Dominic Stone
Dihydropyridine receptors (DHPRs) are voltage-gated Ca2+ channels that are expressed in diverse cell types, including skeletal and cardiac muscle. In cardiac muscle, the DHPR appears to lack the γ subunit, which is present in skeletal muscle DHPRs. The cardiac DHPR is well-adapted for Ca2+-entry dependent excitation-contraction (EC) coupling, producing a large, rapidly activating Ca2+ current. This influx of Ca2+ through the DHPR channel induces further Ca2+ release from the sarcoplasmic reticulum (SR), a process known as calcium-induced calcium release. This mechanism is crucial for initiating muscle contraction in cardiac muscle.
| Characteristics | Values |
|---|---|
| DHPR full form | Dihydropyridine Receptors |
| DHPR in cardiac muscle | Expressed in cardiac muscle |
| DHPR in other muscles | Expressed in skeletal and smooth muscle |
| DHPR function | Voltage-gated Ca2+ channels |
| DHPR in cardiac muscle function | Ca2+ entry-dependent EC coupling |
| DHPR in skeletal muscle function | Small, slowly activating Ca2+ current |
| DHPR in cardiac muscle structure | Lacks the γ subunit |
| DHPR in skeletal muscle structure | Consists of five subunits (α1, α2, β, γ, and δ) |
| DHPR in cardiac muscle mechanism | Activates RyR-2, causing a large release of Ca2+ from the SR |
| DHPR in skeletal muscle mechanism | Interacts with RyR-1 without requiring Ca2+ entry |
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What You'll Learn
DHPRs are voltage-gated Ca2+ channels
Dihydropyridine receptors (DHPRs) are voltage-gated Ca2+ channels. They are expressed in diverse cell types, including skeletal and cardiac muscle. The DHPR senses depolarization of the T-tubule membrane and opens its Ca2+ channel, allowing Ca2+ to enter the cell.
In skeletal muscle, there is a very high concentration of DHPRs, situated in the T-tubules. In cardiac muscle, DHPRs are expressed in the heart, brain, and a number of other tissues. The DHPR isoform plays a critical role in determining the nature of EC coupling. For example, in cardiac muscle, DHPRs are well-adapted for Ca2+-entry dependent EC coupling, producing a large, rapidly activating Ca2+ current. In contrast, skeletal muscle DHPRs are adapted to produce a small, slowly activating Ca2+ current, triggering SR Ca2+ release by a mechanism that does not require Ca2+ entry.
The DHPR has an asymmetrical main body joined by a hook-like extension. The main body is composed of a "trapezoid" and a "tetrahedroid". The skeletal muscle DHPR consists of five subunits (α1, α2, β, γ, and δ), one of which (α1) forms the Ca2+ channel and has the DHPR binding site. The opening of the pore in L-type calcium channels takes place in the α1 subunit.
DHPRs are critical for muscle contraction, secretion, integration of synaptic input in neurons, and synaptic transmission. They are also involved in excitation-contraction (EC) coupling in the heart, where Ca2+ entering the cardiac DHPR activates RyR-2, causing a large additional release of Ca2+ from the sarcoplasmic reticulum (SR). This process is known as Ca2+-induced Ca2+ release (CICR) and is mediated by ryanodine receptors (RyRs). In skeletal muscle, DHPRs and RyRs exhibit reciprocal signaling, with the Ca2+ release activity of RyR-1 controlled by the DHPR and the Ca2+ channel activity of the DHPR controlled by RyR-1.
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DHPRs are expressed in skeletal and cardiac muscle
Dihydropyridine receptors (DHPRs) are voltage-gated Ca2+ channels that are expressed in skeletal and cardiac muscle. In skeletal muscle, there is reciprocal signalling between the skeletal isoforms of DHPR and the ryanodine receptor (RyR), specifically RyR-1. Here, the Ca2+ release activity of RyR-1 is controlled by DHPR, and the Ca2+ channel activity of DHPR is controlled by RyR-1. In cardiac muscle, DHPR interacts with RyR-2, which is also the predominant isoform in the brain.
