- (A) In an experiment, 2mg of a substance ‘A’ dissolved in 4.5 ml sterile solvent was injected as a bolus into the femoral vein of an intact frog. It was observed that the frog’s heart rate increased significantly.
(B) The same solution as in (a) when applied directly on the heart of the same frog after exposing the heart, the heart rate did not change.
(C) The same solution as in (a) when injected to an intact cat femoral vein, the heart rate did not change significantly.
From the above observations, which one of the following statements is most likely to be correct?
(1) Substance ‘A’ is stimulatory on heart and the effect was inotropic.
(2) Substance ‘A’ acted in the brain of frog and also might have released other hormones to increase heart rate.
(3) Substance ‘A’ could not have acted on the brain but must have induced other substances in the blood to increase the heart rate.
(4) The increased heart rate was merely due to increased volume of the heart muscles.Mechanism of SNS-Mediated Heart Rate Increase
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Neurotransmitter Release:
Sympathetic nerve endings release norepinephrine (noradrenaline), a catecholamine that binds to β1-adrenergic receptors located on the sinoatrial (SA) node pacemaker cells and cardiac myocytes. -
Receptor Activation and Signal Transduction:
Activation of β1-adrenergic receptors stimulates the Gs protein-coupled receptor pathway, leading to increased cyclic AMP (cAMP) production and activation of protein kinase A (PKA). -
Effects on Cardiac Pacemaker Cells:
PKA phosphorylates various ion channels, including L-type calcium channels, increasing their open probability and thus the inward calcium current. This enhances the slope of diastolic depolarization in SA node cells, accelerating the rate at which threshold potential is reached and thereby increasing the heart rate. -
Enhanced Contractility:
Sympathetic stimulation also increases myocardial contractility via enhanced calcium handling, improving stroke volume alongside heart rate.
Supporting Evidence from Research
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Studies show that norepinephrine is the main neurotransmitter involved in sympathetic regulation of heart rate.frontiersin+2
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Increased sympathetic activity is directly linked with faster heart rates and greater myocardial contractility, critical in stress, exercise, and pathological states.
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Parasympathetic nervous system, in contrast, releases acetylcholine and slows heart rate.
Why Other Options Are Incorrect
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Adrenaline (Option 1): Though circulating adrenaline (epinephrine) from the adrenal medulla can increase heart rate, it is not the neurotransmitter directly released by sympathetic nerve terminals.
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Acetylcholine (Option 2): Released by the parasympathetic vagus nerve and slows heart rate.
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Dopamine (Option 4): A precursor in catecholamine biosynthesis but not the neurotransmitter released at sympathetic nerve endings acting on the heart.
Summary Table
Neurotransmitter Role in Heart Rate Regulation Released By Norepinephrine Increases heart rate via β1 receptors Sympathetic nerve terminals Acetylcholine Decreases heart rate Parasympathetic vagus nerve Adrenaline Circulating hormone, increases heart rate Adrenal medulla Dopamine Precursor neurotransmitter Various neurons, not SNS cardiac terminals
Conclusion
The neurotransmitter released by the sympathetic nerves to increase heart rate is:
Norepinephrine
Understanding these mechanisms is essential for managing cardiovascular physiology and diseases involving autonomic dysfunction.
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2 Comments
Varsha Tatla
September 17, 2025Done sir
Aakansha sharma Sharma
October 3, 2025(2) Substance ‘A’ acted in the brain of frog and also might have released other hormones to increase heart rate.