Review S2 Bsf Exam 1: Regulation Of Circulation

Front 1

Regulation of blood distribution and blood pressure is under what 2 types of control?

Back 1

Systemic control and local control

Front 2

Examples of systemic control of blood distribution/pressure are:

Back 2

Neuronal (central and peripheral nervous systems)
Hormonal (endocrine system)

Front 3

Examples of local control of blood distribution/pressure are:

Back 3

Locally produced humoral factors
Locally applied physical factors

Front 4

T/F

Local regulatory mechanisms can override systemic mechanisms, neural or hormonal.

Back 4

True!

Front 5

What are 3 intrinsic factors of peripheral circulation regulation?

Back 5

Autoregulation
Endothelium
Tissue metabolites

Front 6

What are 2 extrinsic factors of peripheral circulation regulation?

Back 6

Neural control, primarily sympathetic
Humoral, via circulating catecholamines

Front 7

Local blood flow is regulated primarily by _________

How does VSMC (vascular smooth muscle cells) adjust blood flow?

Back 7

tissue oxygen levels

when oxygen levels drop, resistance increases (vascular smooth muscle contraction) to decrease flow & increase perfusion (increase O2)

Front 8

Increased metabolic activity in an organ leads to (increased/decreased) vascular resistance & (increased/decreased) blood flow

What is this called?

Back 8

decreased resistance
increased flow


active hyperemia

Front 9

A brief period of ischemia lead to a quick (increase/decrease) in flow, then a return to normal.

What is this called

Back 9

increase in flow
(tissue anaerobic metabolites regulate increase)


reactive hyperemia

Front 10

List local vasodilators
(vasodilators, decrease resistance)

Back 10

andenosine
histamine
prostacyclin
Low O2, high CO, H (poor perfusion)
High K (increased osmolality)

Front 11

What is the name of the local factors that endothelial cells can synthesize and secrete in regulation of blood flow?

Back 11

Endothelium-derived vasoactive substances

Front 12

Local vasodilators (decrease/increase) vascular tone under normal conditions, and local vasoconstrictors (decrease/increase) vascular tone.

Back 12

Decrease, increase

Front 13

What do endothelium-derived vasoactive substances act on?

Back 13

Specific receptors or ion channels

Front 14

What does flow-induced vasodilation require?

Back 14

An intact epithelial lining

Front 15

Is endothelium-derived relaxing factor (EDRF) or nitric oxide (NO) an endothelium-derived vasoconstrictor or vasodilator?

Back 15

Vasodilator

Front 16

Is prostacyclin (PGl2) an endothelium-derived vasoconstrictor or vasodilator?

Back 16

Vasodilator

Front 17

Is endothelin (ET) an endothelium-derived vasoconstrictor or vasodilator?

Back 17

Vasoconstrictor

Front 18

Are EDCF1 and EDCF2 endothelium-derived vasoconstrictors or vasodilators?

Back 18

Vasoconstrictors (endothelin derived constricting factor-1 and 2)

Front 19

T/F

NO contributes to direct vasodilation.

Back 19

True!

(flow dependent and receptor mediated)

Front 20

How does NO contribute to indirect vasodilation?

Back 20

By inhibiting vasoconstrictor influences.
It inhibits angiotensin II and sympathetic vasoconstriction.

Front 21

What is the anti-thrombotic effect of NO?

Back 21

It inhibits platelet adhesion to the vascular endothelium.

Front 22

What is the anti-inflammatory effect of NO?

Back 22

It inhibits leukocyte adhesion to vascular endothelium and scavenges superoxide anion.

Front 23

What is the anti-proliferative effect of NO?

Back 23

It inhibits smooth muscle hyperplasia.

Front 24

A decrease/lack of NO may result in what 4 things?

Back 24

Vasoconstriction (e.g., coronary vasospasm, elevated systemic vascular resistance, hypertension)

Thrombosis (due to platelet aggregation and adhesion to vascular endothelium)

Inflammation (due to upregulation of leukocyte and endothelial adhesion molecules)

Vascular hypertrophy and stenosis

Front 25

What is NO produced from?

With what enzyme?

Back 25

L-arginine, via nitric oxide synthase (NOS).

Front 26

Which endothelial form of NOS is Ca2+ dependent and is always produced?

Back 26

Constitutive NOS (cNOS; type III)

Front 27

Which endothelial form of NOS is Ca2+ independent and is present during times of inflammation (induced by bacterial endotoxins and cytokines)?

Back 27

Inducible NOS (iNOS; type II)

Front 28

T/F

NO is a stable molecule and has a relatively long half-life.

Back 28

False!

NO is a very unstable molecule (gas), so it's short lived.

Front 29

What is the general mechanism of action of NO?

Back 29

NO diffuses into the smooth muscle cells, activates soluble cGMP, and causes smooth muscle relaxation

Front 30

How does cGMP (activated by NO) decrease intracellular Ca2+ concentrations?

Back 30

Increased intracellular cGMP inhibits calcium entry into the cell.

Front 31

How does cGMP (activated by NO) lead to hyperpolarization and relaxation?

Back 31

By activating K+ channels.

Front 32

How does cGMP (activated by NO) activate myosin light chain phosphatase?

Back 32

By stimulating a cGMP-dependent protein kinase that activates it.

Front 33

Acetylcholine, bradykinin, substance-P
,↑K+, histamine, adenosine, and ↑H+(acidosis) all stimulate what?

Back 33

NO release

Front 34

The range of systemic arterial pressures between ~70-180 mmHg (depending on the organ) is called what?

