We all know that the sympathetic nervous system, or SNS, is responsible for raising heart rate and causing our pupils to dilate. But what does it do with all of those elevated hormones when it reaches its destination?
It could be any of the following:
– inhibits other branches of the ANS
– activates beta receptors in smooth muscle cells along blood vessels which causes them to release nitric oxide (NO)
– activates alpha receptors which causes vascular smooth muscles to contract which increases blood pressure and reduces capillary diameters leading to a reduction in both blood flow and leakage from vascular beds. There is a large amount of research that links this with cardiovascular diseases.
More specifically, the SNS releases epinephrine, norepinephrine (noradrenaline), and dopamine at any of the above “destinations”. All three can also cause an increase in the heart rate, but they also act on other organs such as the skeletal muscle and liver and cause many of their functions to be switched on. For example, dopamine is involved in gastric motility and secretions. If you give a drug that blocks the action of dopamine in the stomach, you will see less gastric emptying time and less secretion. If you block alpha-receptors, you will see an increase in heart rate because this cycle is dependent on sympathetic stimulation.
This article examines the effects of the SNS on the skeletal muscle. You will learn about two actions of epinephrine, one action of norepinephrine and three actions of dopamine.
In muscle cells, epinephrine causes calcium ion channels to open and calcium ions begin to flow into the cell (movement of calcium from outside to inside). Ca2+ triggers a signaling molecule called troponin C which causes the heart to beat faster. This is a positive feedback loop in which calcium release causes calcium receptors to send a signal to troponin C which causes more calcium release, etc.
Norepinephrine also works in the same way as epinephrine but it increases the speed at which calcium channels open up. It also causes more troponin C to be produced. In addition, norepinephrine sends signals for the myocardium to contract and reduce its resting membrane potential, so that more calcium ions are free to enter the cell and trigger additional muscle contraction and faster heart rates.
Dopamine reduces contraction of the smooth muscle cells which causes blood vessels to widen and allows for more blood flow to be directed to the heart. It also causes the heart muscle itself to contract, which helps with cardiac output.
Dopamine can increase or decrease (inhibit) the heart rate because it works through different receptors. There are D1 and D2 receptors that act as an agonist (stimulant) or antagonist (inhibitor) of doapmine. The D1 receptor is found in the sinoatrial node (SA) and can both increase and decrease heart rate. However, the D2 receptors are located in the ventral tegmental area of the brain stem and will inhibit the SA node. Drugs that block D2 receptors can cause mania and psychosis.
Drugs that activate alpha-1 adrenergic receptors can also slow heart rate by decreasing norepinephrine release from sympathetic neurons. This action is mediated by activation of alpha-1 receptors in the sinoatrial node when norepinephrine binds to its receptor. The mechanism through which these drugs slow heart rate is called presynaptic inhibition, which I will explain in more detail further down this article.
An increase in norepinephrine from the SNS can also inhibit parasympathetic action, unless there is a direct connection between the two systems where one system can “see” the other.
Stimulation of presynaptic alpha-2 adrenergic receptors causes vasodilation and a fall in blood pressure. Stimulation of presynaptic alpha-1 or -2 adrenergic receptors causes vasoconstriction and an increase in blood pressure. This effect is seen with drugs such as phenylephrine which are alpha agonists. However, this effect can differ in different vascular beds (the bed around your heart would be different than a leg vessel).
