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WEEK 21:
Control of Blood Vessels: Peripheral Resistance:
| Question | Answer |
|---|---|
| all resistance vessels are innervated by | SNS |
| what happens when arterial pressure falls | SNS nerve terminals release noradrenaline onto vascular smooth muscle cells causing them to contract |
| contraction is mediated by | a1-adrenergic receptors acting via IP3 signaling pathway causing Ca2+ release from sarcoplasmic reticulum |
| resistance is directly related to (2) | length of vessel and viscosity of fluid |
| resistance is inversely related to (1) | vessel radius |
| blood vessel radius depends on (3) | active tension exerted by smooth muscle, passive elastic properties of wall (elastin and collagen), and blood pressure inside vessel and pressure outside the vessel |
| LaPlace's Law | wall tension is equal to the radius x pressure |
| what size blood vessels tend to rupture | larger blood vessels (as bigger radius and more pressure which makes more wall tension) |
| hormones causing vasodilation (2) | atrial natriuretic peptide (ANP) and BNP |
| hormone causing vasoconstriction (3) | AngII (by binding to angiotensin AT1 receptors on VSMCs following IP3 pathway), ADH (binds to vasopressin receptors on VSMCs), and adrenaline/noradrenaline (bind to a1-adrenergic receptors on VSMCs) |
| zona glomerulosa | mineralocorticoids (aldosterone) |
| zona fasciculata | glucocorticoids (eg cortisol) |
| zona reticularis | gonadocorticoids (eg oestrogens) |
| medulla | adrenaline, noradrenaline (chromaffin cells) |
| layers of the adrenal cortex from outside to inside (3) | zona glomerulosa, zona fasciculata, and zona reticularis |
| prostaglandins are formed via | cyclooxygenase from arachidonic acid pathway |
| 2 main pathways of arachidonic acid metabolism (2) | involving cyclooxygenase (COX) and lipoxygenase pathways |
| endothelium is an important source of a number of | vasoactive PGs, made from arachidonic acid |
| dilators of endothelium (2) | PGE and PGI2 |
| constrictors/ vasoconstrictors (2) | PGF and thromboxane A2 |
| chemical mediators causing vasodilation (3) | histamine, NO, and PGI2 |
| chemical mediators causing vasoconstriction (1) | A2 (TXA2) |
| NO | potent gas vasodilator that acts on both arteries and veins |
| when is NO made | following a rise in intracellular Ca2+ concentrations |
| half life of NO | less than 10 seconds in vivo (meaning that its action remain highly localised) |
| nitroglycerin use | relieve pain of angina |
| how do nitrates like nitroglycerin work | break down and release NO in vivo causing arterial and venous vasodilation to lower ventricular afterload and preload |
| preload | how much the heart muscle stretches before it contracts |
| afterload | resistance the heart must overcome to eject blood |
| metabolic products cells release causing vasodilation | adenosine, lactate, K+, H+ and CO2 causing vasodilation |
| when are metabolic products like adenosine released | when blood flow increases to promote vasodilation to lower blood flow back to normal |
| contraction of myogenic mechanisms is mediated by | stretch-activated Ca2+ channels in VSMC membranes to protect capillaries from surges in arterial pressure |
| resistance vessels in many circulation constrict reflexively when? | when intraluminal pressure rises to protect capillaries from surges in arterial pressure |
Created by:
kablooey
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