Autonomics Flashcards Preview

Cardiology Exam 1 > Autonomics > Flashcards

Flashcards in Autonomics Deck (23):

What are the relative affinities for epi v NE for alpha and beta receptors?

* a1a2: NE>Epi
* If extremely high conc of epi it will bind alpha receptors (ex- epi pen) and cause overall vasoconstriction

* Beta1: NE= Epi

* Beta2: Epi >NE
* Epi is not released from neurons but released right into bloodstream via adrenal gland; in exercise it inc blood flow to skeletal muscle, coronary arteries and liver for glucose liberation (beta 2)


Baroreceptor Reflex

* Negative feedback to stabilize BP in normal range (set point is about 92mmHg)
* Stretch receptors inc firing rate w/ stretch; but they adapt so only code acute change r

* Receptors in aortic arch —> CN X afferents —> nodose ganglion —> nucleus tractus solitarius

* Receptors in carotid sinus —> CN IX afferents —> petrosal ganglion —> nucleus tractus solitarius

* Result? Inc firing —> inc parasymp and dec symp outflow —> dec HR and dec contractility while dec TPR b/c less sympathetic vasoconstriction AND Dec firing —> dec parasymp and inc symp —> inc HR and contractility while inc vasoconstriction and thus TPR


What is the neural baroreceptor circuit?

* Baroreceptors —> nucleus tractus solitarius which then influence both sympathetic and parasympathetic systems

* Sympathetic: NTS —> CVLM (GABAergic) —> - RVLM —> IML (interomediolateral cell column)

* Parasympathetic: NTS —> Nucleus Ambiguus

* So RVLM fires less when inc pressure/inc stretch to dec sympathetic NS to lower BP AND RVLM fires more when dec pressure/less stretch to then inc sympathetic NS to inc BP


What happens when baroreceptor reflex is removed?

* Ex) cervical SC injury

* Greater fluctuation in BP but still stays around set point b/c angiotensin II; but b/c angiotensin II is a hormone it is slower than NS hence takes more time and greater fluctuation

* These patients can still compensate w/ parasympathetic withdrawal


Bainbridge Reflex

Atrial stretch receptors (or low pressure receptors) sense changes in volume SO…inc venous return —> inc firing —> vagus nerve —> nucleus tractus solitarius —> inc HR and contractility AND inhibit release of vasopressin for posterior pituitary (vasopressin normally inc reabsorption of water so now less reabsorption to dec blood volume and thus venous return)



* Atrial Natriuretic Factor (ANF) - Released from atria if venous pressure/atrial stretch is high

* B-Type Natriuretic Peptide (BNP)- released from VENTRICLE in response to inc tension
* Diagnostic signal of increased L ventricle pressure and L ventricle dysfunction

*Overall goal of both = vasodilation (dec return and after load to dec workload of heart)
* Works on hypothalamus - less vasopressin
* Works on kidney - inc GFR to inc NaCal and water secretion (lower volume) and dec renin
* Works on adrenal - less aldosterone (less reabsorption of water and salt)
* Works on medulla - dec BP



(or arginine vasopressin)

* Synthesis is stimulated by…
* High osmolarity (too concentrated) - osmoreceptors
* Dec atrial stretch (low blood volume) - atrial stretch receptors
* Dec BP - baroreceptors

* Synthesis in neurons, then release by posterior pituitary

* Target - collecting duct epithelium in kidney to insert more aquaporin channels so more water reabsorbed —> inc volume, inc BP and more dilute


Renin-Angiotensin System

* JG cells in kidney detect low BP and make renin (JG cells detect renal artery pressure and innervated by sympathetic NS)

* Liver cells make angiotensinogen

* Renin is then enzyme for conversion of angiotensinogen to angiotensin I

* Angiotensinogen (renin) —> angiotensin I (ACE) —> angiotensin II

* ACE or angiotensin converting enzyme is in blood vessel endothelium

***ACE inhibitors are used as to dec BP (hyperkalemia as side effect b/c less aldosterone so less K+ secretion)

***Selective Angiotensin2, Type 1 antagonists block only receptors in blood vessels and adrenal cortex where aldosterone is produced so less is effects


