Circulation II

when cardiac afterload increases, the heart requires _

more energy to eject blood

how does afterload affect ejection

slows ventricular ejection

increased HR and ventricular contractility eventually cause what effect on venous/arterial system

decreased venous pressure

increased arterial pressure

dilating skeletal muscle arterioles has what effect

decreases systemic vascular resistance

exercise requires what adjustments (5)

increased HR

increased ventricular contraction-relaxation rate

increased contractility

decreased systemic vascular resistance

increased venous tone

what does most blood shift to during exercise

skeletal muscle

where does the greatest amount of blood shift away from during exercise

liver and kidneys

where does blood flow remain constant during exercise

brain

capillaries are more numerous in _

metabolically active tissues

what is the sensor for arterial pressure

baroreceptors

where are baroreceptors found

vagal nerves of the aorta

carotid sinuses

how does the arterial pressure reflex work

vagal afferents signal to the medulla

adjustment of sympathetic activity

why does BP drop during heart attack

lack of blood FLOW + high resistance

what impacts resistance the most in the CV system

arteriole tone

what factors influence pressure gradients

contractility

HR

venous volume

when does angiogenesis occur

growth

response to exercise or injury

cancer metastisis

growth factors for angiogenesis

vascular endothelial growth factor (VEGF)

fibroblast growth factor (FGF)

intrinsic mechanisms for controlling regional blood flow via arteriorle tone

1. bayliss myogenic response

2. local metabolic vasodilators

3. paracrine regulation

where are intrinsic methods for controlling blood flow via arteriole tone powerful

brain

heart

skeletal muscle

kidney

extrinsic mechanisms for controlling blood flow via arteriole tone

1. sympathetic vasoconstriction

2. hormones (ADH, renin-angiotensin-aldosterone, catecholamines)

hormones that control arteriole tone

vasopressin (ADH)

renin-angiotensin-alodsterone

catecholamines

when MAP is normal, _ is the major determinant of blood flow

arteriole radius

what primarily determines arteriole radius

smooth muscle contraction

where is myogenic regulation of blood flow very pronounced

renal and cerebal arterioles

blood volume is a key variable in determining _ (2 things)

perfusion pressure

cardiac contraction strength

how does myogenic control of arteriole tone work

increase in transmural pressure opens stretch activated cation channels that depolarize the muscle cells and cause contraction

insufficient oxygen supply to tissues causes the formation of _

vasodilator metabolites

metabolite released due to low oxygen

adenosine

cellular response to increased CO2/lactate/decreased pH

K channel activity increases

increased concentration of extraceullar potassium stimulates _

K channel activity

increased tension and arteriole wall pressure have has what effect on arteriole

opens Ca++ channels

increased muscle contraction

increased resistance

lower blood flow

mechanisms that adjust vascular resistance to maintain constant flow when perfusion pressure changes are considered _

autoregulation of blood flow

autoregulation of blood flow is not _

a reflex

what is active hyperemia

an increase in blood flow to an organ or tissue that is triggered by increased metabolic activity or demand

blood flow to an organ is proprotional to _

its metabolic activity

metabolic factors that promote vasodilation

decreased oxygen

increased CO2 / acidic conditions

increased extracellular K concentration

release of ATP, ADP, adenosinte

the release of ATP, adenosine, and ADP activates _

GPCRs that open K channels and activate Ca pumps

what is the mechanism of active hyperemia

activate K channels

increase hyperpolarization of smooth muscle

turn off voltage gated Ca channels

less contraction

=vasodilation

active hyperemia produces what effect

vasodilation of arterioles

blood flow being increased after a brief period of ischemia is termed _

passive (reactive) hyperemia

during ischemia, _ accumulate in the tissue

vasodilatory substances

vasoactive substances produced by cells in the vicinity of arterioles

autacoids

what are cells that release autocoids

endothelial cells

blood cells

fibroblasts

what do endothelial cells secrete

vasodilators ( nitric oxide and prostacyclin)

what effect does nitric oxide have

promotes synthesis of cGMP

what effect does prostacyclin have

promotes cAMP synthesis

impacts of endothelial derived factors

smooth muscle tone

smooth muscle proliferation

platelet inhibition

regulation of monocyte function

in health, endothelium factors are:

