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BIOL-3602 > ROT 2: Mammalian Smooth Muscle > Flashcards

ROT 2: Mammalian Smooth Muscle Flashcards

1
Q

Shape of a smooth muscle cell/fiber

A

they are simple, short, spindle shaped cells

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2
Q

T/F smooth muscle cells are multinucleated

A

false. they are single nucleated.

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3
Q

Difference between myofilaments (actin and myosin) in smooth muscle compared to skeletal muscle

A

actin and myosin filaments of smooth muscle do not have the highly ordered arrangement into bands that is apparent as striations in skeletal and cardiac muscles.

they are IRREGULARLY arranged so smooth muscle contractions are slower and generate less force.

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4
Q

T/F smooth muscle is not prone to muscle fatigue

A

true.

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5
Q

Visceral smooth muscle is a ____ of muscle cells

A

syncytium

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6
Q

how does a synctium allow depolarization of one smooth muscle cell to quickly depolarize a neighboring cell?

A

electrical current is easily conducted from one cell to another via gap junctions.

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7
Q

T/F: smooth muscle cell action potentials are generated without input from either the motor or autonomic nervous system.

A

true. contractions can occur spontaneously by unergoing rhythmic oscillations in membrane potential.

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8
Q

what is a spike?

A

when the rhythmic oscillations in membrane potential occasiunally reach threshold.

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9
Q

during a spike, the action potential spreads, causing a rise in cytosolic ____, and a wave of muscle contraction is initiated.

A

ca2+

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10
Q

muscle tonus

A

a baseline level of long term sustained contraction

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11
Q

which two nerve plexuses are associated with visceral smooth muscle of the gut? What do these do?

A

1) auerbachs (myenteric)
2) meissners (submucousal)

can enhance or supress the rhythmicity and tonus in the intestinal smooth muscle/

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12
Q

Auerbachs and Meissners nerve plexuses together make up the _____ nervous system. This nervous system can then be modified by the ___ nervous system.

A

Auerbachs and Meissners nerve plexuses together make up the ENTERIC nervous system. This nervous system can then be modified by the AUTONOMIC nervous system.

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13
Q

when a drug mimics the action of the parasympathetic nervous system, it is considered to be a ____

A

parasympathomimetic drug.

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14
Q

Parasympathetic control of the gut is through _____ PREganglionic fibers which synapse with ____ neurons. These neurons are then stimulated to release ____ at the neuromuscular junctions.

A

parasymp control is through CHOLINERGIC PREGANG fibers which synapse with ENTERIC neurons. When stimulated, these enteric nuerons then release ACETYLCHOLINE at neuromuscular junctions.

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15
Q

the receptors of the neuromuscular junction between enteric neurons and smooth muscle cells of the intestine are ____ type cholinergic receptors

A

MUSCARINIC. Muscarinic cells are only found on effector cells,

but cholinergic nicotinic receptors are on all autonmic (SNS and PNS) ganglia. Responds to Ach released from both para and symp. preganglionic fibers.

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16
Q

Parasympathetic stimulation _____ smooth muscle tonus and rhythmicity. Muscarinic receptors can be blocked by the addition of _____ (drug)

A

Parasympathetic stimulation ENHANCES smooth muscle tonus and rhythmicity (promotes digestive gut function).

Muscarinic receptors can be blocked by the addition of ATROPINE(drug).

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17
Q

sympathetic input is via __-___ receptors located on the axon terminals of the enteric (post ganglionic neurons), or on the axon terminals of the preganglionic parasympathetic fibers.

A

alpha-adrenergic receptors.

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18
Q

Release of NE from the sympathetic POST GANG fibers stimulates the ___ receptors, which ____ the release of Ach from the enteric neurons or the preganglionic parasympathetic neurons. What is this phenomena known as?

A

Release of NE from the sympathetic POST GANG fibers stimulates the ALPHA receptors, which PREVENTS the release of Ach from the enteric neurons or the preganglionic parasympathetic neurons.
This is known as PRESYNAPTIC INHIBITION

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19
Q

what does presynaptic inhibition do to smooth muscle?

A

reduces uscle tonus and rhythmicity by preventing Ach release at either the pre or post ganglionic neuron of the autonomic nervous system. Inhibition facilitated by stimulation of the sympathetic nervous system.

