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Physiology > General Physio > Flashcards

General Physio Flashcards

1
Q

Negative feedback

A

Controller with a programmed set-point value & effectors–>adjust regulated variable to the set point.

Ex. Thermoreceptors & Shivering, Glucose & Beta cells for insulin

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2
Q

Body fluid compartments

A

ICF-30 L

ECF- Interstitial fluid (bathes cells/NO proteins) = 12L & Plasma (contains proteins) = 3L.

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3
Q

Downhill Transport (high to low concentrations)

A
  • Goes with the conc. gradient
  • Simple diffusion (Channels)- Water passes rapidly through channels
  • Facilitated diffusion (carrier molecule) another molecule moves in with Na+ Glut transport. EX. D & L glut transporter
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4
Q

Uphill transport (low to high concentrations)

A

Use energy to move ions against conc. gradient.

  • Primary=Na+K+ pump (digitalis stalls pump @ E2)
  • Secondary=Uses ATP indirectly due to Na+K+ pump which maintains gradient for the transport of ions with Na+. Ex. SGLT (antiport, symport)
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5
Q

Edema

A
  • Imbalance of filtration & absorption

- Capillary filtration (out) exceeds capillary absorption (in)

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6
Q

Passive Electrical Properties of a Membrane

A
  • Resistance is reciprocal of conductance & capacitance

- Conductance-depends on the amount of channels on a membrane and measures the ease of ions flowing across membrane.

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7
Q

What promotes K+ entry into muscle?

A

Insulin & beta adrenergic catecholemines

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8
Q

What promotes K+ excretion @ Nephron?

A

Aldosterone & Angio II

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9
Q

AP at a Neuron

A
  1. Dendrites receive synaptic input (ligand gated)
  2. Cell body integrates GRADED excitatory/inhibitory potentials
  3. IF threshold is reached AP starts @ Axon Hillock
  4. AP travels down Axon (myelinated)
  5. Release of NT @ presynaptic terminal
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10
Q

Threshold

A

The intersection of gNA & gK is threshold of AP.

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11
Q

Myelin sheaths

A

High resistance & Low conductance, which allows for NO energy to be lost and travel down the axon FASTER.

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12
Q

Auto immune disease that De-mylenates PNS

A

MS and is treated with Interferon Beta (slows progression)

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13
Q

Fast Chemical Synapses

A
  • Ligand gated ion channels (ionotropic)

- ex. Acetylcholine receptor (cholinergic/nicotinic)

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14
Q

CNS agonist/antagonist to AChR

A
  • Nicotine=agonist

- Curare competes with ACh=prevention of excitation of skeletal muscle.

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15
Q

Slow Chemical Synapses

A
  • ACh receptor has a G protein associated with it.
  • Slower due to cascade effect and NOT a direct channel to let ions in.
  • metatropic
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16
Q

What are 3 main categories of NT?

A
  1. Small molecule (ACh, AA, Purines)
  2. Peptides (3-36 AA in length-Substance P)
  3. Membrane soluble (Gases/NO & Lipids/Endocannabanoids)
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17
Q

Hemicholinium

A

Inhibits choline from re uptake into Presynaptic terminal through Na+ cotransport

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18
Q

Acetylcholinesterase

A

Enzyme produced @ cell body and it located in synaptic cleft. Degrades ACh to choline to be recycled

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19
Q

Peptide NTs

A

Start of as Pro-peptides & packaged into vesicles @ cell body (endorphins/substance P)

  • Contained in LARGE dense core
  • Carried down by Fast axonal transport
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20
Q

Synaptobrevin

A

SNARE protein that binds with Synataxin & SNAP-25(Membrane proteins)–>which allows for exocytosis

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21
Q

Synaptotagmin

A

located on vesicle and are triggered by Ca+2 to bind to cell membrane

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22
Q

Botulinum

A
  • Cleave snare proteins=inhibit exocytosis

- Motor neurons receive APs BUT no exocytosis (ACh) means NO chem. signal to contract= PARALYSIS

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23
Q

Tetanus

A
  • Similar to Botulinum in contraction and cleaving snare proteins.
  • This toxin targets inhibitory interneurons in Spinal cord.
  • GABA is not released=Hyper excitable motor neurons
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24
Q

Neuron in CNS

A
  • Excitatory=Glutamate
  • Inhibitory=GABA
  • Never reach threshold
  • FXN: Integration of many inputs
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25
Q

