SAQs Flashcards
List a total of 5 essential roles of the L-type Ca2+ channel in the heart for excitability and
initiating Ca2+ release from sarcoplasmic reticulum?
Excitability: L-type Ca2+ channels play a vital role in cardiac cell excitability by allowing the influx of Ca2+ ions upon membrane depolarization.
Action Potential Initiation: These channels contribute to the initiation of the action potential in cardiac myocytes by facilitating the depolarization phase.
Contraction Initiation: The influx of Ca2+ through L-type channels triggers Ca2+-induced Ca2+ release from the sarcoplasmic reticulum, initiating myocardial contraction.
Coupling Excitation-Contraction: L-type channels are a key link between the electrical excitation of the cardiomyocyte membrane and the mechanical contraction of the heart muscle.
Regulation of Heart Rate: The activity of L-type Ca2+ channels influences the heart rate by determining the rate of depolarization and contraction, affecting overall cardiac rhythm.
In summary, L-type Ca2+ channels in the heart are crucial for excitability, action potential initiation, initiation of Ca2+ release from the sarcoplasmic reticulum, coupling excitation-contraction, and regulation of heart rate.
Ca2+ release during excitation-contraction coupling is terminated by different means in skeletal
and cardiac muscle. How is termination of Ca2+ release regulated in skeletal and cardiac muscle
cells?
Termination of Ca2+ Release in Skeletal Muscle:
In skeletal muscle, termination of Ca2+ release is primarily regulated by the closure of the dihydropyridine receptor (DHPR) Ca2+ channel. As the action potential ends, DHPRs in the transverse tubules sense the declining membrane depolarization, leading to closure of the DHPR channel. This prevents further Ca2+ influx, reducing the Ca2+ concentration in the cytoplasm and allowing Ca2+ to dissociate from troponin, leading to muscle relaxation.
Termination of Ca2+ Release in Cardiac Muscle:
In cardiac muscle, the termination of Ca2+ release is mainly governed by the active reuptake of Ca2+ into the sarcoplasmic reticulum (SR) by the Ca2+-ATPase (SERCA). As the action potential repolarizes, the L-type Ca2+ channels close, reducing the Ca2+ influx. SERCA actively pumps Ca2+ back into the SR, lowering cytoplasmic Ca2+ levels. This reuptake facilitates muscle relaxation by promoting Ca2+ dissociation from troponin.
In summary, in skeletal muscle, termination of Ca2+ release is regulated by DHPR channel closure, while in cardiac muscle, active Ca2+ reuptake by SERCA is the primary mechanism for terminating Ca2+ release.
Consider this hypothetical scenario: a person is born with a mutation in the prolactin receptor
that results in severely reduced (only 20% of normal) signalling via the Jak/STAT signal
transduction pathway.
Based on your understanding of the regulation of prolactin, what would you expect as an
outcome in this individual in terms of
A. prolactin concentrations in blood, in a non-lactating state
A. Prolactin Concentrations in Blood, Non-Lactating State:
A. In a non-lactating state, the mutation in the prolactin receptor resulting in severely reduced Jak/STAT signaling would likely lead to elevated prolactin concentrations in the blood.
Reasoning: Prolactin regulation involves a negative feedback loop. When prolactin levels are low, the hypothalamus secretes more prolactin-releasing hormone (PRH) to stimulate the anterior pituitary to release prolactin. Elevated prolactin then inhibits the hypothalamus, reducing PRH secretion and subsequently lowering prolactin release. In this scenario, reduced signaling through the Jak/STAT pathway due to the mutated receptor would compromise this feedback mechanism. As a result, the negative feedback on prolactin release would be attenuated, leading to increased prolactin concentrations in the blood.
Consider this hypothetical scenario: a person is born with a mutation in the prolactin receptor
that results in severely reduced (only 20% of normal) signalling via the Jak/STAT signal
transduction pathway.
Based on your understanding of the regulation of prolactin, what would you expect as an
outcome in this individual in terms of
B. milk production in the mammary gland, in a lactating state
B. Milk Production in the Mammary Gland, Lactating State:
B. In a lactating state, the mutation in the prolactin receptor resulting in severely reduced Jak/STAT signaling would likely lead to decreased milk production in the mammary gland.
Reasoning: Prolactin plays a crucial role in milk synthesis and lactation by stimulating mammary gland development and milk production. Prolactin binding to its receptor activates the Jak/STAT pathway, leading to the expression of genes involved in milk production and secretion. In the scenario of reduced Jak/STAT signaling, the ability of prolactin to stimulate milk synthesis and secretion would be compromised. As a result, the lactating individual would likely exhibit decreased milk production in the mammary gland.
First explain the somatomedin hypothesis for the endocrine regulation of growth.
Then describe how this hypothesis has been modified since its inception many decades ago.
In your answer use endocrine terms to differentiate where growth signals act.
