Local and Systemic Control Flashcards by Danielle Hayes

What is ohm’s law?

Q(flow)= pressure differences/ resistance

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Blood flows when pressure exceeds (blank)

resistance

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Flow =(blank)/resistance

MAP

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(blank) can be changed by changing resistance of the vasculature or the pressure gradient in the circulation.

Blood flow

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What is poiseuille’s law?

R =8nl/pir4
n=blood viscosity
l=blood vessel length
r=radius of the vessel

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Blood flow is directly related to the pressure and the (blank)

4th power of the radius

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blood flow is (blank) related to the length of the vessel segment and viscosity of the blood.

inversely

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Changing the (blank) of a vessel will change the resistance of this vessel the most.

radius

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What are the regulatory mechanisms of peripheral circulation?

adjustment of pump output
changes in diameter of resistance vessels
Alteration in capacitance of vessels (veins)
changes in extracellular fluid volume

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What is the dual control of the peripheral circulation?

Local (intrinsic) mechanisms

Systemic (extrinsic) mechanisms

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The peripheral circulation is under dual control: centrally through the (blank), and locally by the conditions in the (blank) of the blood vessels.

nervous system

immediate vicinity

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In some areas of the body, such as the skin and splanchnic regions, (blank) predominates, whereas in others, such as the heart and brain, this mechanism plays only a minor role.

neural regulation of blood flow

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What are the two types of local (intrinsic) mechanisms?

metabolic and myogenic

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What are the two types of metabolic local (intrinsic) mechanisms?

release of vasodilators, nutrient deficiency for vascular smooth muscle

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What are the two types of myogenic local (intrinsic) mechanisms?

sudden stretch and reduced stretch

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What do local (intrinsic) mechanisms effect?

Pressure flow autoregulation
Active hyperemia
Reactive hyperemia

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Can vascular smooth muscle maintain basal tone when there is nutrient deficiency?

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(blank) is constant flow under varying pressures

autoregulation

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(blank) of blood flow is the acute return of the flow back to normal shortly after the arterial pressure changes from normal.

Autoregulation

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The myogenic theory of autoregulation invokes a role for (blank) as the controlled variable in the vasculature.

arteriolar wall tension

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Sudden stretch of small blood vessels will cause the smooth muscle of the vessel wall to (blank) (possible mechanism – activation of stretch-activated cation channels that are permeable for Ca2+)

contract

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The vascular smooth muscle contracts in response to an (blank) across the wall of a blood vessel. The resulting vasoconstriction will maintain a . (Without vasoconstriction, blood flow would increase as a result of the increased pressure).

increase in pressure difference

constant flow

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(blank) is the maintenance of a constant blood flow in the presence of a change in arterial pressure

autoregulation

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The changes in blood flow in response to overall homeostasis (e.g., the dilation of coronary arteries when the energy requirements of the heart increase during exercise) are not classified as (blank)

autoregulatory processes.

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Blood flow is trying to be constant so (blank) is altered to maintain this

resistance

Autoregulation is only when you have (blank) , you do not utilize autoregulation when stressed via exercise (this is increased output, NOT changes in pressure)

increased or decreased pressure

Do you utilize autoregulation when stressed via exercise (increased output, not changes in pressure)?

(blank) cannot be maintained at extreme changes in mean arterial pressure.

Autoregulation

The safe range for blood flow is about 80-125% of normal and usually occurs at arterial pressure of (blank) due to active adjustments of vascular resistance.

60-160 mm Hg

(blank) is increased blood flow caused by increased tissue activity

ACTIVE HYPEREMIA

(blank) is blood flow above control level upon release of an arterial occlusion

REACTIVE HYPEREMIA

When would you have active hyperemia?

exercise

When would you have reactive hyperemia?

skeletal muscle contracts and compresses blood vessel, when contraction of skeletal muscle ends the blood is free to move through the vessel

Why do you want vasoconstriction in pressure flow autoregulation when you have high blood pressure?

Since you are sensing an increased difference in pressure than you need to increase resistance proportionally to maintain flow

WHat two things cause release of vasodilator substances?

deficiency of 02 and increased metabolism

Deficiency of 02 and nutrients in the vascular smooth muscle inhibits the ability of what?

muscle to contract

These are potential candidates for (blank) * (increase) CO2 * lactic acid * (decrease) pH * K+ * PO4 * PgI2 * adenosine * ATP * (decreased) O2 * increased osmolarity

vasodilator metabolites

Large amounts of (blank) can cause vasoconstriction. Small amounts of (blank) can cause vasodilation.

