Final answer:
Calcium ions play a critical role in smooth muscle contraction by entering the cell through sarcolemma channels, binding to calmodulin, and activating MLCK, which leads to muscle contraction. The small diameter of smooth muscle fibers allows for quick diffusion of calcium, negating the need for T-tubules. Other hormones can indirectly influence muscle contractility by affecting calcium transport.
Step-by-step explanation:
The student has asked about the mechanism by which calcium affects the contractility of the intestinal muscle. In smooth muscle cells, such as those found in the intestine, calcium ions (Ca2+) play a critical role in initiating contraction. Although these muscle cells have a limited sarcoplasmic reticulum (SR) for calcium storage, they possess calcium channels in their cell membrane (sarcolemma) that allow the influx of extracellular Ca2+ during an action potential.
When a smooth muscle cell is stimulated, calcium channels on the sarcolemma open, allowing Ca2+ to enter the cell from the extracellular space. This calcium then binds to calmodulin, triggering a cascade of events that lead to the activation of myosin light-chain kinase (MLCK). Activated MLCK, in turn, phosphorylates the light chains of myosin heads, which enables them to form cross-bridges with actin filaments, leading to muscle contraction.
Without T-tubules, which are not present in smooth muscle, the smaller diameter of these muscle fibers allows Ca2+ to diffuse readily throughout the cell, ensuring an even and rapid response to signaling. Other regulatory factors such as parathyroid hormone and adrenal glucocorticoids can influence intestinal calcium transport, thereby affecting muscle contractility indirectly.