Motor endplate of Skeletal fiber

A
  • Always excitatory=ACh
  • Always reaches threshold=Muscle AP=Contraction
  • FXN- relay of single signal
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26
Q

Efferent & Afferent

A

Afferent=sensory commands back into CNS

Efferent=motor outgoing from CNS

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27
Q

Purkinje Cells

A
  • Found in cortex (gray matter) of cerebellum
  • Dendritic tree that receives synapses about movement/posture
  • They are inhibitory release GABA
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28
Q

Microgila

A

-Immune in CNS that scavenge damaged cells & protect against infection

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29
Q

Astrocytes

A
  • Contribute to BBB & CS fluid
  • Direct influence on quantity of NT released at presynaptic terminal (ATP)
  • Help with the re uptake of NT
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30
Q

Gray matter/White matter

A
  • Gray matter: Cell bodies, dendrites, & axon terminals

- White matter: tracts/commissures bundles of myelinated axons

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31
Q

Astrocytes & NTs

A
  • Astroglial cells release glutamine (precursor to glutamate)
  • EAAT (excitatory AA transporter) terminate glutamate action
  • VGLUT (vesicular glutamate transporter) load glutamate into vesicles to presynaptic IF these ATP dependent pumps stop glutamate remains in cleft.
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32
Q

Ependymal cells

A

-Line the ventricles of the brain and central canal of SC.

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33
Q

Stroke

A
  • Glutamate excitotoxicity –> ischemia
  • deprived O2 (hypoxia) = no ATP = transporters not working
  • Glutamate builds up in cleft = excess Ca+2 in post synapse = Activates proteases that lead to cell death (necrosis)
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34
Q

Broca’s area

A
  • Initiates speech
  • Located in frontal lobe
  • Connected to Wernicke’s through arcuate fasiculus
  • Damage = expressive aphasia (can understand when spoken to NOT when speaking)
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35
Q

Wernicke’s area

A
  • Understanding spoken language
  • Located in temporal lobe
  • Connected to Broca’s per arcuate fasiculus
  • Damage = receptive aphasia (words make no sense)
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36
Q

Mechanoreceptors

A
  • Arterial baroreceptors in carotid detect changes in MAP

- Show negative feedback mech.

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37
Q

Dorsal root ganglion

A
  • part of afferent (sensory)
  • Detect touch, pain, temp., itch, proprioception.
  • Part of PNS
  • Gray matter
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38
Q

Stretch “myotatic” reflex

A
  • Monitors length of muscle
  • Monosynaptic = one synapse in CNS
  • AP travels into ventral horn (bypasses DRG)
  • AP @ pre-synaptic terminal (interneuron) in ventral horn releases NT glutamate
  • Glutamate = EPSP = AP at Efferent muscle endplate
  • ACh –>EPP –> Contraction
  • NO neurons from brain EXCEPT cerebellum
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39
Q

Stretch reflex “reciprocal coordination”

A
  • Antagonists NT is needed to relax flexors
  • While Glutamate is released = release of inhibitory NT Glycine or GABA
  • IPSP @ motor end plate = relaxed hamstring
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40
Q

Somatosensory Cortex:Parietal lobe

A
  • Fine touch, proprioception, vibration cross over @ the LVL of Medulla
  • Pain, temp., and coarse touch cross @ midline of Spinal cord
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41
Q

Parasympathetic

A
  • Cervical & Sacral region
  • Long Pre & Short Post
  • “Rest & digest”
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42
Q

Sympathetic

A
  • Thoraco & Lumbar region
  • Short Pre & Long Post
  • “Flight or fight”
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43
Q

Adrenergic receptors

A
  • Epinephrine & Norepinephrine from post ganglion
  • Sympathetic pathways
  • Alpha 1 & 2, Beta 1 & 2
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44
Q

Cholinergic Muscarinic receptors

A
  • ACh from post ganglion/pre
  • Parasympathetic pathways
  • Metabotropic = slow synapses
  • M1, M2, M3
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45
Q

Pregangilonic fibers

A
  • Both Sympathetic/Para use ACh –> Nicotinic receptor

- Antagonist for CNS nACh receptor = hexamethonium

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46
Q

Sweat Glands

A
  • Presynaptic ganglion = ACh/nicotinic
  • Postsynaptic ganglion = ACh which binds to Muscarinic receptors
  • Sympathetic cholinergic neurons
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47
Q