Potassium

What does adensosin do and when is it released?

it is a vasodilator and it s released under hypoxia

What are EDRF? DO they have receptors?

relaxation factors secreted by endothelium | They each have their own receptors on endothelial cells

Endothelial cells can sense (blank) which will induced them to release (blank)

stress | relaxation factors

There is a (blank) between endothelium and adjacent smooth muscle cells.

functional interaction

Endotoxin cytoking, L-arg, shearing forces, acetycholine, bradykinin substance P insulin, NOS can induce what to be made?

NO (citrulline too)

What does NO do?

it creates cGMP to cause relaxation

Endothelium lines arterioles (and virtually all blood | vessels). So it experiences the (blank) associated with flow.

shear stress

Where does autoregulation take place?

liver, brain and kidney

With increased (blank) endothelium releases factors, in particular EDRF

flow (and increased shear stress)

EDRF (=NO) activates (blank), which increases cGMP increases sequestering of intracellular Ca2+, less calcium means less contraction

Increased blood flow allows for release of factors from vessel endothelium which results in dilation and (blank) velocity through vessel.

decreased

What are the two systemic (extrinsic) mechanisms?

Humoral (hormonal) and Neural

What are the systemic (extrinsic) mechanisms of humoral function?

``` Adrenal medullary hormones RAAS Endothelins Kinins Natriuretic peptides ```

What are the systemic (extrinsic) mechanisms of neural function?

Sympathetic (heart and blood vessels) | Parasympathetic (heart >> blood vessels)

Stimulation of the nerves to the adrenal glands | causes release of both (blank) and (blank) in the systemic circulation.

epinephrine (80 %) and | norepinephrine (20 %)

What do Alpha 1 receptors do?

-Vasoconstriction -Increased peripheral resistance -Increased blood pressure

What do Beta 1 receptors do?

-Tachycardia -Increased myocardial contractility

What do Alpha 2 receptors do?

-Inhibition of NE release -Vasoconstriction (veins>arteries)

What do Beta 2 receptors do?

-Vasodilatation -Slightly decreased peripheral resistance

What is the most common way catecholamines cause vasoconstriction?

alpha 1 activation

What are present at presynaptic junctional receptors that regulate release of norepinephrine

Alpha 2 activation

(blank) adrenal medullar hormones effect all receptors but mostly the betas

epinephrine

(blank) affects only A1, A2 and B1

norepinephrine

(blank) affects only B1 and B2

isoproterenol

``` What causes this: INCREASED Heart rate Increase Stroke volume Increase Cardiac contractility Decrease Venous capacitance Increase coronary flow Increase muscle flow Decrease kidney flow Increase splachnic flow ```

