Physiology of the Autonomic Nervous System

A class of drugs that stimulate the sympathetic nervous system by mimicking the effects of norepinephrine and epinephrine.

A drug that increases heart rate and contractility, and dilates bronchioles.

A drug used to treat heart failure, increasing heart rate and contractility.

A drug that constricts blood vessels, increasing blood pressure. It also constricts bronchioles and pupils.

A drug that dilates bronchioles. It also dilates blood vessels in skeletal muscles.

Sympathetic Nervous System (SNS) uses two key receptors: Nicotinic Acetylcholine Receptor (nAchR) at preganglionic synapses and α/β-Adrenergic Receptors at postganglionic synapses for norepinephrine release.

An increase in blood pressure triggers a decrease in the SNS activity and an increase in the PNS activity to counteract the elevated pressure.

Acetylcholine receptors on the endothelium initiate vasodilation by releasing Nitric Oxide (NO) signals.

Antidiuretic hormone (ADH) directly activates V2 receptors in the kidney to increase water absorption.

Ryanodine receptor releases calcium ions from the sarcoplasmic reticulum in cardiomyocytes.

The Sarco/Endoplasmic Reticulum Ca^2+^ ATPase (SERCA) is responsible for reuptake of calcium ions into the sarcoplasmic reticulum in cardiomyocytes.

Nicotinic Acetylcholine Receptor (nAchR) is the receptor at both preganglionic synapse of the SNS and PNS.

Muscarinic Acetylcholine Receptor (mAchR) is the receptor at postganglionic synapse of the PNS.

Vascular resistance is inversely proportional to the 4th power of the vessel's radius. This means that a small change in radius can lead to a large change in resistance.

The sympathetic nervous system (SNS) increases the release of several hormones including aldosterone, angiotensin II, and ADH. However, it does not directly increase the release of ANP (atrial natriuretic peptide).

Natriuretic peptides work by increasing intracellular levels of cGMP. This differs from other signaling pathways like cAMP signaling.

Increased cardiac contractility leads to an increase in cardiac output. The heart pumps more blood per beat, resulting in higher output.

Hydralazine is a vasodilator that can lower blood pressure by multiple mechanisms, including:

• Activation of potassium channels to hyperpolarize cells, reducing excitability.
• Inhibition of IP3 receptor, which reduces calcium release from intracellular stores.
• Decrease in reactive oxygen species (ROS).

Activation of M3 muscarinic acetylcholine receptors (M3-AchR) on bronchial smooth muscle causes bronchoconstriction, leading to narrowing of the airways.

When both alpha 1 and beta 2 adrenergic receptors are activated in vascular smooth muscle, the alpha 1 adrenergic signal (vasoconstriction) typically dominates.

Succinylcholine quickly activates nicotinic acetylcholine receptors (nAchR) on skeletal muscle, but it then desensitizes the receptors, leading to a reduction in muscle activity. It is also known to cause rapid onset, but short duration paralysis.

Non-depolarizing neuromuscular blocking agents act as competitive antagonists of nAchR. They block the binding of acetylcholine to the receptor, preventing muscle contraction.

Baclofen is a GABA-B agonist that hyperpolarizes neurons, reducing their excitability. It also decreases calcium influx.

Milrinone, a phosphodiesterase 3 (PDE3) inhibitor, increases intracellular cAMP levels in the heart, leading to increased contractility. It also inhibits PDE3 in vessels, leading to vasodilation.

PKA (protein kinase A) increases cardiac contractility by enhancing calcium cycling through phosphorylation. It phosphorylates the following:

• Ryanodine receptor 2 (RyR2)
• L-type calcium channel (LTCC)
• Phospholamban (PLB)

The correct order for alpha 1 adrenergic receptor affinity is:

1. Norepinephrine
2. Epinephrine
3. Phenylephrine

The sympathetic nervous system (SNS) plays a significant role in cardiovascular regulation, increasing heart rate, contractility, and vasoconstriction. It does not directly increase the release of ANP.

Hydralazine is a vasodilator that can lower blood pressure by multiple mechanisms, including:

• Activation of potassium channels to hyperpolarize cells, reducing excitability.
• Inhibition of IP3 receptor, which reduces calcium release from intracellular stores.
• Decrease in reactive oxygen species (ROS).

ANP (atrial natriuretic peptide) is a hormone released from the heart that helps reduce blood pressure by promoting sodium and water excretion. It works by increasing intracellular cGMP levels.