Cardio exam 3... pray for me

What are some of the manical factors affecting CVP and venous return. what is the relationship vetween venous pressre and central venouspressure when standing and when reclining

Gravity

1. reclinig= relatively uniform blood distribution

2. Standing= gravity acts on vascular volume and blood accumulates in the lower extremites

   1. venous presure in the feet can reach 90mmhg

   2. reduction of preload and sv by frank starling in the right ventricle

   3. systematic areterial pressure falls more than 20mmhg upon standing

      1. orthostatic hypostension

Skeletal muscle pumps

1. 1 way valves allow blood to return to the heart (prevents back flow)

2. deep veins are surrounded my msucles = causes compression that opens and clsoes the vlaves

3. uses rhymatic contractions to enhance enous return and CO

Wat is the map equation

MAP = CO (SVxHR)xSVR

What causes varcose veins

1. damage in the valve sof the veins which causes swelling and venous twitingg

what is the resporatory pump

• increaed rate and depth of breathin increases venous return and CO

What are some of the factors affecting CVP

1. blood voulme (positive assotiaion

2. cardiac outuput (negative association)

3. SVR (negative association)

4. venous compliance (negatinve association)

5. muscle pumps (postive assoication

6. resporatory pump (positive association)

7. postural changs (reclining or squatting increases central venous pressure.)

What is the relationship betwen venous returnand cardiac output

Venous return = map - RAP/SVR

• venous return acan equal cardiac output in stayd state conditions 

• bloodflwo through the entire system (CO or VR) depends on cardiac fucntion or systemic vascular function

• sysstemic vascular and cardiac curves  guton lots

Describe the interdependance of CO and VR. what are the 2 rules

REturn supports output

1. cardiac output is dependant on preload. reload is determeind by filling pressure (CVP)

Output creates return

1. high hrs can cause a lwoer CVP

2. lower hrs can cause CVP to increase

What are the functions of the medulla, hypothalamus an dhiger centers to controlingautonomic innercation. what are the structures involved

Medulla

• contains cell bodies for parasympathetic and sympatheti efferent nuerons

hyppothalamus

• pareaventricular nucleas and dorsal medial nucleas 

  • they integrates and mdulate medullary neuronal activyt

• higher centrs

  • cerebral cotes, limbic, and midbrain structures

    • connect with the hypothalamus and meddual to modculate activty during emotaional stres

  • Top down control

Understanding the diagram (medulla). How does functional autonomic control from sympatheic, vagal, and nts (receptor afffernetns) impact lbood vessle sand the heart (all in the medulla)

1. only one parasympathetic or sympathetic cna be turned on

Sumpathetic activity controled by the hypothalamus

1. increases vasoconstriciton of the blood vessles

2. increase contractility of the heart

3. reduces activity of vagal nerves

vagal nerves

1. reduces the activity of sympathetic structures

2. controlled bby NTS from receptor afferents

3. reduces contraciitlity of the heart

nts

• impacted by the hyothalamus and receptor afferents

• increases vagal activity

What is parasympathetic innervation from the medulla. what is the DVSN and NA

DVn -dorsal vagal nucleus

NA- nucleus ambiguous

• reduces SA nodal firing (negative choromotrofy

• slowls AV conduction (negative dromotrophy

• minimal impact on ionotrophy bc parasympathetic primarlay impats the aorta

• afferent nerves modualte activity of the vagla neruon

  • baroreceptors from the NTS

What is the anatomy of parasympathetic innervation: pregangion fiers

postgangion fivers

wehre do they work. what hcan they impact

preganglionic fivers

• efferent fivers synapse within or near the target tissue and form small ganglia

• they projet form the cs to a ganglion (cluster cell of vodie)

short postgangion fivers

• innervate secific tissue cites

• cell body is in the gangion long pre gannlgion

• not ture gangion will tyically synase in or near target tissue short post gangion fiver innervates local target tissue

Increased ns activit can cause

• ACH induced direct vasodialation (genitals)

  • Indirect vasodialation by stimualtion productio nof vasodialttory substances (gi circulation)

    • enhances blood flow to promote nutrient pickup

What is the function of sympatheic innervation. what does it originate form and what doe sit impact

originates from nneurons in the medulla (Rostral ventrolateral medulla RVLM)

