Dominic Stone
Cardiac muscle cells contain dihydropyridine receptors (DHPRs), which are voltage-gated Ca2+ channels located in the exterior membranes. DHPRs are a crucial component of excitation-contraction (e-c) coupling, a mechanism that enables the transduction of exterior-membrane depolarization in Ca2+ release from the sarcoplasmic reticulum (SR). In cardiac muscle, the inward flux of Ca2+ through DHPRs triggers the opening of ryanodine receptors (RyRs), leading to calcium-induced calcium release. This process is distinct from skeletal muscle, where Ca2+ is not required for RyR activation. Ultrastructural studies reveal functional differences in the DHPR/RyR reciprocal association between cardiac and skeletal muscles. While DHPRs and RyRs are in close proximity in both muscle types, DHPRs form tetrads only in skeletal fibres, allowing Ca2+ independent coupling.
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What You'll Learn
Dihydropyridine receptors (DHPRs) are voltage-gated Ca2+ channels
In skeletal muscle, DHPRs and RyRs are in close proximity, forming a direct conformational link. The DHPRs in skeletal muscle are located in the T-tubule membrane, where they sense the depolarization of the action potential. This interaction between DHPRs and RyRs in skeletal muscle allows for Ca2+-independent coupling, with the RyRs acting as the Ca2+ release channel.
In cardiac muscle, the ratio of DHPRs to RyRs is much smaller, and only a limited number of DHPRs are linked with RyRs. The cardiac DHPR is well-adapted for Ca2+ entry-dependent EC coupling, producing a large and rapidly activating Ca2+ current. This inward flux of Ca2+ through DHPRs triggers the opening of RyRs, resulting in calcium-induced calcium release.
The molecular architecture of DHPRs remains a subject of ongoing research. While the skeletal DHPR has been studied through cryo-electron microscopy, revealing an asymmetrical main body composed of a "trapezoid" and a "tetrahedroid", the molecular architecture of the eukaryotic, multiple-subunit Ca2+ channel complex is yet to be fully understood.
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Ryanodine receptors (RyRs) are intracellular Ca2+ release channels
Ryanodine receptors (RyRs) are a class of intracellular Ca2+ release channels that are present in various forms, including animal muscles and neurons. They are involved in several important Ca2+ signalling phenomena, such as neurotransmission and secretion. In striated muscle, RyR channels are the primary pathway for Ca2+ release during the excitation-contraction coupling process.
The RyR channels are expressed in many cell types, including skeletal and cardiac muscle. In skeletal muscle, there is reciprocal signalling between the skeletal isoforms of the DHPR and the RyR (RyR-1), where the Ca2+ release activity of RyR-1 is controlled by the DHPR, and the Ca2+ channel activity of the DHPR is controlled by RyR-1. Dyspedic skeletal muscle cells, which lack RyR-1, exhibit a significant reduction in L-type Ca2+ current density and a loss of excitation-contraction coupling.
In cardiac muscle, the RyR-2 isoform is predominant and plays a critical role in excitation-contraction coupling. The inward flux of Ca2+ through DHPRs triggers the opening of RyRs, leading to calcium-induced calcium release. Ryanodine binds to RyRs and can lock them in a half-open state at nanomolar concentrations, causing a Ca2+ leak from intracellular stores. This leaked Ca2+ is rapidly removed by the strong surface membrane Ca2+ extrusion mechanisms in cardiac muscle, preventing total depletion of Ca2+ stores.
The RyR channels are the largest known ion channels, with weights exceeding 2 megadaltons. Their structural complexity enables a wide range of allosteric regulation mechanisms. While the signals that activate RyR channels are generally known, the specific mechanisms involved in modulation and termination of the channels are still being studied and remain unclear.
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Excitation-contraction (e-c) coupling in muscle cells
In skeletal muscle, there appears to be reciprocal signalling between the skeletal isoforms of both DHPR and RyR (RyR-1). The Ca2+ release activity of RyR-1 is controlled by DHPR, and the Ca2+ channel activity of DHPR is controlled by RyR-1. Dyspedic skeletal muscle cells, which do not express RyR-1, lack excitation-contraction coupling and have a significantly reduced L-type Ca2+ current density.
In cardiac muscle, the inward flux of Ca2+ through DHPRs following depolarization triggers the opening of RyRs (calcium-induced calcium release). The cardiac DHPR is well-adapted for Ca2+-entry dependent EC coupling, producing a large, rapidly activating Ca2+ current. However, this feature is maladaptive for skeletal muscle, where large Ca2+ currents could lead to depletion of Ca2+ from the transverse tubules.
Ultrastructural studies have revealed functional differences between skeletal and cardiac muscle. In skeletal muscle, DHPRs form tetrads, representing the structural DHPR/RyR link that allows Ca2+ independent coupling. In cardiac muscle, the key structural element enabling DHPRs and RyRs to interact is their close vicinity to each other.
