Compare the effect of acetylcholine on cardiac muscle with its effect on skeletal muscle. Can you explain the mechanistic basis for the difference

The action of the neurotransmitter acetylcholine, released by the vagus nerve in the heart, slows the heart rate and weakens the force of contraction. The skeletal muscle has the ability to perceive a stimulus and respond to it. As regards skeletal muscles, the stimulus is chemical in nature: acetylcholine released by the motor nerve ending. The response of the muscle fiber is the production and propagation along its membrane of an electrical current (action potential) that causes muscle contraction.

Explanation:

Acetylcholine is one of the most abundant neurotransmitters in the central and peripheral nervous system. Acetylcholine receptors are nicotinic (ionotropic) and muscarinic (metabotropic GPCR). In skeletal muscle of adults, acetylcholine binds to the alpha subunit of the nicotinic channel, which are two of the five subunits that make up the pore of this channel. Acetylcholine released by the nerve ending binds to the receptor in the sarcolemma and triggers an electrical current - the action potential. This spreads along the sarcolemma and causes a signal to pass from the T tubule to the sarcoplasmic reticulum in the triad, which then releases calcium ions (Ca ++). Once the calcium ions are released, by diffusing between the actin and myosin protein filaments, they cause the myofibrils to contract. On the other hand, in cardiac and smooth muscle cells, acetylcholine binds to 7M proteins, which do not function as channels, but are typical members of the GPCR class A superfamily. One of the physiological mechanisms of acetylcholine is the regulation of the heart rate, through the mobilization limited to the inner face of the plasma membrane of the dimer bg of protein G. This dimer transduces the specific binding of the ligand with its receptor in the plane of the membrane, thanks to its proximity with the ion channel or with enzymes bound to the plasma membrane. This can be done because its g subunit remains attached to the inner face of the membrane.

it has to be understood that the sea water contains a huge amount of sodium and chlorine ions and if they enter the cell of the atlantic cod fish, the cell will shrivel and the fish will die. to avoid such a condition, the fish uses active transport for the purpose of removing the ions against the gradient.

explanation:

the atlantic cod is not a maritime osmoconformer. its native application of salts is less than that of the seawater it lives in. it is continually falling water from the gills to the ocean via osmosis.

countering that, the fish is going to be swallowing seawater. but since its internal collection of salts is lower than seawater, the fish will want to go free of excess salt, and since that's going upon a gradient, then active transport, requiring energy, must be used to pump out the salt. much marine fish use the organs to filter out the salt and these fish discharge very straight urine.