Control of blood flow Flashcards
What are the two primary systems involved in the control of blood flow in different organs?
Sympathetic (neuronal) and Endocrine (hormonal) systems.
What are autocoids in the context of blood flow control?
Local hormones that influence blood flow.
What does “active hyperaemia” refer to in local blood flow control?
The increase in blood flow to tissues based on their metabolic activity.
What is “flow autoregulation” in blood flow mechanisms?
The ability of tissues to maintain a consistent blood flow despite changes in perfusion pressure, involving local myogenic and metabolic factors.
What role does the sympathetic nervous system play in blood vessel control?
The sympathetic nervous system, using noradrenaline, regulates blood vessel constriction and dilation via central control.
Which part of the nervous system is responsible for central control of blood vessel tone?
The sympathetic nervous system.
What is the role of sympathetic nerves in the vasculature?
Sympathetic nerves cause vasoconstriction, especially in the spleen, kidneys, skin, and muscles, by releasing noradrenaline that acts on α₁ receptors.
Why is the sympathetic nervous system important for blood flow?
It redistributes blood flow and increases total peripheral resistance (TPR) to raise mean arterial pressure (MAP).
What neurotransmitter and receptor are associated with parasympathetic nerves in vasodilation?
Acetylcholine acting on muscarinic receptors.
Which organs are primarily affected by parasympathetic-induced vasodilation?
Salivary glands, pancreas, intestinal mucosa, and penis.
Does parasympathetic nervous system (PNS) activation affect total peripheral resistance (TPR)?
No, PNS activation has no significant effect on TPR as it affects only a few vascular beds.
In the provided image, what do the red and green structures represent?
Red represents smooth muscle cells, and green represents sympathetic nerve fibers.
What two types of hormonal control regulate blood vessels?
Hormones in the blood and autocoids (local hormones).
What are autocoids, and what role do they play in vascular control?
Autocoids are local hormones that mediate both direct and indirect dilation or constriction of blood vessels.
What layer of the blood vessel is targeted by hormones to regulate vessel tone?
Hormones primarily act on the smooth muscle layer to regulate vasoconstriction or vasodilation.
What is the role of the renin-angiotensin system in blood vessel control?
The kidneys release renin, which converts angiotensinogen into angiotensin II, causing vasoconstriction and raising total peripheral resistance (TPR) in response to reduced blood volume.
How does anti-diuretic hormone (vasopressin) affect blood vessels?
Released by the posterior pituitary in response to dehydration, it causes vasoconstriction to help maintain blood pressure.
What is the effect of adrenaline on blood vessels?
Adrenaline, released from the adrenal glands via SNS activation, can cause vasoconstriction or vasodilation depending on the receptors it acts upon.
How does atrial natriuretic peptide (ANP) influence blood vessel tone?
ANP is released by the atria in response to increased blood volume and promotes vasodilation, lowering TPR.
What are the two opposing effects of vasoactive hormones on TPR?
Angiotensin II: Raises TPR in response to low blood volume.]
ANP: Lowers TPR in response to high blood volume.
Which neurotransmitter is more important at rest in mediating SNS effects on the cardiovascular system?
Noradrenaline
Where is adrenaline secreted from, and under what conditions does its secretion increase?
Adrenaline is secreted by the adrenal medulla, with increased secretion during stressful situations such as fight or flight, hypotension, and hypoglycaemia.
What receptor does noradrenaline primarily act on to cause vasoconstriction?
α₁ receptors, which mediate vasoconstriction via IP₃/DAG signaling.
What receptor does adrenaline act on to increase heart rate and cardiac contractility?
β₁ receptors, which act via cAMP signaling.
What is the effect of adrenaline acting on β₂ receptors?
It causes vasodilation in skeletal muscles and the heart via cAMP signaling.
How much do adrenaline blood levels increase during stress?
Blood levels of adrenaline rise fivefold during stress.
Which local hormones are released by resident or infiltrating immune cells to cause vasodilation?
Histamine and Bradykinin.
What role does nitric oxide play in blood vessel regulation?
Nitric oxide, produced by the endothelium, mediates vasodilation.
Which local hormone is released by cardiac muscle to induce vasodilation?
Adenosine
What is the effect of thromboxane on blood vessels, and what cells release it?
Thromboxane, released by activated platelets, causes vasoconstriction.
