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Adreneric receptors

sans or pans

on what do they react

sympathetic Nepi

NE<E

B1: Heart, kidney

B2: lungs, arteries, uterus, neuromuscular 

B3: adipose tissue 

 

NE>E

a1: bloodvessels (skin, kidney. not heart vessels.) 

a2: presynaptic nerve 

 

cholineric receptors

 

ACh: Natural agonistfor N+M receptors

nicotinic: (fast-ion)

N1:Neuro-muscular ending, ion channel 

N2:Autonomic ganglia adrenal gland

muscarinic: 

M1:Autonomic ganglia EPSP, IP3/DAG

M2:Heart Presynaptic, cAMP

M3:Smooth muscles+ glands, cAMP

what protein makes NE to E

phenylethanolamine-N-methyltransferase 

PNMT

a1 agonist

what does it result in 

pro sympatetic 

Gq coupled: need Ca2+

vasoconstriction bloodvessels

a1 stimulation->vasoconstriction: 

what happens to veins, what happenss to arteries

 

and renin release

arteries:

+bloodpressure

+ after load    + diastolic pressure

+ total peripheral resist.  + BP

veins:

+preload  +systolic pressure

- lower volume stays in the veins

 

renin:

decreases

a1 antagonist

phentolamine 

block a1 receptors: 

a2 agonist

anti sympathetic

inhibitory effect 

Gi coupled receptor : lower cAMP

 

noradrenaline binds; leads to decrease NE

anti-insuline 

beta receptor stimulation

inhibitory except:

  • heart
  • hormone 
  • metabolism

B1 agonist

Gs : increase cAMP 

heart and kidney

cardiac output +

kidney renin release + (hormone)

 

+ chromotopic = HR+

+dromotropic =conducting+

+ inotropic = contractillity +

B2 agonist

Gs: cAMP

Bronchi (arteries, uterus..)

RELAX: smooth muscle, bronchi, vasodilation

- total perif. resistance

- afterload

- diastolic pressure

- bp

B2 antagonist

propanolol

metoprolol

 

B3 agonist

lipolysis

+ metabolism; burn fat

 

NE binds on 

a1 

a2

b1 <3

 

E binds on 

a1

a2

B1 <3

B2 lunggg

bloodvessels contraction 

 

not parasympathetic fibers

NE extravascular side

E intravascular side