The skeletal DHPR is expressed at high levels only in skeletal muscle, while the cardiac DHPR is expressed in the heart, brain, and other tissues. The skeletal DHPR consists of five subunits (α1, α2, β, γ, and δ), with α1 forming the Ca2+ channel and containing the DHPR binding site. The cardiac DHPR, on the other hand, appears to lack the γ subunit, which contributes to the different mechanisms of excitation-contraction (EC) coupling in skeletal and cardiac muscle.
In skeletal muscle, DHPR functions as a voltage sensor and a slowly activating Ca2+ channel, controlling the release of Ca2+ from the sarcoplasmic reticulum (SR). This mechanism does not require the entry of extracellular Ca2+. In contrast, the cardiac DHPR is well-adapted for Ca2+ entry-dependent EC coupling, producing a large, rapidly activating Ca2+ current. This rapid activation of the cardiac DHPR triggers a large release of Ca2+ from the SR, a process known as calcium-induced calcium release.
The differences in the isoforms of DHPR expressed in skeletal and cardiac muscle are significant. The large Ca2+ currents produced by the cardiac DHPR would be maladaptive for skeletal muscle, potentially leading to depletion of Ca2+ from the transverse tubules. Conversely, the small, slowly activating Ca2+ current produced by the skeletal DHPR is better suited to the needs of skeletal muscle, preventing Ca2+ depletion while still triggering SR Ca2+ release.
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DHPRs are involved in excitation-contraction coupling
Dihydropyridine receptors (DHPRs) are voltage-gated Ca2+ channels that are expressed in diverse cell types, including skeletal and cardiac muscle. In cardiac muscle, DHPRs play a crucial role in excitation-contraction (EC) coupling, also known as excitation-contraction pairing (E-C pairing). This process is initiated by the entry of Ca2+ through the DHPR channel, which results in a further release of Ca2+ from the sarcoplasmic reticulum (SR). This mechanism is known as calcium-induced calcium release.
The cardiac DHPR is specifically adapted for Ca2+-entry dependent EC coupling. It produces a large, rapidly activating Ca2+ current, making it well-suited for triggering the release of Ca2+ from the SR. This rapid activation of Ca2+ channels is a key feature of excitation-contraction coupling in cardiac muscle. The influx of Ca2+ through DHPR channels induces a larger release of Ca2+ from the SR, which is essential for cardiac muscle contraction.
In contrast, skeletal muscle exhibits a different mechanism of EC coupling. In skeletal muscle, DHPRs function as voltage sensors and slowly activating Ca2+ channels. The voltage sensor controls the release of Ca2+ from the SR, and this process does not require the entry of extracellular Ca2+. Instead, the skeletal DHPR interacts directly with the ryanodine receptor (RyR-1) to regulate Ca2+ release. This highlights the distinct roles of DHPRs in cardiac and skeletal muscle EC coupling.
The cardiac DHPR appears to lack the γ subunit, which is present in the skeletal DHPR. This difference in subunit composition likely contributes to the divergent mechanisms of EC coupling between the two muscle types. The absence of the γ subunit in cardiac DHPR may be a factor in its adaptation for Ca2+-entry dependent EC coupling. Furthermore, the DHPR in cardiac muscle is involved in sensing the depolarization of the T-tubule membrane, which triggers the opening of its Ca2+ channel, allowing Ca2+ to enter the cell.
In summary, DHPRs are integral to the process of excitation-contraction coupling in cardiac muscle. The entry of Ca2+ through DHPR channels triggers a larger release of Ca2+ from the SR, which is a critical step in cardiac muscle contraction. The cardiac DHPR is specifically adapted for this rapid and Ca2+-entry dependent mechanism, showcasing the importance of DHPRs in maintaining the proper functioning of cardiac muscle.
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DHPRs are sensitive to dihydropyridines
Dihydropyridine receptors (DHPRs) are voltage-gated Ca2+ channels that are expressed in skeletal and cardiac muscle. They are also known as L-type channels and are sensitive to dihydropyridines, a class of drugs that includes nitrendipine, nisoldipine, nifedipine, and BayK 8644. These drugs affect the L-type Ca2+ channel current present on ventricular cardiomyocytes. The cardiac DHPR is adapted for Ca2+-entry dependent EC coupling, producing a large, rapidly activating Ca2+ current. This is in contrast to the skeletal DHPR, which produces a small, slowly activating Ca2+ current.