What is the primary factor in metabolic control of blood flow?
Tissue metabolites, which are produced locally during metabolic activity.
How do tissue metabolites affect blood vessels?
Tissue metabolites cause direct vasodilation to increase blood flow to meet metabolic demands.
Which layer of blood vessels responds to tissue metabolites for metabolic control?
The endothelium and smooth muscle layers respond to tissue metabolites for vasodilation.
What is active hyperaemia?
It is the increase in blood flow to skeletal and cardiac muscles to match the increased metabolic demand during activity.
What sequence of events happen during exercise?
Which two muscle types are primarily involved in active hyperaemia?
Skeletal and cardiac muscles.
How do tissue metabolites affect vascular smooth muscle?
Tissue metabolites directly act on vascular smooth muscle to cause hyperpolarization and vasodilation.
What happens to potassium ion (K+) levels during increased metabolism?
Extracellular potassium levels (K+) increase due to potassium efflux from metabolizing cells.
How do potassium ions contribute to vasodilation?
Increased K+ opens potassium channels on smooth muscle cells, causing hyperpolarization and reduced calcium influx, leading to vasodilation.
What is the role of hydrogen peroxide (H₂O₂) in this process?
Increased H₂O₂ from metabolism contributes to opening potassium channels, promoting hyperpolarization and vasodilation.
What is the relationship between CO₂, H₂O, and HCO₃⁻ in smooth muscle?
CO₂ and H₂O are converted to HCO₃⁻ (bicarbonate) and H⁺, which can influence pH and smooth muscle relaxation.
What role does calcium (Ca²⁺) play in vascular tone?
Voltage-gated Ca²⁺ channels regulate calcium entry into smooth muscle cells, affecting contraction; hyperpolarization decreases Ca²⁺ influx, promoting relaxation.
How does the Na⁺/K⁺ pump contribute to smooth muscle function?
The pump helps maintain ionic balance by actively transporting 3 Na⁺ out and 2 K⁺ in, indirectly influencing hyperpolarization.
What metabolic changes lead to increased vasodilation?
Increased metabolism raises CO₂, H₂O₂, and extracellular K⁺, triggering mechanisms that open potassium channels and reduce calcium influx, leading to smooth muscle relaxation.
What is myogenic control in blood vessels?
It is the ability of smooth muscle in blood vessels to respond to changes in pressure or stretch to maintain consistent blood flow.
What triggers the activation of stretch-activated channels in vascular smooth muscle?
Increased stretch of the blood vessel wall.
What ion flows into the smooth muscle cell through stretch-activated channels during myogenic contraction?
Sodium (Na⁺).
What is the effect of sodium influx on the smooth muscle cell membrane?
Sodium influx causes membrane depolarization.
How does membrane depolarization lead to contraction in vascular smooth muscle?
Depolarization activates voltage-gated calcium (Ca²⁺) channels, allowing calcium influx, which triggers muscle contraction.
What is the role of calcium (Ca²⁺) in myogenic contraction?
Calcium binds to contractile proteins, initiating smooth muscle contraction.
How are adjacent smooth muscle cells coordinated during myogenic contraction?
Gap junctions allow the spread of electrical signals, coordinating contraction across cells.
What is flow autoregulation in blood vessels?
It is the process by which blood flow is maintained relatively constant despite changes in perfusion pressure.
Which two mechanisms are combined in flow autoregulation?
Myogenic control and metabolic control.
How does myogenic control contribute to flow autoregulation?
Myogenic control reduces blood flow in response to increased pressure by causing smooth muscle contraction.
How does metabolic control contribute to flow autoregulation?
Metabolic control increases blood flow in response to the accumulation of metabolites in active tissues.
What triggers myogenic contraction in response to increased perfusion pressure?
How does vessel size affect the relative importance of metabolic vs. myogenic regulation?
The importance of metabolic regulation increases as the diameter of resistance vessels decreases.
What triggers the release of nitric oxide (NO), prostacyclin, and EDHF from the endothelium?
Stimuli such as acetylcholine (from PNS nerves), bradykinin, histamine (autocoids), and flow-induced shear stress.
What is the role of nitric oxide (NO) in vascular control?
NO causes vasodilation by relaxing the smooth muscle.
Which molecule triggers the release of endothelin from the endothelium?