Chromaffin cells

A
  • Secreted by adrenal medulla
  • 80% epinephrine & 20% norepinephrine
  • directly into blood stream NO post ganglion
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48
Q

ANS receptors

A
  • Metatropic (slow response) due to GPCR
  • GPCR have 7 segments & 3 part transducer molecule (alpha, Beta, Gamma)
  • Alpha subunit binds to GDP = OFF/Binds to GTP = ON
49
Q

Exceptions to reciprocal innervation

A
  • Smooth muscle of blood vessels
  • Sweat glands
  • Both receive only sympathetic innervation
50
Q

Sympathetic innervation

A
  • Alpha 1 receptors on arterioles of smooth muscle bind to NE = contraction
  • Beta 2 receptors on arterioles of skeletal muscle bind to Epi = relaxation
  • Flight or Fight = More blood flow to muscles and conserving blood to organs EXCEPT liver which dilates for production of glucose = energy
51
Q

Reciprocal innv. of Iris

A
  • Parasympathetic = innv. circular muscle constricts = pupillary reflex
  • Atropine = antagonist of ACh/muscarinic receptors –>pupil remains open
  • Sympathetic stim = contracts radial muscles opens up pupil to see more.
52
Q

Inactivation enzymes

A
  • MAO (in mitochondria of varicosity) & COMT (cytoplasm of varicosity) = sympathetic
  • Acetylcholine esterase in synaptic cleft = parasympathetic
53
Q

Salivary glands

A
  • receive innv. from both symp & parasymp BOTH stimulate salvia secretion
  • Sympathetic = Beta 1
  • Parasympathetic = muscarinic
54
Q

ACh receptors (parasympathetic) @ the SA Node

A
  • Agonist = muscarine (increases K+ perm, hyper polarizes, slows heart)
  • Antagonist = atropine (blocks effect of ACh/muscarine = Speeds heart)
55
Q

Myofibrils

A
  • Thick myosin = Contractile
  • Thin myosin = Contractile
  • Tropomyosin & Troponin = regulatory filament
  • Titin & Nebulin = organizational proteins
56
Q

H Zone

A
  • Contains only thick filaments
  • Bisected by M line & anchor thick filaments
  • Shortens on contraction
57
Q

I Band

A
  • Contains only thin filaments
  • Bisected by Z disk & anchor thin filaments
  • Shortens on contraction
58
Q

Sacromere

A
  • Is the functional unit of the muscle
  • Is comprised from Z disk to Z disk
  • Several myofibrils make up sacromere
59
Q

A band

A
  • Is comprised of thick and thin filaments

- On contraction it does NOT shorten

60
Q

Titin & Nebulin

A
  • Titin: extends from M line to Z disk & gives the property of “spring back” to sacromere. Associated w/Thick filaments
  • Nebulin: extends from Z disk and runs along the length of the thin filament. Enhance optimal X-bridge action.
61
Q

Myosin & Actin

A
  • Myosin tails point towards M line & Heads point towards Z disc
  • Actin/thin filaments contain site of attachment troponin & tropomyosin covers the site.
  • They do NOT shorten during contraction
62
Q

Myosin characteristics

A
  • 6 chains (2 heavy head, hinge-neck, and tail & 4 light chains-2 on each neck)
  • Each head binds individually to actin
  • Head bound to ADP=attached to actin
  • Head bound to ATPase hydrolyzes energy for x-bridge and it continues with Ca present.
63
Q

Actin characteristics

A
  • Cytoplasmic Ca+2 binds to Troponin
  • Ca+2 shifts tropomyosin and exposes actin
  • 1 Tropomyosin = 7 G:actin monomers & 1 TN
64
Q

Calsequestrin

A

-Calcium ions bound to this protein intracellularly in the SR of skeletal muscle

65
Q

T tubule

A
  • AP conducted on surface of membrane travels down the tubule
  • Depolarization of tubule leads to Ca release from SR
  • DHPR (dihydropyridine receptor) voltage sensitive
  • RyR (ryanodine receptor) acts as the cap on SR - DHPR opens RyR = Ca+2 released
66
Q

Motor unit/s

A
  • Skeletal muscle have a very # of motor units
  • AP’s can recruit more motor units to cause a greater contraction
  • Fine motor control ex. Eye 1n-10 fibers
  • Coarse control ex. Leg 1n-100’s fibers
  • Motor units recruited from small–>large
67
Q

