Lab 2: Contractility of Visceral and Vascular (Aorta) Smooth Muscle

Purpose: To illustrate differences in function/control between smooth muscle from the jejunum and from the aorta. It also
demonstrates that as in other muscles, calcium is required for contraction.

The sympathetic nervous system produces relaxation of the gut muscle while diverting blood to active skeletal muscle.
During exercise, vascular smooth muscle of the aorta contracts in response to sympathetic influences, creating a more
rigid tube which rapidly propagates an elevated pressure pulse to the periphery.
Mechanical differences in smooth muscles:
1. Myogenic pacemaker activity and propagation of the excitatory process are evident in the jejunal smooth
muscle but not in the smooth muscle from the aorta.
2. The major physiologically active agents, epinephrine and acetylcholine, have converse effects on the two
muscles
a. Epinephrine causes relaxation of jejunal smooth muscle and contraction of the aorta
b. Acetylcholine causes increased contractility of the jejunal smooth muscle but causes relaxation of the
aorta when it is in the contracted state (following stimulation with epinephrine)
Jejunum Aorta
Epinephrine α Relax (1) Contract (3)  epinephrine makes aorta contract
β Relax (1) Relax (1)  epinephrine makes jejunum relax
Acetylcholine Contract Relax

Lab Experiment
Jejunum Aorta
Control
Epinephrine Relax Contract
Acetylcholine Contract Relax
Effects of Calcium
Ca2+ free Relax Relax
Epinephrine No change Small increase in contraction
Acetylcholine Small increase in contraction No change/slight decrease in
contraction
Replace Ca2+
Epinephrine Same as control (relax) Same as control (contract)
Acetylcholine Same as control (contract) Same as control (relax)
High Ca2+
Receptors and Blocking Agents
High K+ Contraction Contraction
Propanolol (β blocker)
Epinephrine Relaxes (1/2 as much as Contracts more than control
without propanolol)
Acetylcholine Same as control (contract) Same as control (relax)
Phentolamine (α blocker)
Epinephrine Relaxes (1/2 as much as Inhibited contraction
without phentolamine) response, slight relaxation
Acetylcholine Same as control (contract) Same as control (relax)
Atropine
Acetylcholine No change No change
Epinephrine Same as control (relax) Same as control (contract)
All blockers and K+ Contraction Contraction
Propanolol: blocks beta adrenergic receptors
Phentolamine: blocks alpha adrenergic receptors
Atropine: blocks cholinergic receptors

Wrap-up Session
In the lab, we looked at two types of muscle. The aorta has a stable Vm while the jejunum exhibits spontaneous rhythmic
contraction.
 Autonomic Nervous System

Sympathetic nervous system

Parasympathetic nervous system

Acetylcholine
Epinephrine

Muscinergic receptors

Adrenergic receptors
Atropine

Alpha Beta

Phentolamine Propanolol
In the smooth muscle laboratory exercise, what procedure (at the arrow) would most likely cause the
changes in muscle force depicted above?
A. Adding acetylcholine to the intestine.
B. Adding acetylcholine to the aorta.
C. Adding epinephrine to the intestine.
D. Adding epinephrine to the aorta.
E. Adding phentolamine to the aorta.
F. Adding phentolamine to the intestine.
Explanation: intestinal smooth muscle is spontaneously active, while the aorta is quiescent.
Epinephrine inhibits intestinal smooth muscle and contracts aortic smooth muscle. Acetylcholine contracts
intestinal smooth muscle, and causes relaxation of epinephrine-contracted aorta (via NO release from the
endothelium). Phentolamine blocks alpha-adrenergic receptors, and would have no effect in the absence of
epinephrine or some other alpha-adrenergic agonist, e.g., norepinephrine.

In the smooth muscle laboratory exercise, addition of atropine to the tissue bath would:
A. contract the aorta and contract the jejunum.
B. relax the aorta and contract the jejunum.
C. contract the aorta and relax the jejunum.
D. relax the aorta and relax the jejunum.
E. have no effect on the aorta or the jejunum.
Explanation: atropine blocks muscarinic cholinergic receptors, causing contraction of the jejunum and
leading to NO release in the aortic endothelium. Atropine itself would have no effect in the absence of
activation of these receptors by acetylcholine, which does not occur in the tissue bath due to the absence
of any parasympathetic nerve input.

In the smooth muscle laboratory exercise, addition of epinephrine to the tissue bath would:
A. contract the aorta and contract the jejunum.
B. relax the aorta and contract the jejunum.
C. contract the aorta and relax the jejunum.
D. relax the aorta and relax the jejunum.
E. have no effect on the aorta or the jejunum.
Explanation: epinephrine causes contraction of the aorta because alpha-adrenergic receptors are
excitatory in vascular smooth muscle. The alpha-adrenergic response predominates in the aorta because
epinephrine has greater alpha-adrenergic activity than beta-adrenergic activity (which is inhibitory in
vascular smooth muscle). In addition, the vascular smooth muscle has more alphareceptors than beta-
receptors. In the intestinal smooth muscle, both alpha and beta-adrenergic receptors are inhibitory

In the smooth muscle laboratory exercise, increased K+ concentrations in the tissue bath would:
A. contract the aorta and contract the jejunum.
B. relax the aorta and contract the jejunum.
C. contract the aorta and relax the jejunum.
D. relax the aorta and relax the jejunum.
E. have no effect on the aorta or the jejunum.
Explanation: increased potassium in the tissue bath causes depolarization of both the aorta and intestinal
smooth muscle, by reducing the diffusion of potassium out of the smooth muscle cells. This causes the
potassium equilibrium potential of the smooth muscle cells to become less negative, which opens voltage-
gated calcium channels. Calcium enters the cell, causing a contraction of both muscle types.