• icncresed SNS firing =

  • increased cardiac stimulation

  • increased chronotrohy dromoropy, and ionotropy

  • increased vsoconstriction

What do barrorreflex affernet neruons impact

the NTS and valal functioning

What is the anatomical structures of sympathetic innervation. parav ertebral gangliea, prevertebral ganglia. how does it travel down. post ganglionic sympathetic fibers

SNS axons leave the medula, travel downw the psinal cord and snapse within the inermediolateral cell colum of the spinal cord

• axons exit at hte thoratic and lumbar sine

preganglionic fibers then synapse within syphatetic paravertebral ganglia (bundle of cells) on both sides of the spinal cord

• or they synapse iwthin prevertebral gangila located in teh abdomen

post gangionic fibers travel to target organs where they inervate the arteires and veins

Draw out and understand the diagram .the remation between the higer structures of the brain. paravertebral gangia

prevertebral ganglia. blood vessles. the heart. the spinal cord. sympathetic projections. cranial nerve x ( vagus nerve)

parasympathetic innervation

1. fiters from spinal cord to pregangionicc fibers from the medolla to preautonomic fivers

1) sympateic project from RVLM down the cord to preganglionic neuron region (thoractic)

• t1 to t12 pregnanglionic nerves

2) synapses onto the pregnalionic neuron which projects out of he cord (paravertebral ganglia)

3? post gangionic neurons projects onto the heart

B/c = paraverebral gnaglia. used to inervate the post gangion neurons that project to the heart and blood vesls

es

C. projects into the post gangion neuron projects in both the heart and blodov essles

D/ synapses to the post gangion projects in the blood vessels form the revertebral ganglia

Describe the impacto f sympathetic and parasympathetic funcitonig on: chronotorphy, ionotropy, dromotrophy, vessles, resistance, and capitance 

how does reciprocal integration aid in acue and ongterm control of blood prssure. what is stronger. waht can alter these functions

reciporcal integration of the PNS and SNS aid in acute control of blood vessle

1. vagal influences are dominant over sympathetic influences of the heart

   1. hr.< sa nodal firing pace

   2. without reciprocal intgration = continuous parasympathetic activity.. no response to external stimulus

2. higer corticla regions alter atuonomic (parasympathetic) functioning

   1. fear

   2. vasovagal synchope

   3. stressd

Draw the dagram Where is ACH and NE released from in the symathetic and parasympathetif ccuntionig

What are the receptors of the parasymathetic system/nerves

what are the receptors of the vagus nerves (hint hint… this is more dominiant)

What dos NE and ACH react with in the effector receptrs… what is the result (the heart)

_{where are parasympathetic things found}

ACH is released from vegas nerves

NE is released from syapthetic nerves 

Sympathetic nerves have alpha 2 and M2 receptors. A2 receptors react with NE. M2 receptors react to ACH

• these slow down NE production

Vagus nerves have no receptors (they are found in the cns at the medulla

NE reacts with 

A2 (found inthe sympatehtic cellls 

• cuts down ne productions

A1 ( in the heart cells)

• increases sympatheic fucntioing 

B1 (highest reception) Heart cells

B2 (found in the heart ceells)

ACH 

• reacts with M2 receptors in the heart cells for parasympatheticc functining 

Draw the dagram Where is ACH and NE released from in the symathetic and parasympathetif ccuntionig

What are the receptors of the parasymathetic system/nerves

what are the receptors of the vagus nerves (hint hint… this is more dominiant)

What dos NE and ACH react with in the effector receptrs… what is the result (the blood vessles)

_{where are parasympathetic things found}

Symatpehtic nerves 

• have a2 receptors  (responds to A2)

• relesase NE

Parasympathetic nervse

• releases ACH

• no receptors on it

note there is no interaction iwthsympathetic nerves because there are barey any parasympathetic nvers in the blood vessles

NE

• responds to a2, a1 (primary) and b2 receptors

ACH respponds to m2 (minimally becuase there is baly any symatheir c nerves in the vvasculatore

how to baaro receptors regulate arterial pressure. where are they found. waht nerves are involved (sinus nerves, glossopharyngela nerve, vagus neerves, aortic nervs)

1. Areterial barorecepotrs are found in the cartoid sinus and the aortic arch

2. the sinus nervve (glossopharyngeal nerve (cranial nerve IX) 

   1. innervates the cartoid sinus

      1. travels from the carotid sinus in the glossopharyngela nerve up to the brainstem wehre they synase at the NTS

