A drug or compound that acts like acetylcholine (ACh). Acetylcholine is a neurotransmitter. In the peripheral nervous system (PNS), acetylcholine activates muscles. In the central nervous system (CNS), acetylcholine tends to cause decreased muscle contractions. These two responses are opposite. ACh Receptor agonists (booster of the effect) are used to treat myasthenia gravis and Alzheimer's disease. ACh receptor antagonists block muscle contractions causing paralysis. The bite of the Black Widow spider does this.
ACh will decrease heart rate/contractile strength, etc. Atropine is a muscarinic ACh receptor (mAChR) antagonist, so blocks the effects of ACh. Adding both together will result in a weak action of ACh that tails off as all the mAChRs become blocked by Atropine.
The effect would be an increase in cardiac output. However, there is a maximum level and then the heart would not have time to fill fully and the output would decrease.
The effect would be an increase in cardiac output. However, there is a maximum level and then the heart would not have time to fill fully and the output would decrease.
A side effect is an unintended effect of a treatment or medication, while a residual effect is a lingering effect that can persist after the treatment or medication has been discontinued. Side effects are typically immediate or short-term, whereas residual effects can last longer and may require monitoring or additional treatment.
Breaking down acetylcholine can lead to muscle relaxation because acetylcholine is a neurotransmitter that stimulates muscle contraction. When acetylcholine is broken down, the signal for muscle contraction is reduced, resulting in muscle relaxation.
Pilocarpine stimulates the release of acetylcholine from parasympathetic neurons. Therefore, it stimulates the effect of vagal stimulation on the heart.
Probably no effect.
Organopesticides will increase the severity of muscle contraction beyond normal conditions. Acetylcholine esterase inhibition will allow a more than normal amount of acetylcholine to bind to receptors.
If the enzyme that breaks down acetylcholine is destroyed, acetylcholine levels in the body will increase. This can lead to overstimulation of muscles and nerves, causing symptoms like muscle twitching, paralysis, respiratory failure, and even death.
In some muscle tissue acetylcholine causes vaso-dilation, but not all. Norepinephrine is the opposite competor/effector of acetylcholine. Acetylcholine is present in all preganglionic fibers, both parasympathetic and sympathetic. Acetylcholine is present in postganglionic parasympatic fibers, where norepinephrine is present in the postganglionic sympathetic fibers. In some tissues acetylcholine causes constriction. Can also reduce heart rate vi the vagus nerve. Acetylcholine is the only neurotransmitter used in the somatic nervous system! Acetylcholine can effect vasodilation by several mechanisms, including activation of endothelial nitric oxide (NO) synthase and prostaglandin (PG) production. In human skin, exogenous Acetylcholine increases both skin blood flow and bioavailable NO levels, but the relative increase is much greater in skin blood flow than NO. So this may lead us to speculate that acetylcholine may dilate cutaneous blood vessels through PGs, as well as NO. In some muscle tissue acetylcholine causes vaso-dilation, but not all. Norepinephrine is the opposite competor/effector of acetylcholine. Acetylcholine is present in all preganglionic fibers, both parasympathetic and sympathetic. Acetylcholine is present in postganglionic parasympatic fibers, where norepinephrine is present in the postganglionic sympathetic fibers. In some tissues acetylcholine causes constriction. Can also reduce heart rate vi the vagus nerve. Acetylcholine is the only neurotransmitter used in the somatic nervous system! Acetylcholine can effect vasodilation by several mechanisms, including activation of endothelial nitric oxide (NO) synthase and prostaglandin (PG) production. In human skin, exogenous Acetylcholine increases both skin blood flow and bioavailable NO levels, but the relative increase is much greater in skin blood flow than NO. So this may lead us to speculate that acetylcholine may dilate cutaneous blood vessels through PGs, as well as NO.
It blocks the nicotinic cholinergic receptors on the muscle that normally bind the acetylcholine released by the motor neuron.
It doesn't.
The parasympathetic division of the autonomic innervation of the heart releases acetylcholine from its varicosities (the sites where neurotransmitter is released). The acetylcholine binds to M-2 muscarinc receptors to mediate the negative chronotropic (slowing of heart rate) effect. This also mediates a negative inotropic (lowering of force of contraction) effect.
A drug or compound that acts like acetylcholine (ACh). Acetylcholine is a neurotransmitter. In the peripheral nervous system (PNS), acetylcholine activates muscles. In the central nervous system (CNS), acetylcholine tends to cause decreased muscle contractions. These two responses are opposite. ACh Receptor agonists (booster of the effect) are used to treat myasthenia gravis and Alzheimer's disease. ACh receptor antagonists block muscle contractions causing paralysis. The bite of the Black Widow spider does this.
ACh will decrease heart rate/contractile strength, etc. Atropine is a muscarinic ACh receptor (mAChR) antagonist, so blocks the effects of ACh. Adding both together will result in a weak action of ACh that tails off as all the mAChRs become blocked by Atropine.
The effect would be an increase in cardiac output. However, there is a maximum level and then the heart would not have time to fill fully and the output would decrease.