Final answer:
ACh binds to nicotinic receptors in skeletal muscles causing excitation, while in cardiac muscles, it affects muscarinic receptors which have an inhibitory effect on heart rate and strength of contractions, in line with the roles of the parasympathetic and sympathetic nervous systems, respectively.
Step-by-step explanation:
Acetylcholine (ACh) serves as a neurotransmitter with different effects on skeletal and cardiac muscles due to the types of receptors present and the intrinsic properties of these muscles. In skeletal muscles, ACh binds to nicotinic receptors at the neuromuscular junction (NMJ), leading to depolarization and muscle contraction. This is facilitated by the release of calcium ions from the sarcoplasmic reticulum, which then interact with the actin and myosin filaments, allowing for the sliding filament mechanism of muscle contraction.
In cardiac muscle, ACh affects muscarinic receptors, which have an inhibitory function, reducing the rate and force of cardiac contractions. This occurs because the parasympathetic nervous system (which releases ACh) serves to conserve energy and slow the heart rate, contrasting with the fight-or-flight responses managed by the sympathetic nervous system.
The hormonal signal from the sympathetic nervous system, involving the release of epinephrine and norepinephrine into the bloodstream, affects many organ systems simultaneously, including causing excitation in skeletal muscles but inhibition in cardiac muscles. Gap junctions and the arrangement of the NMJ influence the response to ACh in each muscle type, hence ACh causes excitation in skeletal muscles while inducing inhibition of cardiac muscles.