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Lab Report- The Smooth Muscle

Lab Report- The Smooth Muscle

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This lab is titled “The Smooth Muscle Simulation.”


My friend, Philip, ate deadly nightshade (Atropa belladonna) berries. Therefore, the problem or objective of the lab was to determine the cause of my friend’s intestinal discomfort to identify the correct drug to relieve his pain. To do that, the lab involved testing the effects of different neurotransmitters on the contraction of smooth muscles in the intestines. These neurotransmitters included epinephrine and acetylcholine.

Background Information

The textbook was useful in understanding the structure of smooth muscle, how this muscle works in the body’s organs, and how single-unit and multi-unit smooth muscle differ. The textbook notes that smooth muscles are not striated and are located on the walls of organs like the intestines, urinary bladder, and uterus (Betts et al., 2017). Regarding contraction, smooth muscles rely on calcium ions though they can maintain contractions even without calcium ions (Betts et al., 2017). Also, since smooth muscle contraction is not voluntary, hormones, the autonomic nervous system, and other factors can trigger smooth muscle contraction. Further, smooth muscles are organized into single-unit and multi-unit smooth muscles. Muscle fibers in single-unit smooth muscles are connected by gap junctions such that muscle contraction occurs in a single unit. Conversely, multi-unit smooth muscle fibers lack gap junctions; therefore, contractions are not electrically coupled and do not spread from cell to cell (Betts et al., 2017).

The THEORY section also provided valuable background information related to the lab. Accordingly, some valuable concepts discussed in this section include smooth muscle, the nervous control of smooth muscle, the smooth muscle contraction mechanism, and the effect of drugs on muscle contraction. Muscles have cells that can contract, thus enabling the particular movement of different body parts. Muscles are classified into three categories: skeletal, smooth, and cardiac. As already noted, smooth muscles are not voluntary, as they are controlled by the autonomic nervous system (ANS). Smooth muscle contraction is controlled by two antagonistic parts of the ANS, the sympathetic nervous system (NS) and the parasympathetic NS. The sympathetic NS has short preganglionic fibers and long postganglionic fibers. Formed by adrenergic fibers, its function is to prepare the body to react to stress or emergencies and decrease the tone and contractility of smooth muscles (, 2022b). Contrariwise, the parasympathetic NS has long preganglionic fibers and short postganglionic fibers. The parasympathetic NS is responsible for the “relaxation response” in the body. It is primarily formed by cholinergic fibers and increases smooth muscle tone and contractility (, 2022a).

Nerve cells release chemical messengers called neurotransmitters to convey impulses or send signals to other nerves, muscles, tissues, or organs. Examples of neurotransmitters include acetylcholine and epinephrine. Acetylcholine (ACh) is released in the parasympathetic NS (, 2018a) and is degraded by the enzyme acetylcholinesterase. Epinephrine, also called adrenaline, acts as a hormone and a neurotransmitter in the sympathetic NS (, 2018b). Notably, smooth muscle contraction in the gastrointestinal (GI) tract does not always rely on a direct neural stimulus because of the action of the myenteric plexus. The myenteric plexus is part of the nervous system that contains ganglia of the parasympathetic NS but functions autonomously to regulate digestion.

Additionally, the THEORY section also explained the experimental setup for this lab. The setup comprised 1) a Tyrode tank with the Tyrode solution for an isotonic environment for the piece of intestine used in the lab, 2) a water bath with thermostat for adequate temperature (37 °C), 3) a force transducer or myograph for converting the mechanical force of muscle contraction into an electrical output signal, and 4) an analysis system for collecting electrical signals from the force transducer and transform them into digital data recorded by software in a computer (, 2017).


The variables in this experiment are two neurotransmitters (epinephrine and acetylcholine) and smooth muscle contraction. The experiment involved changing the neurotransmitters and observing their effect on the contraction of smooth muscle in the intestines.


Acetylcholine will increase smooth muscle contraction.

Epinephrine will cause smooth muscle contraction to increase in force and frequency.


Experiment Variables

During the lab, pieces of rat intestines were subjected to different neurotransmitters. The pieces of rat intestines were first experimented with epinephrine and then acetylcholine. The impact of epinephrine and acetylcholine on smooth muscle contraction was then observed.