5 Things Angiotensin II Does

* Stimulates vasopressin from pituitary

* Stimulates thirst (so drink to inc volume)

* Stimulates medulla for sympathetic outflow —> inc HR and vasoconstriction

* Aldosterone release for more reabsorption

* Potentiates release of NE from sympathetic terminals


Adrenergic Crisis

* Sudden, marked inc in circulating catecholamines (from adrenal or spillover from neurons)

* Extreme tachycardia and inc BP

* Causes - cocaine OD (most common), intoxication w/ amphetamines, pheochromocytoma (tumor in adrenal), ingesting Tyramine in food when on MAO-inhibtors, clonidine/beta blocker/opiate/alcohol withdrawal. MI, subarachnoid hemorrhage, panic attack, etc


Catecholamines v. Non-Catecholamines

* Catecholamines - epi, NE, dopamine and isoproterenol- potent but not stable (broken down by MAO and COMT) so not given orally usually

* Non-catecholamines - stable but less potent so can give orally


Epi v. NE

* Epi- (beta >alpha) inc HR and contractility; induces bronchodilation; if high dose then binds alpha —> vasoconstriction to inc BP for perfusion in cardiac arrest

* NE- (alpha>beta) mainly vasoconstrictor; mainly used for shock to inc BP



Dopamine- effects depend on dose;

@ low dose…bind DA receptors and inc coronary, renal, splanchnic flow;

@ intermediate… binds beta1 to inc contractility;

@ high dose binds a1 for vasoconstriction to inc BP




* Isoproterenol- (BETA only) similar effects as exercise; inc contractility, inc HR, inc conduction and vasodilation; downside= inc O2 demand while vasodilation dec
coronary flow so risk of heart ischemia

* Dobutamine - (BETA only) also inc contractility but less inc HR and less vasodilation so less O2 demand than iso





Beta 2 Agonists

* Terbutaline/albuterol- short acting beta 2 agonists for bronchodilation in asthma and COPD

* Salmeterol/formoterol/arfomoterol- long-acting beta 2 agonists for asthma and COPD (only used in combination w/ gluccocorticoids in persistent asthma)

* Ritodrine/Terbutaline- beta 2 agonist that dec intensity and frequency of uterine contractions in premature labor (inc cAMP to remove more Ca++ from vascular smooth muscle)






* Phenylephrine - a1 agonist so vasoconstriction (in nasal and eye formulations); decongestant

* Oxymetazoline- a1 agonist to reduce red eye/allergic eye (helps conjunctiva infection NOT ciliary infection)

* Tetrahydrozoline- a1 agonist so vasoconstriction dec nasal blood flow and nasal mucosa swelling; decongestant




a1 agonist in CNS; stimulants

modanifil>adrafinil in potency

modanifil in elderly and attention probs

adrafinil in narcolepsy and excessive daytime sleepiness



a2 agonist in RVLM so provides neg feedback to RVLM —> dec sympathetic outflow; used as anti-hypertensive but 2/3rd line





* Amphetamine- CNS stimulant; works indirectly by releasing monamines like NE from their storage sites and competing for re-uptake

* Methamphetamine- central effects; works indirectly to inc sympathetic effects; side effects are tachycardia and inc BP

* Ephedrine- MIXED; alpha and beta agonist plus inc NE release






ADHD Drugs

* Methylphenidate (Ritalin) - blocks re-uptake of NE and dopamine + stimulant CNS effects

* Dexamphetamine - promotes release of NE and dopamine and competitive inhibitor of catecholamine re-uptake

* Buproprion - inhibits neuronal re-uptake of NE and dopamine

* Atomoxetine - selective inhibition of NE re-uptake




Selective a1 antagonists

* Prazosin/Doxazosin/Terazosin- a1 antagonist to treat hypertension; block vasoconstriction

* Alfuzosin/Tamsulosin/Silodosin - a1 antagonist to treat BPH



selective a2 antagonist; inhibits a2 negative feedback on sympathetic NS so inc sympathetic NS so inc BP



* non-selective alpha antagonists; limited use b/c side effects but anti-hypertensives