34: Physiology Of Smooth Muscle Flashcards
SR in smooth muscle
Present, but much less developed than skeletal -> less Ca storage
Bc of smooth muscle SR, what must it rely on?
Extracellular sources of Ca
Release of Ca from SR in smooth muscle: 3 steps
- Extracellular activates G protein (Ach, other neurotransmitter, H, etc.)
- Gq protein activated -> IP3/DAG produced
- IP3/DAG cause Ca release from SR
Two ways Ca enters smooth muscle from ECF
Voltage gated Ca channels, ligand-gated Ca channels
Extrinsic vs intrinsic innervation of smooth muscle
Extrinsic: ANS - allows CNS to control
Intrinsic: independent of CNS
Muscarinic receptors M1, 3, and 5 vs M2, 4 in smooth muscle
M1,3,5: excite some smooth muscle in the gut
M2,4: inhibits some smooth muscle (relaxes)
Alpha vs beta adrenergic receptors in smooth muscle
Alpha: contraction of vascular smooth muscle
Beta: inhibits gut and bronchial smooth muscle
Major inhibitory influence on smooth muscle
Nitric oxide (NO)
How does NO work?
Acts via cGMP mechanism, and doesn’t require a membrane-bound receptor because its very lipid soluble - floats right in there
Hormone receptors on smooth muscle
Localized on the blood-side of the muscle
Four hormones examples that can control smooth muscle
Epi, cholecystokinin, oxytocin, angiotensin
Example of a paracrine agent working on smooth muscle and how it works
NO: secreted by endothelium, acts on adjacent smooth muscle -> vasodilation
Mechanical means of activating smooth muscle
Stretch or damage to vascular walls -> contraction
Two reasons smooth muscle use less overall ATP
- Myosin isoform is slower -> fewer cross bridges per unit time
- Latch mechanism
Latch mechanism of smooth muscle
Pi can be removed from myosin any time during cross bridging, and the cycle will still continue without the Pi - but this then makes myosin/actin very low affinity for ATP binding, so takes a long time for actin and myosin to dissociate -> stuck contracted
