2F Adrenal Medulla review

How much epinephrine in circulation comes from adrenal glands?

100%

How much norepinephrine in circulation comes from adrenal glands?

30% (70% comes from postganglionic sympathetic neurons)

How does the adrenal cortex regulate adrenal medullary function?

Adrenal cortical GCs: inhibit neuronal differentiation, stimulate PNMT expression

Preganglionic sympathetic neurons receive signals from …

Primary center neurons in hypothalamus/brainstem

Preganglionic sympathetic neurons synapse on …

Postganglionic sympathetic neurons in ganglia

-chromaffin cells in adrenal medulla

Preganglionic sympathetic neurons release …

Acetylcholine (ACh)

Where are nicotine ACh receptors located?

Membrane of chromaffin cells

-net increae in intercellular cations

How does this intracellular change promote Catecholamine synthesis & release?

Increased cytoplasmic [Ca] signals exocytosis of secretory vesicles.

How are Catecholamines circulated?

Unbound or loosely bound to albumin

How are catecholamines inactivated?

inactivated inside cells after receptor binding

• receptor-hormone complex endocytosis

What enzymes inactivate intracellular catecholamines?

Monoamine oxidase (MAO)

Catecholamines-o-methyl transferase (COMT)

What receptors do epinephrine & norepinephrine bind?

Adrenergic receptors expressed throughout the body

Adrenergic receptors are what type of receptor?

GPCRs

ß(1,2,3) = primarily Gs-linked

∂1 = primarily Gq-linked

∂2 = primarily Gi-linked

What are the effects of beta2-Adrenergic receptors?

Gs-linked GPCRs: increased cAMP inhibits MLCK activity, causes smooth muscle cells to relax

What are the effects of alpha2-Adrenergic receptors?

Gi-linked GPCRs: inhibit cAMP reduced MLCK inhibition, increases smooth muscle cells contraction.

What are the effects of alpha1-Adrenergic receptors?

Gq-linked GPCRs: increased Ca influx from ER activates MLCK, increases smooth muscle cells contraction.

What clinical signs would you expect with excess production of adrenal catecholamines?

Tachycardia, hypertension, & nervousness

What clinical signs would you expect with deficient production of adrenal catecholamines?

Adrenal medulla is not an essential organ, other sources of catecholamines

What is the difference between pharmaceutical agonists and antagonists?

Pharmaceutical agonists bind receptors & induce physiologic effects

Pharmaceutical antagonists bind receptors & do not induce physiologic effects

What is the difference between sympatholytic & sympathomimetics?

Sympatholytics oppose effects of postganglionic sympathetic neurons receive signals activity by inhibiting.

Sympathomimetics produce effects resembling postganglionic sympathetic neurons receive activity