In skeletal muscle, DHPRs function as voltage sensors that interact with RYRs to release calcium needed for muscle contraction. This function does not require calcium permeation through the DHPR channel. The DHPR senses depolarization of the T-tubule membrane and opens its Ca2+ channel, allowing calcium to enter the cell. This calcium entry triggers intracellular calcium release for excitation-contraction coupling. In addition to this fast calcium release, depolarization of skeletal myotubes also evokes slow calcium waves that involve the cell nucleus.
The cardiac DHPR appears to lack the γ subunit, which is present in the skeletal DHPR. This difference likely explains the different mechanisms of excitation-contraction coupling in skeletal and cardiac muscle. The cardiac DHPR is encoded by a single gene, CACNA1C, located on chromosome 12p13.3. The human cardiac α1C subunit is composed of 2157 amino acids.
The effect of BayK on the cardiac DHPR is mediated by a Ca2+-independent connection between the DHPR and RyR. BayK increases ryanodine binding to intact ferret ventricular myocytes, but this effect is eliminated by mechanical disruption of SR-sarcolemmal junctions. BayK also has no influence on SR Ca2+ release in skinned guinea pig atrial fibers. Thus, while BayK can have direct effects on the RyR, it appears that its primary effect is through the DHPR.
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DHPRs are activated by depolarization
Dihydropyridine receptors (DHPRs) are voltage-gated Ca2+ channels expressed in diverse cell types, including skeletal and cardiac muscle. They play a crucial role in excitation-contraction (EC) coupling, which is the process that initiates muscle contraction.
In cardiac muscle, DHPRs are activated by depolarization of the T-tubule membrane. This depolarization opens the DHPR's Ca2+ channel, allowing Ca2+ to enter the cell. The DHPR senses this depolarization and triggers the release of Ca2+ from the sarcoplasmic reticulum (SR), a process known as Ca2+-induced Ca2+ release (CICR). This release of Ca2+ is essential for EC coupling in cardiac muscle.
The cardiac DHPR appears to lack the γ subunit, which is present in the skeletal muscle DHPR. This difference contributes to the distinct mechanisms of EC coupling in skeletal and cardiac muscle. The cardiac DHPR is well-suited for Ca2+ entry-dependent EC coupling, producing a large and rapid Ca2+ current. In contrast, the skeletal muscle DHPR generates a smaller and slower Ca2+ current to trigger Ca2+ release from the SR without requiring Ca2+ entry.
The DHPR's role in EC coupling is closely associated with the ryanodine receptor (RyR). In cardiac muscle, the DHPR activates the RyR, leading to a substantial release of Ca2+ from the SR. This activation occurs through either chemical or mechanical coupling mechanisms. The DHPR-RyR interaction is not fully understood, but it is known that they are in close physical proximity to each other.
In summary, DHPRs are activated by depolarization, which initiates a series of events leading to muscle contraction. The specific mechanisms vary between skeletal and cardiac muscle, with the cardiac DHPR relying on Ca2+ entry to activate EC coupling. The DHPR's interaction with the RyR is a critical aspect of this process, highlighting the complex nature of EC coupling in muscle cells.
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Frequently asked questions
DHPRs, or dihydropyridine receptors, are voltage-gated Ca2+ channels. They are a type of L-type channel.
Yes, DHPRs are expressed in cardiac muscle. They are also found in skeletal muscle and smooth muscle.
DHPRs play a critical role in excitation-contraction (EC) coupling in cardiac muscle. They function as rapidly-activated calcium channels, allowing the influx of calcium into the cell and triggering the release of more calcium from the sarcoplasmic reticulum (SR).
The cardiac DHPR is well-adapted for Ca2+-entry dependent EC coupling, producing a large, rapidly activating Ca2+ current. In contrast, the skeletal DHPR produces a smaller, slower current and triggers SR Ca2+ release without requiring Ca2+ entry.
No, the cardiac DHPR appears to lack the gamma subunit.