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20
Q

beta adrenergic receptors on smooth muscle cells themselves respond to ___ and ___ in the blood.

A

epinephrine and norepinephrine.

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21
Q

Beta-adrenergic receptors can be selectively blocked by _____ and selectively stimulated by _____. Stimulation of beta receptors ____ smooth muscle tonus and rhythmicity.

A

Beta-adrenergic receptors can be selectively blocked by PROPRANOLOL and selectively stimulated by ISOPRETERENOL. Stimulation of beta receptors INHIBITS smooth muscle tonus and rhythmicity.

22
Q

Primary location of alpha and beta adrenergic receptors

A

alpha receptors are found on pre gang and post gang (enteric) neurons, and their activation results in the prevention of acetylcholine release

beta receptors are found directly on the smooth muscle tissue of an organ, and their activation results in the inhibition of smooth muscle

23
Q

Why does smooth muscle contract when there is no stimulus?

A

it can spontaneously depolarize with no innercation due to spontaneous oscillations in membrane potential that can trigger depolarization that spreads to other smooth muscle cells.

Gap junctions allow for depolarization spreading. Although the gut is able to contract by itself, the motility of the gut is influenced by plexuses. The plexuses (auerbachs and meissners) are inbetween circular smooth muscle and longitudinal smooth muscle, and their influence allows for peristalsis to occur.

24
Q

How can peristalsis occur if the gut can essentially do whatever it wants because it can contract with no nervous system innervation?

A

Although the gut is able to contract by itself, the motility of the gut is influenced by plexuses. The plexuses (auerbachs and meissners) are inbetween circular smooth muscle and longitudinal smooth muscle, and their influence allows for peristalsis to occur.

25
Q

What is the composition of Tyrode’s solution?

A

It resembles Ringer’s solution, but contains magnesium, a sugar (usually glucose) as an energy source and uses bicarbonate and phosphate as a BUFFER instead of lactate. Some variations also include phosphate and sulfate ions.

26
Q

Why is it good that we have glucose and oxygen in tyrodes solution?

A

they are salient molecules for oxidative phosphorylation and respiration. ATP production and thus smooth muscle contraction in this lab could not be possible.

27
Q

What was observed when the intestine was bathed with K+ free Tyrodes?

A

K+ free tyrodes causes K+ efflux from membrane according to concentration gradient. Makes membrane more negative (hyperpolarization) and thus contractions may be slower or less strong. (SMALLER AMPLITUDE)

28
Q

What is the effect of K+ enriched tyrodes solution when bathed on smooth muscle?

A

K+ excess solution causes K+ to move INTO the smooth muscle cells according to the gradient, which causes membrane potential to become LESS polarized. May FACILITATE contraction.

In lab, K+ enriched tyrodes resulted in LARGER and more FREQUENT visceral contractions.

29
Q

What is the effect of Ca2+ enriched tyrodes solution when bathed on smooth muscle?

A

Ca2+ enriched tyrodes may cause Ca2+ to enter the cell and cause an upset in positive charges within the cell. may also FACILITATE contractions of smooth muscle due to the influx fo Ca2+ in the ICF. Causes depolarization to threshold easier.

In this lab, we saw LARGER and more FREQUENT visceral contractions in the presence of Ca2+ enriched Tyrodes solution.

30
Q

What is the role of the AUTONOMIC NS in the control of Gut activity? How is this illustrated by the application of acetylcholine and NE to the gut in this experiment?

A

Ach: will cause an increase in tonus shift on smooth muscle.

Ach binds to the muscarinic receptors on the smooth muscles and increases the muscles permeability to Na+ and K+. This would result in more AP spikes, with stronger and more frequent contractions.

NE application will result in PRESYNAPTIC INHIBITION by binding to alpha-adrenergic receptors on either the preganglionic cholinergic neuron or the post ganglionic ENTERIC neurons, preventing them from release Ach. (autonomic neuron would release Ach to enteric neuron, and enteric neuron would typically release Ach onto smooth muscle).

NE could also act on BETA adrenergic receptors on the smooth muscle of the gut itself, also facilitating a decrease in muscle tonus.

31
Q

Draw the expected tonus shift when Ach is added, and when Ne is added.

A

see notes.