Back 34

Autoregulatory range


(outside this range autoregulation doesn't work)

Front 35

a) What results when there is a change in perfusion pressure, at constant levels of tissue metabolism?

b) What type of intrinsic factor is this?

Back 35

a) An alteration of vascular resistance to maintain constant blood flow.

b) Autoregulation

Front 36

What would happen to blood flow in response to a sudden drop of perfusion pressure,
w autotregulation?

w/o autoregulation?

Back 36

autoregulation- blood flow would decrease & then return to normal w/i few min

no autoregulation- blood flow would decrease but would not readjust to normal

Front 37

(Local) Peripheral blood flow is controlled mainly by the (parasympathetic/sympathetic) system

Back 37

sympathetic

(via control of vessel (arteries, arterioles, & veins) resistance- contraction/dilation)

Front 38

Capacitance vessels (veins) are (less/more) responsive to sympathetic stimulation and (less/more) responsive to vasodilator metabolites.

Back 38

More, less

Front 39

Approximately how much of the blood in the body can be mobilized in response to stimulation of sympathetic nerves?

Back 39

Approximately 1/3

Front 40

When does sympathetic stimulation constrict veins and augment the cardiac filling?

Back 40

In exercise

Front 41

What are the 5 parts to the (systemic) vascular neural reflexes?

Back 41

1.Receptors/sensors (baroreceptor & chemoreceptor)
2. Afferent pathway (toward the CNS)
3. Coordinating center (in CNS (medulla))
4. Efferent pathway (away from the CNS)
5. Effectors (smooth muscle cells, pace maker cells) that act on control variable to correct the situation (e.g., Increase/decrease blood pressure, increase/decrease heart rate)

Front 42

Arterial baroreceptors are mechanoreceptors, detecting what?

Are they low or high pressure?

Back 42

Stretch receptors


High pressure receptors (large systemic arteries)
^(detect high BP via increased stretch--> decrease HR in response)

Front 43

What are the 2 afferent pathways of arterial baroreceptors? (where do they come from and what nerves do they travel)

Back 43

Carotid sinus → glossopharyngeal nerve → CNS

Aortic arch → vagus nerve → CNS

Front 44

What is the baroreceptor-mediated rapid response to an increase in BP?

Back 44

↑Blood pressure → Inhibit activity of the vasoconstrictor center in the medulla →

Effect: ↓BP and ↓ HR

(decrease BP does opposite)

Front 45

What is the baroreceptor-mediated long-term response to an increase in BP?

Back 45

↑BP → ↓ release of angiotensin II, aldosterone, and ADH →

Effect: ↓plasma volume

(decrease in BP has opp effect)

Front 46

___________ is responsible for maintaining MAP

Back 46

baroreceptor

Front 47

T/F

Arterial baroreceptors are activated by a decrease in systemic blood pressure.

Back 47

False!

Arterial baroreceptors are activated by an INCREASE in systemic blood pressure.

Front 48

Activation of baroreceptors (decreases/increases) heart rate and (decreases/increases) blood pressure.

Back 48

Decreases, decreases

Front 49

Is vascular tone a slow or fast response to a fall in arterial pressure?

Back 49

Fast response

Front 50

Which hormones regulate vasoconstriction in response to a fall in arterial pressure?

Back 50

Catecholamines: Epi, Norepi
alpha1, alpha2

Vasopressin (ADH) - mediated via V1A receptor in the vascular smooth muscle

Angiotensin II - mediated via AT1 receptor in the vascular smooth muscle

Front 51

Which hormone regulates vasodilation in response to a fall in arterial pressure?

Back 51

Catecholamines: Epi, Norepi
beta2 - vasodilation

Front 52

What hormones cause an increase in plasma volume in response to a fall in arterial pressure? And how do they do this?

Back 52

Vasopressin (ADH)
V2 receptor: water reabsorption in the kidney (↑plasma volume)

Angiotensin II
Renin-angiotensin-aldosterone system: (↑plasma volume via aldosterone effect)

Front 53

Are cardiopulmonary baroreceptors low or high pressure stretch receptors?

Back 53

Low pressure stretch receptors

Front 54

Where are cardiopulmonary baroreceptors located?

Back 54

In the vena cava, right atrium, right ventricle, and pulmonary vessels (“right heart”).

Front 55

Which receptors' activity depends on pressure in the pulmonary circuit?

Back 55

Cardiopulmonary baroreceptors

Front 56

Activation of the cardiopulmonary receptors causes (vasoconstriction/vasodilation), (decreases/increases) plasma volume and (decreases/increases) blood pressure.

Back 56

Vasodilation
decreases plasma volume
decreases BP

(depressor effect)

Front 57

What is the role of ANP (released from atria) in cardiopulmonary reflex?

Back 57

*directly vasodilates--> decreasing BP
*decreases renin--> decreases Ang II & Aldosterone
--> natriuresis (water loss/diuretic)--> decrease blood volume--> decreases BP

Front 58

SV= EDV-ESV

How is EDV controlled?

Back 58

local sympathetics-->increased peripheral vascular resistance--> increased venous return--> increased EDV

Increased EDV--> increases SV--> increases CO

Front 59

SV= EDV-ESV

How is ESV controlled?

Back 59

systemic sympathetics---> increase HR & contractility--> decrease ESV

decreased ESV--> increased SV--> increased CO

Front 60

Increased CO (increases/decreases) BP

Back 60

increases BP

(increased peripheral resistance also directly increases BP)

Front 61

What is the MOST IMPORTANT factor in maintaining BP & CO?

Back 61

blood volume!