Autonomics Flashcards
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)
ANF v BNP
- 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
Vasopressin
(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
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
Dobutamine
- 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
Albuterol
Salmeterol
Terbutaline
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)