32
Q

what is the mechanism of action and the effects on small intestine mobility on isoproterenol

A

Isoproterenol is a BETA AGNOIST. It likes beta 1 and beta 2 receptors on smooth muscle. Does a similar thing as NE but seems to like BETA 2 receptors more than NE and epinephrine.

Recall: 2= inhibitory, 1= excitatory

Exerts a NEGATIVE (inhibitory) tonus shift on smooth muscle. since it favors BETA 2 receptors.

33
Q

isoproterenol favors beta ___ receptors over beta ____ receptors

A

iso favors beta 2 more than beta 1

34
Q

what is the mechanism of action and the effects on small intestine mobility on propranolol followed by isoproterenol and NE

A

propranolol is a BETA ANTAGONIST. blocks both beta 1 and 2 receptors. At first wouldn’t see any change.

After you add isoproterenol, which is a beta agonist, you would ideally NOT SEE ANY CHANGE because the beta 2 sites are BLOCKed by propranolol.

You may see some NEGATIVE TONUS CHANGE by NE because the beta blocking affects of propranolol are wearing off, but ideally, if you block the beta receptors with a beta antagonist, NE/Epinephrine or isoproterenol should not be able to exert their effects.

35
Q

Propranolol is a beta _____

A

antagonist. A competitive inhibitor

36
Q

what is the mechanism of action and the effects on small intestine mobility on atropine applied BEFORE Ach?

A

atropine blocks muscarinic receptors on the gut. No stimulatory affect of Ach on the enteric-smooth muscle synapse if atropine is present, because Ach cannot make contact with the muscarinic receptors.

37
Q

cholinergic receptors in pre-ganglionic neurons that synapse with the enteric neurons are called ___

A

nicotinic receptors

38
Q

receptors on smooth muscle that respond to Ach released by (post gang) enteric neurons are called _____

A

muscarinic cholinergic receptors.

39
Q

what is the mechanism of action and the effects on small intestine mobility on serine applied after Ach

A

Serine is an ANTIacetylcholineesterase. It PREVENTS breakdown in the synaptic cleft. Therefore, if serine allows for an extended affect of ACH, you should see a prolonged POSITIVE SHIFT in muscle tonus.

40
Q

How are the effects of neurotransmitter substances terminated at synapses?

A

1) degradation in the cleft by enzymes. The components are usually reuptaken into presynaptic neuron where the precursors are recycled into new transmitters.
2) diffusion away from the cleft. Astrocytes may take it up to prevent it from continuing to exert its effects
3) reuptake as a whole into presynaptic neurons.

41
Q

Name places where you’d find beta 1 adrenergicreceptors

A

found in heart at the SA NODES and the ventricular myocardium

42
Q

name places where you’d find beta 2 receptors

A

smooth muscle of the gut. Stimulation of these receptors would stop the gut from digesting. (2= inhibitory)

43
Q

name places where you’d find alpha 1 receptors

A

arteriolar SMOOTH muscle. (1= excitation) triggers general vasoconstriction, which is generally facilited by epinephrine hormone

44
Q

name place hwere you’d find alpha 2 receptors.

A

on pre syn (afferent) and post syn (enteric neuron in this case) neuron endings. Inhibits the release of acetylcholine.

45
Q

epinephrine has higher affinity for beta ___ than NE

A

Beta 2

46
Q

Ranke E, NE, and IP in terms of their affinity for beta 2

A

IP > E&raquo_space; NE

47
Q

Why can isoproterenol exert larger affects than NE in the same amount?

A

because iso has stronger affintiies for both beta 1 and beta 2 receptors (but higher affinity for beta 2)

48
Q

T/F: both alpha 1 and alpha 2 receptors have higher affinities for NE rather than E

A

false. epinephrine hormone binds to both alpha 1 and alpha 2 receptors stronger than NE.

49
Q

Nicotonic receptors are typically found at the synapse between pre and post gang neuron in the PNS AND SNS. Which organs also have Nicotinic receptos?

A

CHROMAFFIN CELLS in the adrenal gland that produce epinephrine and NE.

Also found on motor end plates of skeletal muscles.

50
Q

T/F: muscarinic cells are found in blood vessels.

A

FALSE. their activation causes excitation in SMOOTH MUSCLE OF GUT and de-excitation in CARDIAC MUSCLE.

51
Q

Muscarinic cells are only found on ____ cells

A

effector cells.

BIOL-3602 (23 decks)

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