Provide a explantion and diagram of the  Intracellular mechanism of smooth muscle relaxation via antagonists such as atropine binding and blocking muscarinic receptors M3.   explain how  Atropine blocks the acetylcholine receptors

Explain the intracellular mechansim of smooth muscle relaxation of agaonist such as mepyrimine and atropine.

High blood K+ concentrations cause depolarization of the restingmembrane potential. Predict and explain the effect of high blood K+levels on smooth muscle function

Acetylcholine molecules are actively transported from the axon to their receptors on the muscle membrane by special transport proteins.

exaplin the intracellular mehcanims of smooth msucle via agonist such as Hitamine and acytycholine.  link hisamine to muscarnic recptors  link acetycholine to a neurotransmittors  Give a diagram for each.

How is the muscular contraction stopped (i.e.: how does a muscle relax after contraction)? 1. The brain stops sending the nerve impulse that commands the muscle to contract, interrupting communication at the neuromuscular junction 2. Acetylcholineesterase (AChE) is released into the synaptic cleft to destroy any remaining Acetylcholine 3. No mechanism is necessary. When the antagonist begins to contract, it forces relaxation and stretch of the agonist muscle. 4. Relaxation occurs as the myosin heads are "snapped" off of the thick filaments. This interrupts the crossbridge and allows for muscles to stretch 5. Relaxation only occurs if the brain sends a "stop" signal to the muscle

Most immediate physiological adjustments to exercise occur prior to any change in tissue metabolic demand for oxygen or nutrients.  This occurs because exercise increases sympathetic nervous system activity.  With your knowledge of exercise and the control of alpha motor neurons by the primary motor cortex of the brain, how does increased exercise influence the sympathetic nervous system?

61.

Neuromuscular Junction: -Activation of nicotinic ACh receptors in the motor end plate results in both Na+ influx into and K+ efflux from the muscle fiber - An action potential in a motor neuron always produces a graded depolarization in the motor endplate and an action potential in the sarcolemma. -Acetylcholine released from the motor presynaptic terminal binds to voltage-gated ACh receptors in the motor endplate. -all of the above -a and b are right

Succinylcholine act as adepolarising agent that prevents repolarization of the somatic motor neuron. Thus, no further ACh is released until drug is cleared. Name another site within the MNJ we could target to prevent muscle contraction, and explain why this would work.