Epinephrine

``` What causes this: DECREASED Heart rate (vagal) Increase Stroke volume Increase Cardiac contractility Decrease Venous capacitance Increase coronary flow Decrease muscle flow Decrease kidney flow Increase splachnic flow ```

Norepinephrine

What causes this: - Vasoconstriction (veins > arteries) - Effect on blood pressure consists of initial depressor response (release of PgI2) followed by sustained increase in blood pressure due to vasoconstriction. - Positive inotropic and chronotropic effect. - Increase plasma levels of ANP, renin, aldosterone, and catecholamines. - Increase release of sympathetic transmission. - Produce bronchoconstriction. - Decrease glomerular filtration rate, renal blood flow, increases Na+ reabsorption.

Endothelins

What is released form endothelial cells and causes vasoconstriction

endothelins

Explain the renin-angiotensin-aldosterone system?

Angiotensin is produced from liver->coverts to angiotensin I-> epithelial cells of lungs produced angiotensin II->ADH (brain) + aldosterone (kidney)-> vasoconstriction + increased water absorbtion (Na and H20)

Explain the Kinin pathway? | What does it do?

active factor XII + plasmin->plasma kallikrein + kininogens-> bradykinin and lyslbradykinin vasodilation

If you block ACE or Kinanase II you will cause (blank).

vasodilation

(blank) is a 28-amino acid peptide that is synthesized, stored, and released by atrial myocytes in response to atrial distension, ANG II stimulation, endothelin and sympathetic stimulation (b-adrenoceptor-mediated).

Atrial natriuretic peptide (ANP)

Elevated levels of ANP and BNP are typically found during (blank)

hypervolemic states (elevated blood volume) and congestive heart failure.

Will you find CNP in the heart? Will you find ANP or BNP in the heart?

No, | Yes

What serves as a counter-regulatory system for the RAAS?

natriuretic peptides

What causes vasodilation and renal effects that lead to natruiresis and diuresis?

natriuretic peptides

(blank) directly dilate veins and thereby decrease central venous pressure, which reduces cardiac output by decreasing ventricular preload.

Natriuretic peptides

(blank) also dilate arteries, which decreases systemic vascular resistance and systemic arterial pressure. Vasodilatation is achieved by the increased cGMP levels (but by a different mechanisms of NO).

natriuretic peptides

(blank) affect kidneys by increasing glomerular filtration rate (GFR) and filtration fraction, which produces natriuresis (increased sodium excretion) and diuresis (increased fluid excretion).

natriuretic peptides

A second renal action of (blank) is that they decrease renin release, thereby decreasing circulating levels of angiotensin II and aldosteron. This leads to further natriuresis and diuresis (water and sodium loss). Decreased ANGII also contributes to systemic vasodilatation and decreased systemic vascular resistance.

Natriuretic peptides

What are the two main action of natriuretic peptides?

Vasodilatation | Renal effects that lead to natriuresis and diuresis

What are the 5 main effects of natriuretic peptides?

``` Decreased blood volume Decreased arterial pressure Decreased central venous pressure Decreased pulmonary capillary wedge pressure Decreased cardiac output ```

What doesnt have B2 receptors?

skin and mucosa cerebral salivary glands veins (systemic)

What are the two feedback loops?

autonomic feedback loop and hormonal feeback loop

the (blank) directly influences the four major variables, peripheral vascular resistance, heart rate, contractile force of the heart, and venous tone.

sympathetic autonomic nervous system

The (blank) directly influences heart rate.

vagus

(blank) directly increases peripheral vascular resistance.

Angiotensin II

an increase in (blank) causes an increase in renal blood flow; an increase in renal blood flow causes a decrease in renin release; an increase in plasma renin causes an increase in angiotensin production, etc.

mean arterial pressure

Circulatory homeostasis for the whole organism is met by a balance between (blank)

metabolic, hormonal and neural influences.

What are the extrinsic factors that effect arterioles?

neural and hormonal

What are the intrinsic factors that effect arterioles?

tissue metabolits local hormones myogenic endothelial factors

There is no (blank) in smooth muscle; instead, Ca2+ regulates myosin on the thick filaments.

troponin

(blank) plays a central role in the excitation-contraction coupling in vascular smooth muscle cell.

Calcium

the (blank) is responsible for the control of total peripheral resistance, arterial and venous tone, and the distribution of blood flow throughout the body.

The Vascular Smooth Muscle

How do you excited vascular smooth muscle and elicit contraction?

Ca++ + calmodulin activates MLCK, which phosphorylates myosin LC20, resulting in cross-bridge cycling.

Vascular smooth muscle lacks (blank) in contrast to skeletal muscle. Ca2+ plays a central role on excitation-contraction coupling in vascular smooth muscle.

troponin and fast sodium channels

(blank) coupling is the predominant mechanism for eliciting contraction of vascular smooth muscle

Pharmaco-mechanical

The activation of Receptor/G protein/PLC/IP3/DAG/PKC pathway leads to (blank)

vasoconstriction and muscle contraction

How does Ca elicit muscle contraction? | What is the clinical focus of this?

Calcium-> MLCK->Myosin + Actin-> contraction -a1, AT, ET, 5HT receptor blockers as antihypertensive drugs.

The inhibition of cAMP/AC/PKA pathway leads to what?

vasoconstriction

Activation of cAMP/AC/PKA pathway causes what? | What is the clinical focus of this?

vasodilation - isoproterenol induced vasodilatation - ischemia/adenosine/vasodilatation

Activation of cGMP/GC/PKG pathway causes what? What is the clinical focus of this?

Vasodilation (relaxation) shear stress -ET, thrombin, atrial distension and ANP release