         1. afferent fibers from the cartoid sinus travel i

      2. the aortic arch barro receptosres are innervated by the aortic nerve (combines with teh vagus nerve) before traveling to the nts

understanding the diagram. wehrea re these nerves found. Glossophryngeal nervs. Aortic arch receptrs. 

where is the sinus nerve. werhe is the bvagus nerve 

ahhhh

HOw does the stres response to barro receptors impact the heart or whateer

arterio barro recepotrs reposnd to stretching of vessel walls produced by an increases in arterial blood ressure

increase in arterial pressure = increase in firing rate of individual receptors and enrves

the aortic arch baroreceptors function simlar to carotids

• have higher threshold pressure fo r firing and are less sensitive than the cartoid sinus receptors

• cartoid baroreceptrs are prdominate acute bp regulators

how does a change in arteriaal pressure imact CO and SVR. draw out the diagram

how does it relate to receptor firing, the CNS. CO and SVR (barroreceptors)

1. low bp decreases arterial blood pressure

2. decreased receptor firing increased

3. stop activation of the NTs (NTS will not inhibit sumpathetic activation)

4. increase in sympathetic nerves and decreases in parasympatheic

5. increase in both CO and SVR

6. both increases arterial rpessure 

Where are additional low pressure rreceptors found in the body

Waht do they respond to 

what is more dominant

riight atrium, low venoatrial junction, and the pulmonary arterial cirnculation

reponses

• they respond to atrial filling and are tnically active

  • increased venous return

  • increaed PNA (acardiac) and reduces SNA due to para sympathetic nerve activation

  • Decreased ADH release - adh come sform pituitary but some comes form the heart

    • used to reudce blood vlume

• As the cardiopulmonaries become more sielent = sns becoems more dominant

  • areterial baroreceptors also help due to low stretch

how does sanding impact parasympathtic and sympathtic activity

1.standing = pooling of blood at the feet = reudced filling ofthe heart = increaed sympathetic activity

ANS responds with baroreceptor reflexis

describe and draw out the valsalva manuver. whatare the different phases and what would happen in changes in alteration

phase 1

• begning of the forced expiration

  • aortic pressure increases due to aortic cpomression and the heart rate decreases refleixively - barro receptors are stimulated 

  • causes reciprocal cahges in bp and hr (decrease

phase 2

• aortic pressure falls during pahse 2

• compression of throatic veins reduces venosurs return and cardiac output = reflex tachcardia occurs (reduced stimulation of the barro receptors

phase 3

• small fall in aortic pressure do the loss of thoractic pressure. increase in heart rate due to reduced barroreceptor stimulation

  increase venous return raises aortic pressure onece again = rediuction in heart raate

phase 4 

• normal cardiac ouptut while svr is elevated from sympathetic activation durigng phase 2

• overshoot in aortic pressure

• heart rate falls a little bit

What are the steps by phases 

phase 1

1. infrease in intrathorastic pressure

phase 2

2. increase in aortic pressure

3. baroreceptor response to drop the bp

4. hr plummets

5. svr and ivc colapse. no vagus return to the heart = reduced s

6. bp drops hr increases to make up for the decreases in stroke volume

phase 3

7. breathing normally

8. small fall in aortic pressure do the loss of thoractic pressure. increase in heart rate due to reduced barroreceptor stimulation

9. increase venous return raises aortic pressure onece again = rediuction in heart rate

10. drops in intrathorastic pressure increase hr

11. the backued up venous return in the heart drops donw hr and increas stroke volume

What ar echemoreceptors and what can they do in the heart

• they cna influence medullary cardiovascular centers drectly or indirectly

  • through altered pulmonary strech receptor activity

• specialied cells located on artieres in the medulla motor blood po2, pco2. orr ph

function is to regulate resporatory activity to maintain arterial stable pressrues

sympathetic funcioning is stimulated by what

• decrease in po2

• increase in pco2

• decrease in blodo ph

what areperipheral chemoreceptors and where are they found

• lcoaeted in small caroitid bodies and aoritc boides. 

