Epithelial transport + Skeletal Muscle EC coupling Flashcards
Draw the basic structure of epithelia and indicate the direction of absorption and secretion. What is epithelial polarity?
Epithelial polarity: the apical and BL membranes have different transport proteins that are independent of each other. The transporters can be linked in series, which allows for vectorial transport
What are the common features of epithelia?
Na+ channel on BLM
K+ channel/K+ leak channel on BLM
Large inward Na+ gradient
Linking transporters in series (e.g. Na+/Glucose transport)
Define transepithelial potential. Use the concept of NaCl absorption in frogs to explain the concept of transepithelial potential. What is the equation to calculate transepithelial potential?
Vte = Vbl - Va
The paracellular pathway describes what? Use the secretion of NaCl to explain how this works.
How the transepithelial potential on the lumen drives the movement of ions towards or away from the lumen, in between the epithelial cells
Describe how potassium is secreted in the kidney collecting duct. What creates the driving force for K+ movement? What would be the effects of adding a dieuretic on the secretion of potassium?
The ENAC channel allows for sodium movement inside the cell, which creates a lumen negative transepithelial potential (Vte). The negative Vte is the driving force for K+ secretion outside the cell.
Adding a dieuretic, e.g. amiloride, blocks the ENAC channel, which prevents Na+ influx, thereby creating a lumen positive potential that prevents K+ secretion. The result is accumulation of intracellular K+, leading hypokalemia.
Describe the types of tight junctions discussed. What is the relationship between concentration gradient and transportation rate for each junction type and why?
Tight junctions and Leaky junctions
Tight: Conc gradient = high b/c tight junctions don’t allow movement of solutes, thus transportation rate will be low (too much energy required to transport things due to high concentration gradient)
Leaky junctions: Conc gradient low b/c easier flow of solutes through the junctions. Transportation rate is therefore high. The junction itself is leakier than the membrane
Define isosmotic water transport. How does this work? How do you calculate the flow rate?
Isosmotic: no detectable osmotic gradient between lumen and interstitium. Water transport is therefore due to aquaporins (water channels, essentially)
Jv = LpA * osmotic pressure (where LpA = permeability based on the # of open channels)
Describe what happens in the case of Cystic Fibrosis. Which ion channel is affected and what are the downstream effects of that?
Downstream effects: mucus buildup allows for bacteria to be trapped, making pts prone to opportunistic infections and such.
Among Skeletal ms, cardiac ms, and smooth ms, which one requires extracellular Ca2+ for its contraction?
Everyone except skeletal ms
Given what we know about cross bridge cycling in Skeletal and cardiac muscle, describe cross-bridge cycling in smooth muscle. What are the unique features about this process? How is this regulated?
Unique features: need MRLC phosphorylation first to initiate cross bridge formation via MLCK
To cause cross bridge detachment, need MLC Phosphatase (remoces Pi from MLC)
Regulation: cAMP >> PKA >> adds P to MLCK >> inactivates enzyme, no cross bridge formation
ROK >> adds P to MLCP >> inactivates enzyme, cross bridge stays in place
Describe the relationship between force and membrane potential
Depolarization of Vm directly proportional to increased force of muscle contraction
Define twitch. What is an afterdepolarization?
The force of contraction that’s generated after a single action potential is fired.
Afterdepolarization - period of slower repolarization due to K+ that’s lingering around the lumen of T tubules
What is the basis of EC coupling in skeletal muscle? Is this present in cardiac muscle as well or no? Describe how EC coupling works in skeletal muscle.
The arrangement of RyR subunits apposed to and aligned with DHPRs.
This is only in skeletal ms.
Describe the process of EC coupling in cardiac muscle (hint: the mechanism is Calcium induced calcium release)
In words (contraction)
Cardiac AP firing activates L-type Ca2+ channels on membrane surface and on T tubules>> Ca2+ flows into cell and binds RyR on SR >> channel opens and Ca2+ exits into cytosol (Ca2+ can then bind Trop C and cross bridges form per usual)
In words (relaxation)
Ca2+ exits the cell via PMCA, NCX, or it gets returned into the SR via SERCA
Interpret the graph. What changes do you see with increasing or decreasing Ica in both ms types?
As [Ca]i decreases in cardiac muscle, Ica decreases and tension does as well, which suggests that Ica is dependent on [Ca]. This is not the case in skeletal muscle, where even as Ica decreases, [Ca]i and tension stay constant. This serves as evidence for Ca-induced Ca release in cardiac muscle.
