Related Experiment Video
Updated: Aug 8, 2026
09:28
A Method of Nodose Ganglia Injection in Sprague-Dawley Rat
Published on: November 25, 2014
Effect of ganglionic blockade on catecholamine secretion in exercised dogfish
The American Journal of Physiology
|December 1, 1983
Summary
Vigorous exercise increases epinephrine and norepinephrine in dogfish. Ganglionic blockade reduced this response, suggesting some neurogenic control over catecholamine secretion, potentially aiding recovery.
Area of Science:
- Comparative Physiology
- Neuroendocrinology
- Marine Biology
Background:
- Exercise triggers significant increases in plasma epinephrine (E) and norepinephrine (NE) in the dogfish (Squalus acanthias).
- The functionality of the sympathetic nervous system in dogfish remains uncertain.
- Investigating the control mechanisms of exercise-induced catecholamine (CA) secretion is crucial.
Purpose of the Study:
- To determine if exercise-induced catecholamine secretion in dogfish is under autonomic neurogenic control.
- To assess the role of neurogenic pathways in mediating the physiological responses to exercise.
Main Methods:
- Experiments involved comparing plasma E and NE levels in control dogfish versus those infused with hexamethonium for ganglionic blockade before exercise.
- Systemic arterial pressure responses during exercise and recovery were monitored in both groups.
Main Results:
- Ganglionic blockade significantly reduced CA secretion during exercise without impairing the fish's exercise capacity.
- Systemic arterial pressure patterns during exercise and recovery were not significantly altered by ganglionic blockade.
- A fraction of CA secretion capacity appears to be under neurogenically related control.
Conclusions:
- The study suggests that some catecholamine secretion in dogfish may be under neurogenic control, though not essential for exercise performance.
- Catecholamines might play a more significant role in the recovery phase following exercise in dogfish.
More Related Videos
Related Concept Videos
01:21G-Protein Gated Ion Channels
GPCRs are primarily responsible for our sense of smell, taste, and vision. The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory organs,...
Sensory organs,...
01:09GPCRs Regulate Adenylyl Cylase Activity
Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
Two...
00:59Direct-Acting Cholinergic Agonists: Pharmacological Actions
Direct-acting cholinergic agonists exert their pharmacological actions by mimicking the effects of acetylcholine on postsynaptic muscarinic receptors to generate parasympathetic responses. These agents elicit a range of physiological responses, including cardiovascular effects. For example, activation of muscarinic receptors induces bradycardia, decreased cardiac output, reduced peripheral resistance, and consequent hypotension. In the eye, stimulation of M3 receptors leads to smooth muscle...
01:23Drugs Acting on Autonomic Ganglia: Stimulants
Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...
01:28Drugs Acting on Autonomic Ganglia: Blockers
Ganglionic blockers inhibit autonomic activity by blocking nicotinic receptors in the autonomic ganglia, suppressing impulse transmission. These blockers lack selectivity between sympathetic and parasympathetic ganglia and are ineffective as neuromuscular junction antagonists. They can be categorized into two groups:
01:27Adrenergic Neurons: Neurotransmission
Postganglionic sympathetic fibers (except those supplying the sweat glands) releasing noradrenaline or norepinephrine are called noradrenergic or adrenergic neurons. Noradrenaline, dopamine, adrenaline, or epinephrine are collectively called "catecholamines" as they contain a catechol moiety and an amine side chain. The five stages of neurotransmitter release involve their synthesis, storage, release, reuptake and metabolism.
Synthesis: Catecholamine synthesis requires tyrosine, which is taken...
Synthesis: Catecholamine synthesis requires tyrosine, which is taken...