• respond to a fall in po2

• an elevation in pco2

• a decrease in ph

what are chentral chemoreceptors. hwere are they foudn and what do they respond to

1. located in the medulla *can directly sense blood bc not surroudned by blood brian barreir)

2. responsd

   1. increased co2

   2. decreaed ph

   3. increased h+ ions

   4. does not detect po2

What hormonesdoes the adrenal medulla secrete

• 80% e and 20% ne

what is the use of pinephrine in the cardiovascular system. waht receptors does it bind to

1. it depeodn son the distribution of cadreneric reepcetors and the afinites of the recpeotrs for epinephrine

   1. primary repsonsive to b receptors (b1 mostly). still reacts ot b2 and a receptors (a andrireceptors)

   2. b1 in the heart

what is the sue of norepinephrine in the heart and what recpetors are they most responsive with

norepinephrine = neurtranspitter and alpha hormoen

• released form sns neoursons as a neurortransmitter

• released form the adrenal medulla as a hormone

afinity for noe for b1 (heart) and a1 (vessles) receptors = greater than a2 and b2 receptros

causes an increase in hr and vasoconstriciotn

What happens if you adminiserter ne and e clinically

(look at terries slide im tired)-

Epineprine

• increase in hr from binding to b1 receptors

• decrease perhiperal resistance because increasei nhr = barroreflex withdraws sympathetic tone

• vasodialation

• increase in CO because e is still present

• arterial pressure and puls pressure widesns but maps stays the same

• tpr decreases =. diastolic pressure decreases ore impactuflly = not a change in map

NE (works more strongly in the vasculature)

• increase pherhiperal resistance. svr/tpr becuase of thea ctivity of a receptors

• ne at the heart but parasympathetics will cancel it out (ne isnt as strong)

• parasympathetics dont have an effect on the vasculature = increase in tpr decreases in co increase in diastolic pressure and increase in map due to increase in diastolic

figure this shit out

What is the function of the RAAS sytem. what does it do and what does it contorl

• impacts blood volue cardiac otuput, and total peripheral resistance

Understanding the RAAS cycle. draw it out

. which factors are the most impactful chainging arterial pressure. what is the fucnction of the kindeys, renin, angiotensinii ace, angeotesin 1 and aldosterone

1. Renin is an enzyme that acts on angiotensiongen

2. Angiotensisin then transforms to angiotensin 1

3. Vascular endothelium (in the lungs) - uses ACE that cleves off two amino acids to from angiotensin II

4. coontroling cardiac output through sv (blood volume) is th emost impactful

What is the fucntion of angiotensin ii in the RAAs system

1. Constricts resistance of vessels = increasing SVR and TPR’

2. Enhances sympatheti andrenic activity (TPR, HR, SV)

3. Acts on the adrenal cortex = aldostrone release (fluid)

4. Stimulates vassopressin release from posterior pituitary (SV, TPR) (ADH)

5. Stimulates thirst centers in the brain (SV) 

6. Stimulates cardiac and vascular hy[ertrophy (SV-long term)

what are teh different ways to manipulate raas and what are the result form them. Aledosterone, ACE, renin. Kindey disfuction. Adrenal corte x disfunciton. DRAW it out

1. Very common for hypertension and heart failure

2. ACE inhibitor s and AT1 receptor blockers do teh following

   1. Decrease arteriol pressure, ventricular afterload, blood volue, and ventricular preload

   2. They inhbit and reverse cardiac and vascular remodeling

Where is renin released from. Where is ANP released form

Renin= the kidneys

AnP = the heart

Waht is ANP and what does it do. What sitmulates ANP release. Draw out the cycle

ANP- atrial natriuetic peptide

1. It is a counterregulatory system for the renin-angiotensin-aldosterone system

2. 28 aminoacid peptide synthesized and stored in response to atrial distension, angiotensin ii stimulation, endothelin, and sympathetic stimulation

3. Elevated ANP are found during hypervolemia and congestive heart failure causes atrial distension)

   1. It helps facilitate offload and create a balance for blood volume volume

• atrial distiension

• sympathetic stimulation

• angiotensin ii

• endothelin

What are the effects of ANp release.draw out the diagram. how is it impacting aldosterone, angeiotensin ii, renin, and caridac ouptut. and the kindesy

1. Decrease in aldostrone, angiotensin 2, renin release = natural diuresis = reductio nin blood volume reduced cvp

Reduced CVP, readuced CO, reduce SVR and overal reduced atrial pressure

how do you modulate ADH (vassopressin (ADH control)). waht is its function. wehre is it released from 