Isotonic

A
  • Change in length over time: Same tension
  • Muscle shortens-Twitch & tension stays constant.
  • Force muscle works against = after load
  • Light load=Fast X-bridging
  • Heavy load=Slow X-bridging
68
Q

Isometric

A
  • Change in tension over time: Same length
  • NO shortening: Muscle is held rigid
  • Elastic properties of muscle are in use ex. Titin
69
Q

Isotonic/Isometric

A
  • Combo of isotonic & isometric contractions produce skeletal muscle action
  • Muscle action does NOT always require “shortening”
70
Q

Metabolic pathways for ATP in skeletal muscle (Creatine)

A
  • Contraction requires hydrolysis of ATP
    1. Creatine phosphate transfers high energy phosphate off ADP. Produced in resting muscle from creatine + ATP. Yields Small amounts and short lived.
  • Good for fast energy
71
Q

Metabolic pathways for ATP in skeletal muscle (Anaerobic glycolysis)

A
  • No O2 required uses glucose or glycogen = Glucose
  • Produces ATP & Lactic acid
  • ATP produced is a bit more than creatine BUT still not effective in all out exertion.
  • Good for fast energy (reserves)
72
Q

Metabolic pathways for ATP in skeletal muscle (Aerobic catabolism)

A
  • Requires O2 + use of 3 classes of fuel (fat,carb,protein) ATP by oxidative phosphorylation (38 ATPs per glucose)
  • Moderate rate of production
  • Lower rate of production BUT higher quantity of energy produced.
73
Q

Slow Twitch Muscle

A
  • Myosin ATPase = hydrolyze ATP slower = fewer X bridges
  • Slow SERCA = Ca ions are slowly returned to SR
  • Contractions longer = 10x longer
  • Muscles that maintain posture & use oxidative phosphorylation
  • Red = MANY myoglobin (shuttle O2 into mitochondria) MANY mitochondria
  • Small diameter
74
Q

Fast Twitch Muscle

A
  • Develop tension quickly = fast glycolytic fibers
  • Tension and relax fast (sprinting/jumping)
  • Anaerobic glycolysis = Fast ATP (not efficient)
  • Have fewer mitochondria = fewer myoglobin
  • Fatigue faster - Better for speed
  • Large diameter
75
Q

Myostatin

A
  • Anti-growth protein, W/O it muscle grows excessively & fat deposition limited
  • Homozygous mutated gene = increase bulk
76
Q

Smooth, Skeletal, Cardiac similarities

A
  • Use X-bridges myosin attaching to actin

- Contraction occurs in all 3 due to cytoplasmic Ca+2

77
Q

Types of Smooth muscle (Tonic)

A
  • Tonic: Always maintain degree of contraction
  • w/o fatiguing using 25-30% X bridging.
  • Low metabolic rates (little O2) = hydrolyze ATP @ slower rate
78
Q

Types of Smooth muscle (Phasic)

A
  • Discrete contractions & relaxation
  • Produce peristalsis
  • Ex. Esophagus & bladder
79
Q

Smooth muscle Properties

A
  • Gap junctions = single unit contraction (intestinal tract & blood vessels)
  • Activity influenced by NT (ACh, Epi) @ post ganglionic
  • In addition: hormones, paracrines(local signals ex. NO), stretch = contraction
  • NO TN/TM mech
80
Q

Single unit

A

-Neuron varicosity = NT = Receptors on smooth muscle membrane = GAP JUNCTIONS spread action potential quickly

81
Q

Multi unit

A
  • Each cell is stimulated individually ex. Eye
  • Varicosities are spread through and within the smooth muscle
  • Allowed contraction to be conc. in different areas
82
Q

Sympathetic Tone

A

-Arterial diameter @ constant baseline contraction w/sympathetic activity
-Tone = Constant NE release from post ganglion
-

83
Q

Smooth muscle contraction

A
  • Actin attached to Dense bodies = cytoskeleton
  • 10-15 actin to 1 myosin head = increases probability to generate tension even when stretched.
  • Ca comes from extracellular & SR (reduced)
  • NO T tubules
84
Q

Calcium & Smooth muscle

A

-Extracellular Ca into smooth muscle (voltage gated, metatropic hormones/NTs) = SR releases more Ca (IP3) = Ca binds to calmodulin (like troponin inSM) = Myosin light chains = MLCK phosphorylation = energizes BEFORE power stroke = Tension

85
Q

Proteins on actin filament (smooth muscle)

