(From Dr. Nardell’s ANS Physiology Handout, by Brian Buschman)
Return to Semester Two Goodies
Return to The Unofficial Ross Page
Facilitated exchange diffusion is when a drug works by stimulating facilitated antiport exchange between itself and NE.
False NTs are able to compete with NE for the mechanism that takes them up into the vesicles. This way the false NT is in the vesicles and is released in place of NE when stimulated.
Epi stimulates both a and b receptors. It’s effects include:
Increase rates, automaticity, conduction, contraction.
It also has decreased cardiac efficiency. Less work is done per unit of O2 consumed.
Visceral and cutaneous vasoconstriction.
Skeletal muscle vasodilatation
Low doses cause decreased TPR so BP drops.
High doses cause decreased TPR and increased cardiac output. This causes increase in systolic pressure, slight increase in MAP and decrease in diastolic pressure.
Bronchiodilation and increased mucus clearance
Smooth muscle relaxation and contraction of the sphincters
Relaxation of various things
Epi does not enter the CNS
Overall decreased aqueous humor pressure. Stimulation of b2 receptors increases production but other sympathetic effects cause the overall effect to be a decreased pressure.
b2 receptors increase sequestration of Ca2+ which increases spindle discharge and causes tremors.
It functions to decrease insulin and increase blood glucose. O2 consumption goes up as discussed with the heart’s decreased efficiency.
Epi causes the secretion of renin
NE is pretty much the same as epi but it does not stimulate b2 so it does not induce:
Adverse effects are like epi. Therapeutic uses include hypotension, shock and to retard absorption of local anesthetics.
Low doses only activate D1 receptors.
Intermediate doses can also activate b1 receptors and cause release of NE.
High doses activate D1, b1 and D2 receptors.
Based on this it’s effects are:
Low doses cause vasodilatation of renal and mesenteric beds.
Intermediate doses have inotropic effects
High doses cause increase HR, hypertension, nausea and vomiting.
Dopamine’s therapeutic use is to help with shock related to poor renal perfusion. It does not cross the blood brain barrier so it cannot be used to treat Parkinson’s.
The major effect is hypertension from the a1 induced vasoconstriction.
Non-catacholamines are not degraded by MAO and COMT so they last longer then epi, NE and dopamine.
Phenylephrine and methoxamine are used to treat orthostatic hypertension, nasal congestion and as a mydriatic.
The main effects of a2 stimulation cause CNS sympathetic outflow stimulation. They also limit the release of insulin bring the primary PNS job or a2 receptors.
It is used to treat bronchospasm and to overcome cardiac conditions requiring increased CO and decreased TPR.
Only stimulates the cardiac functions. Causes increase in BP, CO and so forth.
Albuterol and terbutaline are the anti-asthmatics as they cause:
They also cause the vasodilatation that is associated with the sympathetic response.
Asthma
COPD
Suppress premature labor
Return to Semester Two Goodies
Return to The Unofficial Ross Page