anti inflammatory

anti hypertensive

anti thrombotic

where are endothelial cells located

between the blood vessel wall and circulating blood

what do endothelial cells detect

chemical substances in blood

physical forces acting on vessel wall

vasodilators released by endothelial cells

nitric oxide

prostacyclin

how does cGMP cause smooth muscle relaxation

induces dephosphorylation of myosin light chains

how does cAMP cause smooth muscle relaxation

activate Ca pumps that remove Ca from cell

vasoconstrictors released by endothelial cells

endothelin

thromboxane

what activates nitric oxide release

calcium

mechanical stress in endothelial cells

why do nitric oxide signals remain very local

they diffuse rapidly across membranes and quickly decompose in blood

what activates platelets

foreign surfaces

collagen matrix

ADP

thrombin

thromboxane

endothelial cells inhibit _

platelet activation

how do endothelial cells inhibit platelet activation

create a barrier between the ECM collagen and blood

secrete prostacyclin and NO

express an enzyme that hydrolyzes ADP (a platelet activator)

endothelin regulates

vasomotor tone

blodo pressure

thromboxane and endothelin activate _

GPCRs

_ dysfunction is a hallmark of cardiovascular disease

endothelial

what do mast cells release

histamine

what stimulate mast cells

pathogens and allergens

what effect does histamine have (arterial/capillary)

relaxation of smooth muscle

increases capillary permeability --> swelling

where are mast cells found

connective tissue of all organs

along the course of small vessels

main local factors that regulate blood flow

nitric oxide

prostacyclin

endothelin

thromboxane

prostagalndins

histamine

what effect does bradykinin have

stimulate endothelial cells to produce nitric oxide

what effect does serotonin have

acts a vasoconstrictor by releasing Ca+ from the ER in smooth muscle

what effect do kinins have

cause inflammation and affect BP

_ release serotonin

platelets adhering to damaged vessels

where in the body is neuronal extrinsic control strongest

skin

gut

kidney

which nervous system has the largest role in regulating blood flow

sympathetic nervous system

_ stimulates the formation of bradykinin

acetylcholine

where do parasympathetic fibers innervate

salivary glands

mucus glands in the mouth

bladder

genitals

shock produces what effect

dilation of systemic vessels (reduces resistance)

drops BP

norepinephrine acts as a _

vasoconstrictor

how does epinephrine cause vasodilation

activating beta2 receptors

high concentrations of epinephrine activate _ receptor

alpha 1

what produces angiotensin II

ACE converts angiotensin I to angiotensin II

angiotensin II causes _

vasoconstriction

where are osmolarity sensors found

hypothalamus

net effect of norepinephrine

increased systemic vascular resistance

what releases ADH

posterior pituitary of the hypothalamus

when is ADH released

in response to increased plasma osmolarity

what effects does ADH have

stimulates water reabsorption in kidney

where is ADH synthetsized

hypothalamus

what causes ADH release beside increased plasma osmolarity

neuronal input from stretch receptors in the left atrium (they detect blood volume)

what does the renin-angiotensin-aldosterone system promote

kidney reabsorption of sodium and water

what starts off the renin-angiotensin-aldosterone system

kidney synthesizes and releases renin when BP is low

when does the kidney release renin

when BP and/or blood volume are low

where is angiotensinogen produced

liver

what converts angiotensinogen to angiotensin I

renin

where is angiotensin converting enzyme produced

lungs

what does ACE do

cleaves angiotensin I to angiotensin II

what does angiotensin II do

upregulates BP, kidney water retention, thirst

what is the renin-angiotensin-aldosterone pathway

kidney releases renin

liver releases angiotensinogen

renin cleaves angiotensinogen to angiotensin I

lungs release ACE

ACE convert angiotensin I to angiotensin II

what cell stimulates JG cells to release renin (and when)

macula densa cells when they detect low Na levels

what mechanism does the brain rely on to keep blood flow constant

myogenic regulation of arterial smooth muscle

which cells actually release renin

juxtaglomerular cells