Classify sympathetic receptors.Enumerate thier site of distribution and functions.Give one test to check the function of SNS and PNS

Reading File
Finding Sources
Finding Sources
Finding Sources
Reading File
Reading File
Reading File
Reading File
Finding Sources
Reading File
Finding Sources
Reading File
Finding Sources
Finding Sources
Finding Sources
Reading File
Reading File
I now have comprehensive information from multiple authoritative textbooks. Let me compile the full answer.

Sympathetic (Adrenergic) Receptors — Classification, Distribution & Function


1. Classification of Sympathetic (Adrenergic) Receptors

Sympathetic postganglionic neurons release norepinephrine (NE) and epinephrine (Epi), which act on adrenergic receptors — all of which are G-protein coupled receptors (GPCRs). Two major classes exist, each with subtypes:
ClassSubtypes
α (Alpha)α₁, α₂
β (Beta)β₁, β₂, β₃
DopaminergicD₁, D₂ (sometimes listed separately)
— Medical Physiology (Boron & Boulpaep), p. 512; Costanzo Physiology 7th Ed., p. 69

2. Distribution and Functions

α₁ Receptors

Details
G-protein / 2nd messengerGq → Phospholipase C → IP₃ + DAG → ↑ intracellular Ca²⁺
Agonist potencyNE ≥ Epi
Selective antagonistPhentolamine, prazosin
Site of distribution & function:
Organ / TissueEffect
Vascular smooth muscle (skin, renal, splanchnic)Vasoconstriction → ↑ peripheral resistance
GI tract sphinctersContraction (sphincter closure)
Urinary bladder sphincterContraction (urinary retention)
Radial muscle of irisMydriasis (pupil dilation)
Pilomotor musclesPiloerection ("goosebumps")

α₂ Receptors

Details
G-protein / 2nd messengerGi → ↓ adenylyl cyclase → ↓ cAMP
Agonist potencyNE ≥ Epi
Selective agonist / antagonistClonidine / Yohimbine
Site of distribution & function:
Organ / TissueEffect
Presynaptic adrenergic nerve terminals (autoreceptors)Negative feedback — inhibit further NE release (key regulatory role)
GI tract wallReduced motility
Presynaptic cholinergic terminals (heteroreceptors)Inhibit ACh release
CNS (locus coeruleus)Sedation, ↓ sympathetic outflow
The adrenal medulla lacks α₂ receptors and is therefore not subject to feedback inhibition — it can deplete catecholamines during prolonged stress. — Costanzo Physiology 7th Ed., p. 70

β₁ Receptors

Details
G-protein / 2nd messengerGs → ↑ adenylyl cyclase → ↑ cAMP → protein kinase A
Agonist potencyEpi > NE
Selective antagonistMetoprolol, atenolol
Site of distribution & function:
Organ / TissueEffect
Heart (SA node)↑ Heart rate (positive chronotropy)
Heart (ventricular muscle)↑ Contractility (positive inotropy)
Kidney (juxtaglomerular cells)↑ Renin secretion
Salivary glands↑ Secretion
Adipose tissueLipolysis

β₂ Receptors

Details
G-protein / 2nd messengerGs → ↑ adenylyl cyclase → ↑ cAMP
Agonist potencyEpi >> NE
Selective agonist / antagonistTerbutaline / Butoxamine
Site of distribution & function:
Organ / TissueEffect
BronchiolesBronchodilation (clinical use in asthma)
Vascular smooth muscle (skeletal muscle)Vasodilation
GI tract wallRelaxation (↓ motility)
Urinary bladder wallRelaxation
UterusRelaxation (tocolysis)
LiverGlycogenolysis → ↑ blood glucose
At physiologic concentrations, β receptors are more sensitive to catecholamines than α₁ receptors. High local NE concentrations (near synapses) are needed to activate α₁. — Costanzo Physiology 7th Ed., p. 70

β₃ Receptors

Details
G-protein / 2nd messengerGs → ↑ cAMP
Selective antagonistSR59230A
Organ / TissueEffect
Adipose tissue (brown fat)Lipolysis and thermogenesis
Bladder detrusorRelaxation

Summary Table (Costanzo / Medical Physiology)

ReceptorLocationSignalKey Effect
α₁Vascular SM, iris, GI sphincters, bladder neckIP₃ / ↑Ca²⁺Vasoconstriction, mydriasis
α₂Presynaptic terminals, GI wall↓ cAMPInhibit NE release (feedback)
β₁Heart, kidney, adipose↑ cAMP↑ HR, ↑ contractility, renin release
β₂Bronchioles, skeletal muscle vessels, GI wall↑ cAMPBronchodilation, vasodilation
β₃Adipose (brown fat), bladder↑ cAMPLipolysis, thermogenesis

3. Tests of SNS and PNS Function

Test for SNS — Cold Pressor Test

Procedure: The subject immerses one hand in ice-cold water for 1–5 minutes.
Normal response:
  • Systolic BP rises by 15–20 mmHg
  • Diastolic BP rises by 10–15 mmHg
Mechanism: Cold activates cutaneous pain fibers → CNS → sympathetic efferent outflow → vasoconstriction → ↑ BP.
Interpretation: A reduced or absent response indicates a lesion in the sympathetic efferent arc. If combined with a normal Valsalva response, this localizes the lesion to the baroreceptors or their afferent nerves (seen in diabetic neuropathy and tabes dorsalis).
— Adams & Victor's Principles of Neurology, 12th Ed., p. 551

Test for PNS — Valsalva Maneuver (Heart Rate Response)

Procedure: The subject forcibly exhales against a closed glottis for ~10–15 seconds (strain phase), then releases.
Normal response:
  • Strain phase: ↑ intrathoracic pressure → ↓ venous return → ↓ cardiac output → ↓ BP → baroreceptors trigger ↑ sympathetic + ↓ parasympathetic → tachycardia
  • Release phase: Venous return rebounds → ↑ BP → baroreceptors trigger ↑ vagal (PNS) tone → reflex bradycardia (overshoot)
Valsalva Ratio = Maximum HR during strain ÷ Minimum HR within 30 s after release
  • Normal: ≥ 1.4
  • Tests vagal (parasympathetic) efferent limb via the cardiac vagus nerve
— Adams & Victor's Principles of Neurology, 12th Ed., p. 551; Costanzo Physiology 7th Ed., p. 172

Sources:
  • Costanzo Physiology, 7th Edition — pp. 69–70
  • Medical Physiology (Boron & Boulpaep) — p. 512
  • Adams & Victor's Principles of Neurology, 12th Ed. — p. 551
  • Guyton & Hall Textbook of Medical Physiology — Ch. 18
This is a shared conversation. Sign in to Orris to start your own chat.