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:
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