Smooth muscle innervation and electrical activity

Mechanism
Exam priority: medium

Smooth muscle is switched on by nerves that release transmitter from beads along the axon, by hormones, by stretch and by its own rhythm.

Updated Nov 13, 2026

Also called: Slow waves, Varicosities, Junction potentials, Myogenic response

See it in 3D: Stomach · Esophagus · Urinary bladder · Trachea

Key points

Resting potential ≈ −50 to −60 mV, about 30 mV less negative than skeletal muscle; spike threshold in visceral muscle ≈ −35 mV.
The upstroke is carried mostly by Ca²⁺ through L-type channels (few fast Na⁺ channels), so it is slow, and the same Ca²⁺ helps trigger contraction.
Slow waves are rhythmic oscillations of membrane potential that do not contract the muscle themselves; spikes fire on their crests and those cause contraction (gut pacemaker).
Stretch depolarizes single-unit smooth muscle and can trigger spikes: hollow organs contract when overfilled; arterioles constrict when pressure rises (myogenic response).
Multi-unit muscle (iris, ciliary muscle, piloerector, vas deferens) is driven by nerves via graded junction potentials, often with no action potential at all.
Hormones and drugs act through receptors: some open channels and change voltage; others (Gq → IP₃) release SR Ca²⁺ with little or no voltage change.

What it is

Autonomic nerves do not form end plates on smooth muscle; they release transmitter from swellings along the axon that diffuses to many cells. The resting potential is less negative than in skeletal muscle, and action potentials are carried mainly by Ca²⁺, which also feeds contraction. Many smooth muscles are also excited without nerves: by stretch, by rhythmic slow waves, or by hormones acting with or without a change in voltage.

How it works, step by step

An autonomic axon runs over the muscle sheet and releases ACh or norepinephrine (or a cotransmitter) from many varicosities.
At diffuse junctions the transmitter travels nanometres to micrometres and reaches many cells slowly; at contact junctions (≈ 20–30 nm, multi-unit muscle) the response is faster.
Receptor activation opens cation or Ca²⁺ channels (depolarization) or K⁺ channels (hyperpolarization), giving a graded junction potential.
In single-unit muscle, when depolarization reaches threshold, L-type Ca²⁺ channels open and a spike spreads through gap junctions to the whole sheet.
Some tissues (ureter, uterus near term, some vessels) hold the depolarization for up to ≈ 1 s (plateau), which prolongs contraction.
Pacemaker cells (interstitial cells of Cajal in the gut) generate slow waves; when a crest crosses threshold, a burst of spikes produces a rhythmic contraction.
Stretch opens mechanosensitive cation channels; the depolarization adds to slow waves and fires spikes, so the organ contracts against the load.
Ca²⁺ entering with the spike plus Ca²⁺ released from SR (IP₃ or Ca²⁺-induced release) activates calmodulin and MLCK, and the muscle contracts.

Regulation

+Stretch: Opens mechanosensitive channels: depolarization and spikes (myogenic tone, emptying of overfilled hollow organs).
+Parasympathetic ACh (M3, gut, bladder, airways): Depolarizes and raises IP₃: more spikes and more SR Ca²⁺ release.
+Norepinephrine on α1 receptors (arterioles, sphincters): Gq → IP₃: Ca²⁺ release and contraction, often with only a small voltage change.
+Oxytocin (uterus near term): Raises Ca²⁺ and spike frequency; receptor number rises at the end of pregnancy.
−β2 agonists, epinephrine (airways, uterus): cAMP opens K⁺ channels and speeds Ca²⁺ removal: hyperpolarization and relaxation.
−NO and other inhibitory transmitters (enteric nerves, endothelium): cGMP lowers Ca²⁺ and Ca²⁺ sensitivity: relaxation, e.g. sphincter opening and vasodilation.

Electrical patterns in smooth muscle

Pattern	What it looks like	Where	Consequence
Spike	Brief Ca²⁺ action potential (≈ 10–50 ms)	Most single-unit muscle (gut, bladder)	Twitch-like contraction; trains summate into tone
Plateau	Upstroke then delayed repolarization (hundreds of ms to ≈ 1 s)	Ureter, uterus, some arteries	Prolonged, strong contraction
Slow waves	Rhythmic oscillation, several per minute, no contraction alone	Stomach, intestine	Sets the maximum rate of peristaltic contractions
Junction potential	Graded depolarization, usually no spike	Multi-unit muscle (iris, vas deferens)	Contraction graded by nerve firing
Pharmacomechanical coupling	Little or no voltage change	Airways, vessels (Gq agonists)	SR Ca²⁺ release and Ca²⁺ sensitization

Clinical notes

Achalasia: loss of inhibitory (NO-releasing) enteric neurons leaves the lower esophageal sphincter unable to relax, and peristalsis in the body of the esophagus fails.
Paralytic ileus after surgery: sympathetic inhibition and inflammation suppress slow-wave-driven spikes, so the gut stops propelling content.
Asthma: airway smooth muscle constricts to ACh, histamine and leukotrienes (Gq); β2 agonists relax it through cAMP.
L-type Ca²⁺ channel blockers relax arterial smooth muscle and lower blood pressure, because vascular spikes and tone depend on Ca²⁺ entry.
Preterm labour: increased uterine excitability (more gap junctions and oxytocin receptors, stronger plateaus) before term; tocolytics reduce Ca²⁺ entry or raise cAMP.

Test yourself

Think of the answer, then tap the question to see it.

Why is the upstroke of a smooth muscle action potential slower than that of a skeletal muscle fiber?

It is carried mainly by Ca²⁺ through L-type channels, which open and close more slowly than the fast Na⁺ channels of skeletal muscle.

A gut segment shows rhythmic slow waves but no contraction. What is missing?

Spikes. Slow waves only bring the membrane near threshold; contraction starts when a crest crosses threshold (≈ −35 mV) and Ca²⁺ spikes fire.

Why does the iris constrict smoothly even though its smooth muscle rarely fires action potentials?

It is multi-unit muscle: each cell is driven by nearby nerve varicosities, and graded junction potentials and Ca²⁺ entry grade the contraction.

How can a Gq-coupled agonist contract airway smooth muscle with almost no change in membrane potential?

Pharmacomechanical coupling: Gq → PLC → IP₃ releases Ca²⁺ from the SR, and Rho-kinase increases Ca²⁺ sensitivity, without needing a spike.

What happens to an arteriole when the pressure inside it suddenly rises, and why?

It constricts (myogenic response): stretch opens mechanosensitive cation channels, depolarizes the muscle and opens L-type Ca²⁺ channels.

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Connections

See it in 3D4

The structures of Durgical's 3D anatomy where it happens.

In Biochemistry1

IP₃, DAG and calcium pathway

In Pharmacology5

← All of physiology

Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: Achalasia (StatPearls (NCBI Bookshelf), 2025); Asthma (StatPearls (NCBI Bookshelf), 2025); Anatomy, Abdomen and Pelvis: Bladder (StatPearls (NCBI Bookshelf), 2025).

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