensive, antianginal, vasodilator and cardiac depressants activities.

In many different cell types, Ca²⁺ entering the cytosol via voltage-gated Ca²⁺ channels regulates enzyme activity, gene expression, and other biochemical processes (Flavell and Greenberg 2008).

Dihydropyridine-sensitive, voltage-gated Ca2+ channels contribute to the resting intracellular Ca2+ concentration of hippocampal CA1 pyramidal neurons.

Voltage-gated channels are proteins that can respond to small changes in membrane potential or the distribution of charge across a phospholipid bilayer. Voltage-gated channels play a vital role in the process of nerve cell communication through their involvement in production of an action potential.

The dihydropyridines are more vascular selective and the non-dihydropyridines are more myocardial selective and tend to reduce the heart rate. Further important differences are between short- and long-acting forms of the calcium channel antagonists.

What is the dihydropyridine receptor in the sarcoplasmic reticulum? ›

Depolarization of the skeletal muscle membrane elicits a change in the configuration of dihydropyridine receptors that in turn triggers sarcoplasmic reticulum (SR) Ca²⁺ release through ryanodine receptors.

Nicardipine may be the most potent overall relaxant of vascular smooth muscle among the dihydropyridines. Peak plasma levels are reached 1 hour after oral administration, with bioavailability of 35%. Plasma half-life is 8 to 9 hours.

The dihydropyridine receptor (DHPR), normally a voltage-dependent calcium channel, functions in skeletal muscle essentially as a voltage sensor, triggering intracellular calcium release for excitation-contraction coupling.

Failure of these calcium channels can result in migranes, ataxia, and also other neurological diseases. Calmodulin is a specific calcium channel sensor, and regulates the functions of the channel.

The L-type channel is the primary route for Ca²⁺ entry into cardiac, skeletal, and smooth muscles. The skeletal muscle L-type channel acts as a voltage sensor for excitation-contraction (E-C) coupling in skeletal muscle, presumably linking membrane depolarization to Ca²⁺ release from intracellular stores.

The dihydropyridines are more vascular selective and the non-dihydropyridines are more myocardial selective and tend to reduce the heart rate. Further important differences are between short- and long- acting forms of the calcium channel antagonists.

Dihydropyridine (DHP) CCBs tend to be more potent vasodilators than non-dihydropyridine (non-DHP) agents, whereas the latter have more marked negative inotropic effects.

Dihydropyridine (DHP) receptors of the transverse tubule membrane play two roles in excitation-contraction coupling in skeletal muscle: (a) they function as the voltage sensor which undergoes fast transition to control release of calcium from sarcoplasmic reticulum, and (b) they provide the conducting unit of a slowly ...

Skeletal muscle excitation–contraction (EC) coupling is initiated by sarcolemmal depolarization, which is translated into a conformational change of the dihydropyridine receptor (DHPR), which in turn activates sarcoplasmic reticulum (SR) Ca²⁺ release to trigger muscle contraction.