A
  • Calponin & Caldesmon regulate contraction
  • Low intracellular Ca no myosin-actin interaction
  • High intracellular Ca = Calmodulin triggers RXN phosphorylates above proteins = x bridging
86
Q

Hormone/NT Ca+2 entry

A

-Hormone/NT on receptor G protein cascade = PLC (phospholipase) - PIP2 (4-5 bisphosphate) - IP3 - Release of intracellular Ca+2 from SR

87
Q

Relaxation of Smooth muscle

A
  • Ca+2 is pumped out (anti-port secondary) and into SR
  • Ca unbinds from CaM
  • MLC phosphatase (dephoso) MLC = Myosin head ATPase activity now decreased
  • Latch State where myosin stays attached tension maintained with NO ATP
88
Q

Properties of Cardiac muscle

A
  • Regulation by Ca influx by TN-TM
  • Uninucleate
  • APs spread through gap junctions @ intercalated discs
  • Heart fills sarcomeres reach optimal overlap
89
Q

Coordinated pumping

A
  • Mech. connections fascia adherens & desmosome = transmit force from cell cell
  • Gap junctions spread electrical APs
90
Q

Desmin

A
  • intermediate protein found in all muscle
  • in cardiac and skeletal forms scaffold around Z discs of adj. myofibrils
  • Anchor for myofibrils to nucleus/cytoskeleton
91
Q

Conducting system of the heart

A
  • SA node–>electrical activity spreads via gap junctions–>Spread is SLOW @ AV node–> Depol through septum/bundle branches–>back up to atrium from apex to base
  • Punkenje cells are LARGEST in heart = non contractile = few myofilaments (high amounts of glycogen, resistant to hypoxia)
92
Q

Contraction of Heart (ventricle)

A
  • Na in flux (0)
  • Na channels inactivate & K channels respond to depol = tiny repol (1)
  • Ca+2 influx increase balance outflow of K+ (2)
  • Ca channels SLOWLY inactivate & K+ continues to leave (3)
  • K+ at equilibrium RMP (4)
93
Q

Ca - Ca release

A
  • T-tubule (not voltage) Ca induced opening
  • RyR opens more Ca from SR
  • High intracellular Ca = Contraction
94
Q

SA node AP

A
  • Phase 0: Inward Ca+2 = upstroke (peak amplitude lower)
  • Phase 3: Outward K+ current = repolarization
  • Phase 4: K channels close, Funny channels open for Na slowly depolar cell
  • NO K+ leakage channels
  • NO phase 1 & 2
95
Q

Effects of sympathetic/Parasympathetic on Heart

A
  • Heart rate = Chronotropic
  • Conduction velocity @ AV node = Dromotropic
  • Contractility = Inotropic
  • Sympathetic = Beta 1
  • Parasympathetic = M2 (atria only)
96
Q

Effects of sympathetic/Parasympathetic on Heart (SA node)

A
  • (+) chronotropic up the influx of Na binding NE to Beta 1 coupled with adenyl cyclase via G proteins
  • Speeds K+ efflux @ phase 3 = faster repolarization = faster HR
  • (-) chronotropic: ACh binds @ M2 = inhibit adenyl cyclase lowers Na influx and increases out K+ = more negative potential
97
Q

Inotropic Reserve

A
  • Intercellular Ca+2 potential to bind to more TN = more cross bridging
  • beta 1 phosphorylation of phospholamben = Increases activity of SR pump = more CA
98
Q

Relaxation of Heart Tissue

A
  • Ca+2 ions unbind from TN
  • Ca+2 pumped into SR by SERCA
  • Ca+2 pumped in extra cellular by Ca pump or NCX (Na gradient maintained by Na/K pump)
99
Q

Length-Tension In Heart

A
  • Filling of ventricles stretches Myocytes = Tension (x-bridge) increases greatly w/Sacromere length
  • Ca binds to TN-C easily the long the length
100
Q

+ inotropic effect

A

-B1 adrenergic receptors (metatropic) = adenyl cyclase = Gprotein = cAMP triggers action of KINASE = phophorylation = DHPR Calcium channels (keep them open longer)

101
Q

Phospholamban

A
  • Increases rate of of Ca+2 pumping into SR
  • Shorter time Ca bound to TN = Increases rate of relaxation between beats (TN-I decreases binding to TN-C=relax)
  • Increases Ca stores in SR = More Ca for Ca induced contraction
102
Q

