PREPARATION FOR EXAM II (NOV 10, 1999)

PROBLEM ASSIGNMENT: Acetylchloline (and some other agonists) have been shown to cause relaxation of arterial segments in vitro (ie, relaxation of the smooth muscle in a bath). However, this effect disappears if the inner, endothelial cell layer of the vessel is first scraped away. Explain.

CHANGES TO READING:

Chapter 10: Omit 363-366; 381-394

Chapter 12: Omit 480-485

READ THE FOLLOWING SECTIONS (not covered in class):

"Diving" (pp 513-514)

"Mammalian fetus" (pp 487)

"Control of the Microcirculation" (pp 510-512)

REVIEW OUTLINE FOR EXAM II

A. NEURON-NEURON SYNAPSES

1. Spatial and temporal summation

2. EPSPs and IPSP (depolarizing vs hyperpolarizing post-synaptic potentials)

3. Synaptic Inhibition

a. post-synaptic inhibition

b.pre-synaptic inhibition (modulation of calcium channels)

(see also parasympathetic pre-synaptic inhibition of cardiac pacemaker cells)

B. MUSCLE PHYSIOLOGY (esp Skeletal muscle)

1. Control of whole muscle tension

a. recruitment of motor units

b.frequency summation/tetanus

c. Series elastic element

2. Internal Organization

a. fibers-myofibrils-myofilaments

b. sarcomeres

c. banding pattern: A band, I band, Z line, H zone

d. Changes in banding patterns with shortening

3. Sarcomere Organization

a. Thick and thin filaments

b. cross bridge attachments

c. length tension relationship (as related to cross bridge overlap)

4. Filament structure

a. Thin filaments

1. G actin polymerization

2. troponin (Ca++ binding) and tropomyosin

b. Thick filament

1. Myosin polymers (tail to tail)

2. myosin as a "molecular motor"

3. "head groups" = cross bridges (ATPase and actin binding properties)

5. Cross Bridge Cycle

a. changes in ATP binding, ATP hydrolysis, product release (ADP and Pi)

b. changes in actin affinity

c. changes in myosin head energy state/position

d. role of actin in accelerating myosin ATPase activity

6.Excitation-contraction coupling

a. role of t-tubules in transmitting APs

b. role of sarcoplasmic reticulum as calcium storage site

c. dihydropyridine/ryanodine receptor complex--couples AP to SR calcium channels

d. Troponin/tropomyosin block of actin binding sites

e. role of SR Ca++-ATPase in muscle relaxation

7.Muscle types

a. properties of cardiac muscle and smooth muscle compared to skeletal

1.myogenic vs motorneurons

2.innervation

3.contraction speed

4. E-C coupling

b.Twitch subtypes

1. slow oxidative

2. fast oxidative

3. fast glycolytic

C. CIRCULATORY SYSTEMS

1.General

a. Characteristics of open vs closed circulatory systems

b. respiratory and systemic circuits

1.. dual-in-line (eg, teleost fish)

2.dual-parallel (eg, mammal): requires division of heart into left/right sides

2. Components of closed systems

a. heart-pump

b. large arteries (high elasticity/pressure storage)

c. arterioles (thick smooth muscle-regulation of flow and resistance-sympathetic innervation)

d. capillaries : single cell layer-exchange site

e. veins: high compliance/volume storage

f. lymphatics: one way system for returning interstitial fluid to vascular compartment

3. Mammalian heart (4 chambers)

a. pattern of flow (ins and outs) major blood vessels associated with each chamber

b.valves (orientation and function)

c. cardiac cycle (atrial-ventricular systole/diastole)- pressure changes

4. Electrical Activity in the Heart

a.. spontaneous APs (autorhythmicity)

b. electrical coupling via gap junctions

c. autonomic NS innervation (SA node and ventricular contractile cells

d. conduction system:

1. SA node: pacemaker (fastest inherent rhythm)

2. AV node: conduction point between atria and ventricles/ delay or pause

3. bundles of His/Purkinje fibers: high speed conduction through ventricular muscle mass- synchonization

e. Cardiac cell APs

1. SA node cell: ramp or unstable baseline due to closing of K+ channels

2. Calcium channels extend length of AP

3. sympathetic and parasympathetic activity affects slope of pacemaker potential

4. ventricular cell: exaggerated Ca plateau (E-C coupling and extends refractory period

f. Electrocardiogram

1. P, QRS and T waves

2. PQ interval

5. Cardiac cycle diagram

a. correlate pressures (atrial, ventricular aortic), ventricular volume changes, and ECG

b. points where pressures intersect: valves open and close (heart sounds)

c. volume changes: filling, isovolumetric phase, ejection

d. end diastolic volume

6. Cardiac Performance

a. Cardiac output = stroke volume X heart rate

b. regulate HR (sympathetic and parasympathetic NS)

c. Regulate stroke volume:

1. sympathetic innervation of ventricular cells (contractility/positive ionotropy)

2. Frank-Starling relationship (length tension)

3. changes in venous return (eg gravity) cause change in end diastolic vol

4. adjustment to gravity (inc venous return): skeletal muscle "pumps", sympathetic venoconstriction

7. Hemodynamics

a. Poiseuille's eq.: Q = P/R where P is mean arterial press and R = total peripheral resistance

b. control of blood flow to tissues --central

1. sympathetic neurons--alpha receptors for norepinephrine mediate vasoconstriction

2. beta receptors for einephrine mediate vasodilation (relaxation)

(but higher doses can cause "spillover" onto alpha receptors--overall vasoconstriction

3. parasympathetic innervation to some blood vessels-vasodilation

4. renin-angiotensin (sympathetic activity on JG cells of kidney--renin release--production of active angiotensin--vasoconstriction

c. Control of blood flow to tissues--local

1. myogenic effect (stretch reflex of smooth muscle

2. active hyperemia--vasodilation in response to elevated tissue metabolism

3. tissue damage inflammation--histamine mediates vasodilation

d. Regulation of arterial blood pressure ( P = Q x R)

1. sensors: baroreceptors (aortic and carotid a) and volume sensors (rt atrium)

2.cardiovascular control center

3. output via sympathetic/parasympathetic flows; hormones

4. effectors: SA node, cardiac contractile cells, smooth muscle of arterioles (regulate resistance), JG cells of kidney (angiotensin)

e. examples (all bidirectional):

1. Baroreceptor reflex: inc BP--stretch of baroreceptors, inc firing rate, dec sympathetic

activity-dec HR, dec SV, dec C.O., dec R, all dec blood pressure

2. Volume receptor reflex: inc blood volume-right atrium stretch:

a. hypothalamus--decrease release of ADH

b. right atrium-release of ANF-inc Na+/H2O excretion

3. Hemorrhage:

a. decreased BP-dec baroreceptor firing-increased sympathetic activity

(reverse of baroreceptor reflex, above)

inc HR, SV, CO, vasoconstriction, inc R, etc

b. renin release-angiotensin-vasoconstriction

c. angiotensin also stimulates release of aldosterone-inc Na+ reabsorption by kidney

d. decreased volume-atrial vol receptors (dec stretch):

increased ADH release

decreased ANF release

increased water recovery (decreased excretion)

f. Microcirculation and capillary dynamics

1. general: size of capillaries, single cell layer, sites of exchange

2. types of transport across capillaries: simple diffusion, across pores (paracellular), transcytosis, bulk flow across pores

3. bulk flow as mechanism for turnover of interstitial fluid

a.blood pressure creates net filtration force

b. colloid osmotic press creates net reabsorption force

c. capillaries vary in Kf or permeability

d. net fluid loss or gain in capillary depends on balance of forces

e. lymphatics vessels take up excess filtered fluid and recycle to blood

f. changes in one force or another upsets balance