sympathetic activity

De Groot points out, in spite of the fact that epinephrine levels and catecholamine excretion are actually not elevated, propranolol ( it is presumed, acting by inhibition of alpha-adrenergic sympathetic activity ) reduces anxiety and tremor in a very useful manner, indicating some of the central nervous system irritability is a manifestation of elevated sensitivity to circulating epinephrine.

This may be involved in its pathology by enhancing sympathetic activity, vasoconstriction, or by some other unknown neurotransmitter-related mechanism.

One common measure of sympathetic activity is skin conductance, which measures how sweaty our palms are and how well they conduct electricity.

Stimulation of the adrenal medulla releases adrenaline ( epinephrine ) into the bloodstream which acts on adrenoceptors, producing a widespread increase in sympathetic activity.

It may also be due to reduction in renin release from the kidneys, and a central nervous system effect to reduce sympathetic activity ( for those beta blockers that do cross the blood – brain barrier, e. g. propranolol ).

* Increased heart rate, stimulated by increased sympathetic activity in order to maintain cardiac output.

This center in the brain increases sympathetic activity, releasing catecholamines into the blood stream.

However, because calcium channel blockers result in a decrease in blood pressure, the baroreceptor reflex often initiates a reflexive increase in sympathetic activity leading to increased heart rate and contractility.

Hence, once the pheochromocytoma has been resected, thereby removing the major source of circulating catecholamines, a situation arises where there is both very low sympathetic activity and volume depletion.

Increased sympathetic activity reduces glandular bloodflow, thereby decreasing the volume of fluid in salivary secretions, producing an enzyme rich mucous saliva.

This occurs because sympathetic activity from the ciliary ganglion is lost thus parasympathetics are not inhibited.

There is a relationship between sympathetic activity and emotional arousal, although one cannot identify which specific emotion is being elicited.

The NTS also sends excitatory fibers to the Nucleus ambiguus ( vagal nuclei ) that regulate the parasympathetic nervous system, aiding in the decrease in sympathetic activity during conditions of elevated blood pressure.

Recent studies have described a subset of POTS patients that appear to have elevated angiotensin II levels coupled with paradoxically reduced absolute blood volume, signs of increased sympathetic activity and reduced peripheral blood flow.

* Clonidine can work in patients with reduced sympathetic activity.

It is especially effective in patients exhibiting symptoms of excessive sympathetic activity.

Horner syndrome is due to a deficiency of sympathetic activity.

The vagal and sympathetic activity constantly interact.

Parasympathetic influences exceed sympathetic effects probably through two independent mechanisms: ( 1 ) a cholinergically induced reduction of norepinephrine released in response to sympathetic activity and ( 2 ) a cholinergic attenuation of the response to a adrenergic stimulus.

It will also affect the postsynaptic alpha 1 and 2 receptors in the nervous system, and so reduce sympathetic activity.