Creado por Evian Chai
hace más de 4 años
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Pregunta | Respuesta |
What is the difference between SNS and PNS effects on Vascular tone? | 1. PNS causes selective vasodilation (salivary glands, pancreas, sex organs, intestine) and doesn't impact TPR 2. SNS redistributes blood and can affect TPR |
What is the difference between adrenaline and noradrenaline? | Noradrenaline maintains myogenic tone and is released constantly Adrenaline is released by the adrenal medulla mainly, and is only during fight/flight. It uniquely binds to B2 |
What occurs when noradernaline binds to B1/A1 receptors? | B1: Increase HR/cardiac contractility A1: Vasoconstriction of most vascular beds |
What occurs when adrenaline binds to B1/A1/B2 receptors? | B1: Increase HR/cardiac contractility A1: Vasoconstriction of most vascular beds B2: VASODILATION of heart/liver/skeletal muscle arterioles |
What do the following hormones cause? 1. Angiotensin II 2. Vasopressin (ADH) 3. Atrial Natriuretic | 1. Vasoconstriction 2. Vasoconstriction, an increase in blood volume 3. Vasodilation |
What signal does the PNS send and what does it do? | ACh, binds muscarinic receptors on pacemaker to lower HR |
What signal does the SNS send and what does it do? | Noradernaline, binds to: 1. B1 receptors on pacemaker (increase HR) 2. B1 receptors on myocardium (increase contractile force) |
What does vascular tone determine? | 1. BP, TPR, CO 2. Distribution of blood |
How does myogenic autoregulation contribute to vascular tone? | Arterioles respond to increase in pressure by increasing contraction Protects glomerulus from too high pressure |
How do Prostanoids (prostaglandins and thromboxanes) affect vascular tone? | Vasoconstrictors: TXA2, PGF2 Vasodilators: PGE, PGI |
How does Bradykinin affect vascular tone? | 1. Vasodilation through production of nitric oxide 2. Increase vascular permeability |
How does histamine affect vascular tone? | Mast cells release to: 1. Vasodilation (nitric oxide) 2. Increase vascular permeability |
How does nitric acid affect vascular tone? | 1. Endothelial nitric oxide synthase in endothelial cells make NO, diffuse to smooth muscle 2. Leads to calcium storage in sarcoplasmic reticulum/no cGMP = no contraction 3. So vasodilation |
What is endothelial nitric oxide synthase in endothelial cells stimulated by? | Laminar flow, Ca2+ |
What are the 5 determinants of BP? | 1. Stroke Volume 2. Heart Rate 3. Total peripheral resistance 4. Central venous pressure 5. Blood volume |
Where are the mechanoreceptors for the baroreceptor reflex located? | Aortic arch and carotid sinus |
What does increased BP lead to? | Increased firing of baroreceptors |
What are the effects of increased baroreceptor firing? | Increases PNS activity (release ACh to pacemaker cells) Decreases SNS activity on cardiac myocates (fall in HR, CO, Contractile force, TPR etc, vasodilation of vessels) Lowered BP |
What nerves do signals from the mechanoreceptors travel to the brain with? | 1. Vagus nerve 2. Glossopharyngeal nerve |
How does blood volume regulate blood pressure in the Short vs. long term? | Short: raise in BV=raise in BP Long: raise in BV=excretion of excess fluid/salt=fall in BV/BP |
What determines blood volume? | Plasma osmolarity |
How does increased osmolarity impact blood volume? | Raise in thirst/ADH/water reabsorption Increase in BV |
What does metabolic hyperaemia occur in response to? What happens? What is the main factor contributing to this? | Excercise Vasodilation Increase in metabolism+vasodilation allows muscles to get more nutrients etc. Local factors are the main factor causing increased blood flow |
What does reactive hyperaemia occur in response to? What happens? | Blood flow cut off Metabolites accumulate and trigger vasodilation until washed out |
How is thermoregulation achieved by the arteriovenous anatomoses? | Cold: Vasoconstriction Hot: Decrease in sympathetic, vasodilation, more blood to surface (dermal venus plexus), more heat loss |
What does the skeletal muscle pump do? | Aids venous return in legs |
Since diastolic pressure is the lowest pressure point in the cardiac cycle, how is BP maintained? | Energy stored in the elastic walls during systole released to mantain |
What does renin do? | Converts angiotensin to angiotensin II |
What does angiotensin II do? | 1. Vasoconstrictor 2. Stimulates ADH release, which increases H20 reabsorption 3. Stimulates release of aldosterone from adrenal gland to increase Na+ reabsorption Increased BV as result |
What does a raise in BV lead to? | 1. Increased BV-->increased central venous pressure detected by mechanoreceptors 2. Vasodilation of afferent arterioles in glomerulus caused by Atrial Natrutiec Peptid-->increased GFR/water excretion 3. Lowered renin/Angiontensin II/ADH 4. As result, diuretics (more urine) and natriuresis (Na+ excretion)-->Lowered BV |
What does pressure natriuresis occur in response to? What happens? | 1. Increased BV 2. local metabolite release in renal artery leads to vasodilation, increased natriuresis 3. Leads to fall in BV/BP |
What is syncope? What is it caused by? | 1. Fainting due to blood/needles 2. Due to increase in PNS (lowered HR/Vasodilation) and lowered SNS (lowered CO/TPR=fall in BP+lowered blood flow to brain) |
What are 3 functional adaptations of the pulmonary circulation? | 1) Low pressure 2) Unaffected by ANS, no metabolic regulation 3) Hypoxic pulmonary vascoconstriction - High CO2 will usually cause vasodilation but here it causes vasoconstriction to reduce blood to unoxygenated areas |
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