Smooth muscle Flashcards

(12 cards)

1
Q

describe the smooth muscle contraction and structure

A

The smooth muscle contraction is slow and tonic.

This relates to its structure: It still has actin and myosin but it no longer has the regulatory component troponin, its spindles are also unorganized which favours tonic contraction.

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2
Q

where can smooth muscle be found (4)

A

vasculature
urinary tract
GI tract
airways

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3
Q

whats the difference between a single unit and multi-unit muscle.

A

a single unit is where some of the muscle fibres are innervated and the stimulation spreads to others via gap junctions.

A multi unit, is when all the fibers are individually innervated and there is little or no communication/.

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4
Q

outline the mechanism of contraction

A

An increase in intacelluar calcium concentration in response to a stimulus activates calcium-dependant calmodulin.

This will go on to activate myosin light chain kinase which phophorylates myosin light chains found in in the mysoin head.

phosphorylisation allows these heads to form cross bridges to the actin chain to facilitate contraction,

much like in skeletal muscle to continue this contraction the heads must be unbound. this is achieve by dephosphorylisation which is carried out by mysoin light chain phosphtase.

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5
Q

where does the calcium influx come from?

A

VG calcium channels triggered by Na+ influx mediated depolarisation

Calcium from intracelluar stores released by the action of IP3.

NON-SELeCTIVE cation channels, like P2x which is a purinoceptor. ~(atp activated)

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6
Q

How do Gq activating ligands cause smooth muscle contraction?

A

Gq will activate phopholipase C whcih will hydrolyse phospholipids to from DAG and Phosphotidyl 4,5 bi phsophate which will eventually form inositol 123 tri phosphate (IP3)

IP3 will cause the release of intracellualar calcium stores. casuing contraction and depolarisation.

depolarisation will cause further influx of calcium via NSCC and VGCCs. Calcium activated chloride channels driving chloride efflux and the DAG activation of protein kinase C which inhibits K+ efflux will help increase membrane depolarisatiopn.

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7
Q

Outline as many ligands as possible that cause smooth muscle contraction via the Gq pathway

A

NA- works via the alpha 1 receptor- aided by co transport with ATP which acts on PRUINOCEPTORS nsccs
so alpha 1 agonists like phenylethrine cause vasoconstriction whilst antags cause vasoldilation.
(Note tyramine can then also cause Vasoconstriction)

Angiotensin II: Acting on the Angiotensin II receptor, angiotenisn I is converted to the active angiotensin II by angiotensin converting enzyme.
Hence inhibitors of ACE can be used to cause vasodilation and an example is Capitropil.

Endothellin: Key here it is Endothelin 1 acting on recpotr Ea and Eb2. hence inhibitors will cause dilation. BQ123

Vasopressin: acting on the V1 receptor this mainly cause vasoconstriction in the kidneys. a common analogue used to recreate this effect is fellypressin. Tends to be used alongside local anesthetics.

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8
Q

Migraines discuss their treatment?

A

Originally treated with ergometrine which is a ergoalkaloid due to its association with 5ht and the constriction or dilation of cerebral blood vessels being the cause of migraines.

More recently migraines have been said to be issues of neurogenic inflamation and there SUMATRIPTAN a 5ht 1 like receptor agonist has been said to be able to act on nerve stemming form the trigeminal nucleus to prejunctionally stop the constriction and dilation of cerebral vessels which would otherwise lead to migraines.

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9
Q

Describe bronchial smooth muscle contraction and relaxation? implication.

A

Contarction is related to ACh M3 activation through the Gq pathway. hence antagonists like Ipatropium bromide can be used to cause bronchial dilation in asthma attacks.

Realxtion mainly stems from Beta 2 adrenoceptor agonisation from the likes of salbutamol which has been shown to acvt quicker in the case of an astham attack. this may be aided by the fact it also inhibits the release of histamine from mast cells

Both drugs would be given via inhalation

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10
Q

what do methyl xanthines do are they any good?

A

These are drugs that are thought to exert there effect by inhibiting phosphodiesterase 1 or by preventing adenosine acting ion adenosine receptors.

However they only work at high concentration so are not very safe.

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11
Q

describe the contraction and relaxation of uterine smooth muscle? application

A

More now related to contraction: innervation by alpha 1 adrenoceptor agonists; oxytocin; m3 Ach agonists, prostoglanDinS E2 AND F2 ALPHA

Oxytocin is used alot in pregnancy to increase the force and rate of contractions. given intravenously there are breaks to allow for oxygenated blood to go to the foetus.
Oxytocin can also be given to induce labour in the case of early abortions.

Relaxation is driven again by beta 2 adrenoceptor agonists, which are commonly given in the case of premature birth

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12
Q

What is calcium sensitization?

A

The smooth muscle can become desenstised to calcium influx. 1 way is the activation of protein kinase C and its activation of CPI-17, or the activation of the G12/13 pathway which will initiate rho signalling-rho gef- rho kinase.

Both of these will inhibit myosin light chain phosphotase preventing the unbinding of myosin heads and their fore their ability to react to the effects of calcium influx on myosin light chain kinase.

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