ADH = increases water reabsorption by the kidnesy

• increasing water permeability of the collecting duct

ADH = nonapeptied hormone relased from the posteiro pituitary

• two principal sites of action: the kidnesy and blood vessels

ADH is antidiuretic via renal v2 receptors

• constricts arterial blood vessles but hte normal physiolgoic oncentrations of AVP are blow its vasoactive range

how do the follwing impact blood volume, cardiac output, and arterial pressure

• sympathetic activity

• vagla activity

• crculating epinephrine

• angiotensin ii

• aldosterone

• AnP

• and vassopressin 

descrobe wju

understand teh diagram… waht does it mean

save meeee

What are the different categories for high blood rpessure: normal, elivated, sage 1-2. sever and hypertensive for both systolic and diastolic 

look at diagram

1. What quantifies severe hypertension vs a hypertension emergency

1. Severe hy[ertension

   1. Death is not imminent

   2. May be harmful to rapixly lower blood pressure

   3. No need to immediatley treate

   4. Not that acutely dangerous

   5. Treatnment starts with pcp

2. Htn emergency

   1. End organ damage is evident

   2. Death is possible

   3. Immediate control of bpis critical 

1. What is the difference between pulmonary and systemic hypertension

1. Pulmonary

   1. Not as well studied

   2. Not as treatable 

   3. Worse prognosis

   4. Comes with comorbidities

2. Systemic hypertension

   1. Common

   2. Mostly treatable 

   3. Common precursor for other ocnditions

1. What are some o the causes of hypertesniosn

1. Typically bigins with hypervolemia

   1. Increased sodium and water retention

2. Renal pressure natiruesis corve is shifted = higher atrial pressure is required to maintain sodium balance

3. Altered kidney filtration and sodium balance in renal disease = shift in pressure naturisis = hypervolimia

1. Understand the diagram. Draw out the kidey RAAS system and understand how kidney disfunction, adrenal cortex disfunction, and how it can i mpac atrial pressure

raghhh

1. How does urine outut and fluid intake impact map in a healthy perosn, untreated, and treated hypertensive person. How does restricted fluid intak eplay into this

1. Waht is essential hypertension (90-95 percent of cases)

1. Diagnosis by exclusion

2. Increased sodium and fluid retention is a primary factor

3. Vascular changes = can contribute to hypertensive states 

   1. Especially with renal disfunction

4. Related to heredity, age, race, and ses

5. Some patients are more strongly influenced by stressful conditions than are normotensive individuals

What is secondary hypertension and how frequent is it found in the body (5%-10% of cases)

1. Renal artery stenosis

2. Renal disease 

3. Hyperaldosterone (primary)

4. Phechromoctoma (cathacholamine- secreting tumor)

5. Aortic coarctation

6. Pregnancy (preclampsia)

7. hyperthyroidms/hypothyrodism

8. Cushing system 

9. Sleep apnea

1. How does dysfunction inthe CNS PNS and gut microbiome impact hypterteions

1. Dysfunction in the Cns

   1. Inhibition of sympathetic outflow (reflex inhibition)

   2. Exaggerating intrinsic firing of sympathic centers

      1. Causes excessive vasoconstriction

      2. Causes excessive sodium retention

2. PNS

   1. Afferent renal nerves are not functioning properly

3. Gut microbiome

   1. Alteredgut microbiota generally impacts bp

   2. Inflammation peripherally and in the cns ude to changes in circulating factors

What are some of the common tyes and factors of secondary hypertension: describe the following 