Lab Procedure Summary

The first step was exploring the smooth muscle and the role of the ANS in smooth muscle contraction. Next, the impact of epinephrine and acetylcholine smooth muscle contraction was examined by putting these neurotransmitters into the water bath containing Tyrode solution and rat intestines. Then, the effect of atropine, a compound found in Atropa belladonna berries, on smooth muscle contraction was examined. This was followed by testing the effects of the drug physostigmine on smooth muscle contraction. The results of each reagent were analyzed to determine whether to accept or reject the hypotheses and thus identify the cause of Philip’s intestinal pain and the effective drug for his discomfort.


Throughout the lab, I kept track of the mechanism of each neurotransmitter and its effect on smooth muscle contraction. I also noted the impact of atropine and physostigmine on smooth muscle contraction. Additionally, I noticed different sound frequencies during the lab process; the sound in the lab was low and calmer, but the sound heard after teleporting to view the animations showcasing different neurological processes was much louder. My lab character could move around the lab and interact with the lab materials and reagents. I expected adrenaline (epinephrine) to increase smooth muscle contraction; however, I observed that it decreased smooth muscle contraction.

Lab Parts

All lab parts were completed easily. Nonetheless, analyzing the results of each variable on smooth muscle contraction required critical thinking so as to identify the best action/drug to combat the effect of the deadly nightshade berries.

Data and Results

Epinephrine decreased smooth muscle contraction, while acetylcholine increased smooth muscle contraction. Additionally, atropine decreased smooth muscle contraction, whereas physostigmine caused muscle contraction to increase in force and frequency, meaning these two are antagonistic. No other patterns between these variables were observed.


Contaminating the reagents would have impacted the accuracy of the data. However, I ensured I used a new and clean pipette tip for each reagent to avoid contamination. This was a virtual lab; therefore, all potential anomalies that could have occurred were eliminated. Besides, the simulation did not alert me of any errors.


Reviewing the Hypothesis

The two hypotheses for this lab were:

Acetylcholine will increase smooth muscle contraction.

Epinephrine will cause smooth muscle contraction to increase in force and frequency.

However, the experiment results revealed that epinephrine decreased smooth muscle contraction, while acetylcholine increased smooth muscle contraction. Therefore, I accepted the hypothesis that “Acetylcholine will increase smooth muscle contraction” and rejected the one stating, “Epinephrine will cause the smooth muscle contraction to increase in force and frequency.” The lab’s findings align with the background information. Notably, acetylcholine functions in the parasympathetic NS, meaning it increases smooth muscle tone and contractility. Conversely, epinephrine is a neurotransmitter in the sympathetic NS, implying that it decreases smooth muscle tone and contractility. Besides, epinephrine binds to alpha and beta receptors, thus causing a relaxation of the smooth muscle. The lab also revealed that physostigmine is a cholinergic receptor agonist since it boosts acetylcholine action by binding to acetylcholinesterase, thus preventing acetylcholine degradation. Therefore, physostigmine increases the tone and contractility of smooth muscles. As such, physostigmine is an effective drug to combat the effects of atropine (decreasing smooth muscle contraction) and help relieve Philip’s intestinal pain.

Moving Forward

The course student learning outcome was constructing scientific descriptions of the muscular system. The Smooth Muscle Lab relates to this learning outcome as it helped in understanding smooth muscle and the mechanism of smooth muscle contraction. After completing the lab, one can describe the characteristics of smooth muscle, the sympathetic and parasympathetic control of smooth muscle, and identify the neurotransmitters and receptors in smooth muscle contraction. All these pieces of knowledge help achieve the course student learning outcome. Nonetheless, completing this lab left me with one question: How is the action of the myenteric plexus regulated?


Betts, J. G., Desaix, P., Johnson, E., Johnson, J. E., Korol, O., Kruse, D., Poe, B., Wise, J., Womble, M. D., & Young, K. A. (2017). Anatomy and physiology. OpenStax, Rice University. (2017, January 5). Experimental setup. Labster Theory. (2018a, March 7). Acetylcholine. Labster Theory. (2018b, November 19). Norepinephrine and epinephrine. Labster Theory. (2022a, July 25). Parasympathetic control of smooth muscle. Labster Theory. (2022b, July 25). Sympathetic control of smooth muscle. Labster Theory.


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Could you please develop the answer in APA format without including the template?

Lab Report- The Smooth Muscle

Lab Report- The Smooth Muscle

Just elaborate answers like a paragraph without including the template. The professor doesn’t want us to include the template anymore.

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