Treppe

A
  • Increased Ca entry into cytoplasm w/increased frequency of APs
  • Over time Ca builds up = Step wise increase in force of contraction over TIME
  • Phophorylation of DHPR by Kinase activity allows more Ca from SR
103
Q

Clot formation (coagulation)

A
  • Thrombus: Clot that plugs whole vessel

- Embolus: Unstable clot breaks off and gets lodged in vessel downstream

104
Q

Plasma proteins

A
  • Participate in blood clotting
  • Carriers of hormones, cholesterol, ions (Fe+2)
  • Signaling molecules (hormones), Extracellular enzymes (plasmin) or cytokines (thrombopoietin)
  • Source for many is the Liver
105
Q

What are platelets?

A
  • Cell fragments split off megakaryocytes
  • NO nuclei
  • Life span of 10 days
  • Wound exposes collagen = platelets contact w/it = ACTIVE = exocytosis (degranulation)
106
Q

Megakaryocytes

A
  • Thrombopoietin (TPO) regulates growth
  • Parent cell of platelets
  • TPO is a cytokine (glycoprotein) secreted by Liver
  • Polypoid = mitosis 7 times
107
Q

Hemostasis

A
  1. Vasoconstriction: triggered by paracrines released from endothelial cells
  2. Platelet plug: Adhesion due to Collagen, intregrins on platelet membrane allow stick. Cytokines = platelet aggregation
  3. Blood Coagulation: platelet–>plug = coagulation cascade triggered by tissue thromboplastin. Clot dissolved by PLASMIN
108
Q

Primary Hemostasis

A
  • Platelet mechanically plugs break in vessel
  • Positive feedback = exposed collagen activates platelets
  • Degranulation/exocytosis of platelet factors = platelet aggregation
109
Q

Degranulation

A
  • Intracellular granules
  • Serotonin: (Vasoconstriction = aggregation)
  • ADP: attracts MORE platelets to area = adhesion/aggregation
  • PAF: activates more platelets (+) feedback triggers production of thromboxane A2 (TXA2) vasoconstrictor, which comes from prostaglandin H2
110
Q

What does Aspirin inhibit?

A

-Enzymes involved in prostaglandin synthesis aka thromboxane syn.

111
Q

Secondary Hemostasis

A
  • Coagulation converts platelet plug into a clot
  • (+) feedback sustain cascade
  • In Cascade inactive plasme proteins converted to active forms
  • TF 3 works w/TF 7 + Ca/phosolipds = Active factor 10
112
Q

Thrombin contributes to?

A
  • Clot formation: Platelet formation & production of fibrin loops back to Factor 11 amplifies cascade = active factors 8/10
  • Down regulation: binds to TM cofactor to activate protein C
  • Clot Dissolution: Active protein C inhibits Factor 5/8 = anti coagulant
113
Q

Meningococcemia (bacterial infection)

A
  • Bacteria (Neisseria) lyses releases endotoxin = activation of factor 7 produces coagulation
  • Edema due to proteins leaking into ECS and fluid follows
  • Petichia thrombi that block vessels = small red/purple spots and can lead to perpura (large red spots)
  • TREAT with PROTEIN C targets factors 5/8
114
Q

What happens to blood sample when ADP is added?

A

-Platelets activation and formation of aggregates aka flakes form

115
Q

Adrengenic receptors affinity for NE/E

A
  • Alpha 1 = NE:activates phospholipase C
  • Alpha 2 = NE: Decreases cAMP
  • Beta 1 = NE & E: increases cAMP
  • Beta 2 = E: increases cAMP
  • Beta 3 = NE: Increases cAMP
116
Q

Chronotropic effect (Heat Rate)

A
  • Sympathetic: Beta 1-up-regulates influx of Na+ funny channels in SA
  • Parasympathetic: M2-down-regulates conductance of Na+ channels & upregulates K+ efflux = more (-) rmp
117
Q

Dromotropic effect (conduction velocity/AV)

A
  • Sympathetic: Beta 1-up-regulates influx of Ca+

- Parasympathetic: M2-down-regulates influx of Ca+ and upregulates K+ efflux = (-) rmp

118
Q

Inotropic effect (contractility)

A

Sympathetic: Beta 1-up-regulates Ca+ influx (phosphorylation of phosolamban)
-Parasympathetic: M2-down-regulates (atria) Ca+ influx & up regulates K+ efflux

Physiology (4 decks)

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