• renal artery stenosis

• renal disease

• primary hyperaldosteronism

• cushing syndrom

• preclapsia

• pheochromocytoma

• hyperothryrodis

• aortic oarctation

• sleep apenae

1. Causes identifiable and possibly treatable

2. Renal artery stenosis: renal artery becomes narrowed (stenoic) = owing to atheroschelrotic or fibromuscular lesions

3. Renal deseisse: damaged kidney nephrons

4. Prymarey hyperaldosteronism: increased secretion of aldosterone by an adrenal adenoma or adrenal hyperplasia

5. Cushing syndrome: excessive glucoracoitd secretion = leads to hye=pertension

6. Preclapsea: occurs in 5% of pregnaies during late second and third trimesters

7. Pheochromocytoma: catehcolamine-secreting tumor (in the adrenal medula)

8. Hyperthyroidis: increase in blood volume and increaed cardiac activity = hypertension

9. Aoritc oarctation: narrowing of the cardiac arch usually distal to the left s ubclavian artery

10. Sleep apnea: a disorder which people stop breathing for short periods of time during their sleep 

1. What are some of the symptoms of cushing syndromeWhen the adrinal glands excrete too mcuh cortosol 

   1. Cns irritablity

   2. Hypertension

   3. Cardiac hypertrophy

   4. Hyperphalsia (tumor on kidneys = really bad)

   5. Obesity

   6. Osthero perossi

   7. Muscle wasting

how can ventricular hyertrophy relae to lala’cslaw

afterload = wall stress 

1. What are some of the compensatory cardiac and ventricular adaptations to high blodpressure

1. Cardiac 

   1. Concentric hypertrophy: more sarcomeres in parallel

      1. Like lifting weights in the gym

      2. Wall stress decrease

      3. Stroke work increases allong with diffusion distance

2. Vascular

   1. Vascular myocite hyertorpy

      1. Narrwoign of the lumen

      2. Reduces complanced

         1. Accelerated cv agin

1. What are some of the therapeutic intervention methods

1. sed to correct secodnary hypertension (treats the underlying cause)

   1. You n eed to addres CO (SV and HR) and SVR

1. What is the most effectiv evaraible when addrsing hypertension (SV vs HR) - what are the pharmalogical methods used

   1. HR

1. HR

   1. Use of beta blockers (typically given with diurents to reduce blood volume)

   2. Uses calicum channel blocker

   3. Not verry effectiv bc SV is more affective in CO

2. SV

   1. Diuretics reduce blood volume (most common treatmetn)

   2. Ace inhibitors

      1. Given with diuretics

      2. Andiotensin 2 type 1 receptor blockers

1. What are som eof the sytemic methods for fixing ypertension

1. Alpha-adrenoceptor antagonist causes vasodialation

2. Other drugs result in dialation

   1. Ace inhbitors

   2. Angiotensin II receptor blocers

   3. Ca+ channel blcoekrs 

   4. Direcet acting arterial dialators (hydralazine)

      1. Treating SVR is usually in combination with treating volume issues

What is the ACD regime for therapeutic interventions

1. AT1 blockatesace in hbitors

2. Calcium channel blclocker

3. Diuretics

1. What are trends in treatnemnt efficacy and what is the mortality and compliccation rates for those untreated

Waht is the NTS

nucleus tractus solitarius.

• afferent fibers from erhiperal baroreceptors and chemoreceptors and resporatory stretch receptors enter here.

• inhibitory interneurons within here project ot the medulala regions to cut back on sympathetic nerves

• enhanses vagal efferent nerve activyt

• recives inmput fromt he hypothatlamus

What is the DVN and NA

• dorsal vagal nuceus and nucleus ambiguus

  • parasympathetic vagal fibers innervating the heart originate from cell boides found here (medulla of the bbrainstem)

reduces sa nodal firing and slwos the av nodal conduction (agal tone)

Describe the valsalva manuver

• reflective test that involves holding your broeath

• increasses the pressure i nthe thoractic cavity = increased pressure in the thoractic vessels = increased aortic copmpression = increased aortic pressure

• results in bradycardia due to barroreceptor stimulation (parasympathetic

What are teh effects of low does epinephrine and norepinephrine in the body

low does E

• increases systolic and diastolic pressure. increases heart rate and areterial puls pressure. very little chagne in map (because they bind to b1 andrenoreceptors = cardiac stimulation)

• b2 receptors = sytemic vasodialation

• map does not chagnge mych bc cardiac output is offset from teh decrese in systemicvascur resistance

Norepinephrine (low doese)

• increase ma and areterial puls pressure. hr increases as well (B1 adrenogenic stimulation)

• decreases due to barroreceptor reffelx. map increases due to a1 andronorecpeotrs = increases svr

Where does PNS activity manafest in the vasculature. ACH and others

ACH- induced direct vasodialation (genetals)

Indirect vasodialation by stimulating production vasodialtory substances in the GI circulation

HOw do parasympathetics synapse to their target tissues

• they project from the cns directlu to the area (pre and post ganglionic cells)

Why are beta 2 vasodialtory in the vasculature but not in the heart

• increases camp production. Camp production is vasodialtory in the blood vessles

• camp improces cont3raction in the heart - increases hr and contractility