Angiotensin II.
Which molecules act on endothelial receptors to stimulate nitric oxide (NO) release?
Autocoids such as bradykinin and histamine.
What enzyme is responsible for producing nitric oxide in the endothelium?
Endothelial nitric oxide synthase (eNOS).
What is the role of L-arginine in the production of nitric oxide?
L-arginine is the substrate used by eNOS to produce nitric oxide (NO).
What happens to intracellular calcium levels when autocoids bind to endothelial receptors?
Intracellular calcium levels increase, activating eNOS to produce nitric oxide.
What is the effect of nitric oxide (NO) on vascular smooth muscle?
NO diffuses to the smooth muscle, causing relaxation and vasodilation.
What is the initial action of nitric oxide (NO) on smooth muscle cells?
NO activates soluble guanylate cyclase (GC), converting GTP to cyclic GMP (cGMP).
What role do potassium (K⁺) channels play in NO-mediated smooth muscle relaxation?
K⁺ channels open, causing hyperpolarization of the membrane, which decreases calcium influx through voltage-gated calcium channels (VGCC).
What is the role of SERCA in smooth muscle relaxation?
SERCA (sarco/endoplasmic reticulum Ca²⁺ ATPase) pumps calcium into the sarcoplasmic reticulum, reducing cytosolic calcium levels.
What does PMCA do in the context of NO action on smooth muscle?
PMCA (plasma membrane Ca²⁺ ATPase) removes calcium from the cell, further lowering cytosolic calcium levels.
How does phosphodiesterase (PDE) affect cGMP levels?
PDE degrades cGMP into GMP, terminating its signaling effects.
What happens to blood flow when an eNOS inhibitor like L-NMMA is used?
Blood flow decreases because NO production is blocked, reducing vasodilation.
whats the sequence of events during anaphylactic shock
What are the three major endothelium-derived factors involved in vascular control?
Prostacyclin (PGI₂), hyperpolarizing factors (EDHF), and endothelin.
What is the function of prostacyclin (PGI₂) in vascular regulation?
PGI₂ causes vasodilation by increasing cAMP levels in smooth muscle and also inhibits platelet aggregation (Stage 2 of clotting).
How do hyperpolarizing factors (EDHF) contribute to smooth muscle relaxation?
EDHF opens potassium (K⁺) channels, leading to membrane hyperpolarization and reduced calcium (Ca²⁺) influx, promoting vasodilation.
What is the role of endothelin in vascular tone?
Endothelin acts as a vasoconstrictor, increasing calcium levels in smooth muscle to promote contraction.
What triggers the release of vasodilating autocoids like prostacyclin and EDHF?
Flow-induced shear stress or the action of vasodilating autocoids on endothelial cells.
Which hormones can stimulate the release of endothelin?
Vasoconstrictor hormones like angiotensin II and thrombin.
How is hydrogen peroxide (H₂O₂) formed in oxidative stress?
Superoxide (O₂⁻) is converted into hydrogen peroxide (H₂O₂).
How is coronary blood flow related to oxygen consumption?
There is a direct, proportional relationship between coronary blood flow and oxygen consumption.
What is the distribution of blood flow at rest for major organs?
How does an increased heart rate affect diastole and perfusion time?
Diastole: Shortens significantly (from 0.5 seconds at rest to 0.13 seconds during exercise).
Perfusion time: Decreases (from 35 seconds/min at rest to 23 seconds/min during exercise).
What equation describes the relationship between flow, pressure, and resistance?
p = pressure
r = resistance
What happens to cerebral arterioles when perfusion pressure increases?
They constrict, reducing flow to maintain it at a normal level.
What happens to cerebral arterioles when perfusion pressure decreases?
They dilate, increasing flow to bring it back to normal.
What prevents cerebral haemorrhage during increased cardiac output or mean arterial pressure (MAP)?
What mechanism restores cerebral blood flow during haemorrhage-induced low perfusion pressure?
What happens in a healthy coronary artery during rest?
large pressure drop across the vasculature supports sufficient blood flow, with partially constricted arterioles maintaining the capacity for increased flow during exercise.
How does stenosis affect coronary blood flow?
Stenosis introduces additional resistance, reducing the pressure drop across the microvessels and thereby reducing blood flow to the cardiac muscle.
