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Questions and Answers
Which type of signaling is associated with the release of hormones from enteroendocrine cells in the GI tract?
What is true about the mechanisms of contraction within the GI tract?
How do depolarization and hyperpolarization affect GI tract activity?
Which statement correctly describes hormonal regulation in the GI tract?
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What role do neurotransmitters play in regulating gut function?
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What is the role of NO (nitric oxide) in muscle contraction?
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How does the CNS aid in the relaxation of smooth muscles?
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What occurs when opioids bind to opioid receptors in the myenteric plexus?
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What happens to calcium levels during stimulation of smooth muscle contraction?
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What is the effect of acetylcholine on the ENS?
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Which receptor type does the ENS possess for adrenergic neurotransmitters?
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Which mechanism leads to the reduction of contraction size in smooth muscle tissues?
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What is a likely mechanism behind constipation associated with opioid drug use?
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What is the primary effect of the influx of Ca2+ through voltage-gated channels in the sarcolemma?
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How does the activation of phospholipase C by a receptor contribute to contraction?
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What is one mechanism through which phasic contractions can be down-regulated?
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Which statement accurately describes the role of hormones and neurotransmitters in muscle contraction regulation?
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What must occur for actin and myosin to form cross-bridges during contraction?
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What effect does increasing myosin light chain phosphatase have on muscle contraction?
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Which of the following signals contributes to the down-regulation of phasic contractions?
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How does stress influence contraction in smooth muscle?
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Study Notes
Smooth Muscle Mechanism of Contraction
- Sarcolemma (cell membrane): Voltage gated Na+ and Ca2+ channels open during depolarization.
- Influx of Ca2+ causes the following events
- Activation of the ryanodine receptor, releasing Ca2+ from the sarcoplasmic reticulum
- Increased contraction facilitated by calmodulin and MLCK
Up-regulation Mechanism 2 – Pharmomechanical Contraction
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Hormones & neurotransmitters bind to their receptors, activating Gαq-signaling pathway.
- Receptor activation triggers phospholipase C activity.
- Production of IP3 induces Ca2+ release from the sarcoplasmic reticulum, enhancing contraction.
Down-regulation of Phasic Contractions
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Hyperpolarization of smooth muscle cells:
- Receptors open ion channels that hyperpolarize cells.
- Slow waves fail to reach threshold leading to no contraction.
- Alternatively, the number of action potentials is reduced.
- Increased activity of Myosin Light Chain Phosphatase (MLCP): This enzyme dephosphorylates myosin, reducing the force of contraction.
- Inhibition of excitatory ENS neurotransmission: Opioid drugs are examples.
Regulation - Examples
Relaxation
- The CNS detects relaxation through senses and sends signals to the ENS via the parasympathetic NS using acetylcholine as a neurotransmitter.
- ENS has muscarinic cholinergic receptors and sends an excitatory signal to smooth muscle.
- Mechanism - Depolarization and increase in Ca2+
Stress
- CNS detects stress via senses and communicates with ENS through the sympathetic NS using adrenaline.
- ENS has α adrenergic receptors, receiving an inhibitory signal from the ENS.
- Mechanism - Increased MLCP activity leads to dephosphorylation of myosin and reduced crossbridge cycling.
Opioid Drugs
- Mechanism: Opioids bind to opioid receptors in the myenteric plexus, inhibiting neurotransmission by ENS neurons. This blocks excitatory signals from reaching the GI smooth muscle.
Regulation - Overview
- Hormones and neurotransmitters primarily regulate the magnitude/strength of contraction.
- They have minimal impact on frequency, which is determined by ICC and varies by region.
- Mechanisms of regulation:
- To increase contraction: Depolarize or increase Ca2+
- To decrease contraction: Hyperpolarize or decrease Ca2+
- Increasing MLCP activity dephosphorylates myosin, reducing cross-bridge cycling
- Blocking excitatory neurotransmission decreases contractions.
Case Study: Elvis Presley
- History: Elvis had a history of opioid drug use, constipation, an enlarged colon, heart disease, and an enlarged heart. These factors contributed to his death.
- Autopsy Findings: Opioids were found in Elvis' system, along with an enlarged colon and heart disease.
- Cause of Death: Cardiac arrest/heart attack.
- Opioid's Impact on GI Tract: Opioid drugs can cause constipation by inhibiting the myenteric plexus, which regulates the complex movements of the GI tract.
Myenteric Plexus
- Location: The myenteric plexus is located within the muscularis propria of the GI tract.
- Function: It regulates the complex movements (peristalsis) and duration of contractions of the GI tract.
- Opioid Impact: Opioids inhibit the myenteric plexus by blocking the excitatory signals from the CNS, contributing to constipation.
- Role in GI Contraction: The myenteric plexus is responsible for coordinating the contractions of the GI smooth muscles, essential for digestion and elimination.
Enteroendocrine Cells
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Function: Enteroendocrine cells are located in the GI tract and release hormones.
- These hormones trigger a cascade of events that influence various bodily functions, including digestion and metabolism.
- Stimuli: The release of the hormone is triggered by a variety of stimuli, including food intake and changes in pH.
- Mechanism: Enteroendocrine cells possess apical receptors that bind to peptide hormones, leading to a slow but sustained release of hormones from the GI tract.
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Description
This quiz explores the various mechanisms behind smooth muscle contraction, including the roles of calcium ions, hormones, and neurotransmitters. It delves into the up-regulation of contraction through the Gαq-signaling pathway and the down-regulation that leads to hyperpolarization. Test your understanding of these intricate processes!