The excitation-contraction coupling phenomenon was first defined by Alexander Sandow as the series of events from the generation of the action potential in skeletal muscle fibres to the onset of muscle tension. Over the past seven decades, significant advances have been made in understanding the morphological, physiological, and pharmacological basis of ECC, aided by improved experimental techniques and the use of fast Ca2+ dyes.
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Differences in the DHPR/RyR reciprocal association
Dihydropyridine Receptors (DHPRs) and Ryanodine Receptors (RyRs) are essential for excitation-contraction (e-c) coupling in muscle cells. DHPRs are voltage-gated Ca2+ channels located in exterior membranes, while RyRs are the Ca2+ release channels of the sarcoplasmic reticulum (SR). The close vicinity of DHPRs and RyRs is the key structural element that allows them to interact with each other in both skeletal and cardiac muscle cells. However, the signalling mechanisms between these two molecules differ between the two muscle types.
In cardiac muscle, the inward flux of Ca2+ through DHPRs following depolarization triggers the opening of RyRs in a process known as calcium-induced calcium release. This process is essential for excitation-contraction coupling, which allows the transduction of exterior-membrane depolarization into Ca2+ release from the SR.
On the other hand, in skeletal muscle, Ca2+ is not required for the activation of RyRs. Instead, the coupling between DHPRs and RyRs involves a direct mechanical link. Ultrastructural studies have revealed that functional differences between skeletal and cardiac muscle can be attributed to variations in the DHPR/RyR reciprocal association. While DHPRs and RyRs are in close proximity in both types of muscle, DHPRs uniquely form tetrads in skeletal muscle fibres. These tetrads represent the structural DHPR/RyR link that enables Ca2+ independent coupling in skeletal muscle.
The isoforms of DHPRs and RyRs expressed in skeletal and cardiac muscle also contribute to their functional differences. In skeletal muscle, there appears to be reciprocal signalling between the skeletal isoforms of DHPRs (DHPR) and RyRs (RyR-1). The Ca2+ release activity of RyR-1 is regulated by DHPR, while the Ca2+ channel activity of DHPR is controlled by RyR-1. In contrast, the cardiac isoform of RyR, RyR-2, lacks the ability to mediate skeletal-type EC coupling and enhance the Ca2+ channel activity of skeletal DHPR.
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DHPRs and RyRs form calcium release units
Dihydropyridine Receptors (DHPRs) and Ryanodine Receptors (RyRs) are essential components of calcium release units in cardiac and skeletal muscle cells. These receptors facilitate excitation-contraction (e-c) coupling, a mechanism that enables the transduction of exterior-membrane depolarization into Ca2+ release from the Sarcoplasmic Reticulum (SR).
DHPRs are voltage-gated Ca2+ channels located in the external membranes of muscle cells. They play a crucial role in regulating the influx of Ca2+ into the cell. On the other hand, RyRs are intracellular Ca2+ release channels found in the SR. They are responsible for controlling the release of Ca2+ from the SR into the cytoplasm.
In cardiac muscle cells, the communication between DHPRs and RyRs is facilitated by their close proximity. The inward flux of Ca2+ through DHPRs triggers the opening of RyRs, leading to calcium-induced calcium release. This process is known as calcium-induced calcium release (CICR). The interaction between DHPRs and RyRs forms a calcium release unit that regulates calcium release in cardiac muscle cells.
Ultrastructural studies have revealed functional differences in the DHPR/RyR reciprocal association between cardiac and skeletal muscle cells. In skeletal muscle, DHPRs form tetrads, which are structural links with RyRs that enable Ca2+-independent coupling. This direct mechanical coupling between DHPRs and RyRs in skeletal muscle differs from the calcium-induced calcium release mechanism observed in cardiac muscle.
The distinct mechanisms of DHPR and RyR interactions in cardiac and skeletal muscle cells highlight the importance of these receptors in maintaining proper calcium handling and excitation-contraction coupling in different muscle types. Further research and understanding of these processes are crucial for comprehending muscle function and developing therapies for muscle-related disorders.
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Frequently asked questions
DHPRs are dihydropyridine receptors, or L-type calcium channels, located in the exterior membranes of muscle cells. They are voltage-gated Ca2+ channels.
Yes, cardiac muscle does have DHPRs. They are located in the surface membrane and T-tubules of cardiac muscle cells.
DHPRs play a crucial role in excitation-contraction (e-c) coupling in cardiac muscle cells. They interact with Ryanodine Receptors (RyRs) to facilitate the release of Ca2+ from the Sarcoplasmic Reticulum (SR), leading to muscle contraction.
The cardiac DHPR is adapted for Ca2+ entry-dependent EC coupling, producing a large and rapid Ca2+ current. In contrast, the skeletal DHPR generates a smaller and slower Ca2+ current to trigger Ca2+ release without requiring Ca2+ entry.
