Smooth muscle is a type of tissue found within the walls of numerous internal organs and structures throughout the body. This muscle tissue is present in the digestive tract, blood vessels, the bladder, and various other hollow organs and passageways. Its primary function involves involuntary actions, meaning it operates without conscious thought, playing a role in processes like moving food through the intestines, regulating blood pressure, and assisting in the expulsion of waste. These actions are fundamental for maintaining proper bodily functions and overall internal stability.
Distinguishing Features of Smooth Muscle
Smooth muscle stands apart from skeletal and cardiac muscle due to several unique characteristics. Unlike skeletal muscle, which is responsible for voluntary movements and appears striated under a microscope, smooth muscle lacks these striations, giving it a “smooth” appearance. This difference in appearance is due to the distinct arrangement of its contractile proteins.
Smooth muscle operates entirely involuntarily, controlled by the autonomic nervous system, hormones, and local factors. It is capable of sustained contractions over long periods, useful for organs that need to maintain tone or exert continuous pressure, such as blood vessels regulating blood flow or the bladder holding urine.
How Smooth Muscle Contraction Begins
The initiation of smooth muscle contraction is a finely tuned process triggered by various stimuli, all ultimately leading to an increase in calcium ions within the muscle cell. Neural stimuli from the autonomic nervous system, including both sympathetic and parasympathetic branches, can prompt contraction or relaxation depending on the neurotransmitter and receptor type. For example, norepinephrine can cause contraction in vascular smooth muscle by activating alpha-1 and alpha-2 receptors.
Hormones also initiate smooth muscle contraction. Hormones like oxytocin can stimulate uterine contractions during childbirth, while epinephrine can have varying effects depending on the specific receptor it binds to in different smooth muscle tissues. These hormones or neurotransmitters can bind to receptors, often coupled with G-proteins, which then lead to the opening of calcium or sodium channels, allowing positive ions to enter the cell.
Local factors within the tissue environment, such as stretch, pH changes, or oxygen levels, also influence smooth muscle activity. For instance, stretching the smooth muscle in the walls of organs like the bladder can directly trigger contraction, helping to propel contents forward. A decrease in oxygen or an increase in carbon dioxide in surrounding tissues can cause blood vessel smooth muscles to relax, leading to dilation and increased blood flow.
The Molecular Contraction Cycle
Smooth muscle contraction begins with an increase in intracellular calcium concentration, which can enter the cell from the extracellular space through L-type voltage-gated calcium channels or be released from internal stores within the sarcoplasmic reticulum. This calcium influx is fundamental for smooth muscle contraction. Once inside the cell, calcium does not directly interact with troponin, as in skeletal muscle, but instead binds to a different regulatory protein called calmodulin (CaM).
Calmodulin, a calcium-binding protein, has four calcium binding sites. When calcium binds to calmodulin, it forms a calcium-calmodulin complex that undergoes a conformational change. This activated complex then binds to and activates an enzyme known as myosin light chain kinase (MLCK).
The activation of MLCK is an important step. Once activated, MLCK phosphorylates the regulatory light chain (MLC) on the myosin molecule by adding a phosphate group. This phosphorylation of myosin light chains is what enables the myosin head to interact with actin filaments. In the presence of ATP, the phosphorylated myosin head forms cross-bridges with actin.
The formation and cycling of these cross-bridges, driven by ATP hydrolysis, cause the actin filaments to slide past the myosin filaments, leading to shortening of the muscle cell and generation of force. Unlike skeletal muscle, where troponin and tropomyosin regulate contraction, smooth muscle regulation primarily involves the phosphorylation of myosin light chains by MLCK.
Contraction Control and Relaxation
The regulation of smooth muscle contraction and its subsequent relaxation involves a balance of enzyme activities and calcium handling. Once contraction is initiated, relaxation requires the dephosphorylation of the myosin light chains. This dephosphorylation is performed by an enzyme called myosin light chain phosphatase (MLCP). MLCP removes the phosphate group from the myosin light chain, which reduces the myosin’s affinity for actin, leading to the detachment of cross-bridges and muscle relaxation.
Reducing the intracellular calcium concentration is also important for relaxation. Calcium is removed from the cytoplasm through several mechanisms. The sarcoplasmic reticulum contains ATP-dependent calcium pumps that transport calcium back into its internal stores. The plasma membrane of the smooth muscle cell also has calcium pumps and sodium-calcium exchangers that pump calcium out of the cell into the extracellular space.
The level of smooth muscle contraction can be modulated by the relative activities of MLCK and MLCP. Factors that increase MLCP activity or decrease MLCK activity will promote relaxation, even without a significant drop in intracellular calcium levels. For example, nitric oxide, a signaling molecule, can diffuse into smooth muscle cells and activate guanylyl cyclase, leading to the production of cyclic guanosine monophosphate (cGMP). An increase in cGMP then stimulates cGMP-dependent protein kinase, which in turn activates MLCP, promoting dephosphorylation of myosin light chains and relaxation. This interplay of calcium levels and enzyme activities allows smooth muscle to maintain varied levels of tone and respond flexibly to different physiological demands.