BMS 300 1st edition Lecture 33Outline of Last Lecture I. Autonomic Regulation -generic 1. CNSPNStarget -parasympathetic branch 1. motor nucleus of the vagus 2. vagus nerve 3. cardial ganglion 4. pacemaker cells 5. acetylcholine 6. G-protein coupled receptor g2iII. Sympathetic branch -spinal cord—intermediolateral gray column 1. T1-L32. sympathetic chain ganglia 3. postganglionic neuron to target III. Role of nerephinophrine -G-protein coupled receptor -G (alpha) sThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.1. increase in cAMP 2. affection HCN channels -Effection contractile cells Outline of Current Lecture IV. Adrenergic receptors contracticity and the vasculature -B1 receptors and contracticity 1. phosphorylation >ca2+ channels >ca2+ pumps V. The vascalature -the tubes into which the ventricles pump blood -closed system of arteries, anterioles, capillaries and veins -resistance to flow- friction along the walls VI. Some equations -ΔP=Rxt -circumference=2π r-area=A=π r2-flow: ΔPπ rt / 8 hLVII. Pressure drop -anterioles VIII. Role of anterioles in both muscle and alpha 1 receptors Current LectureRecap last lecture: -we had drawn a box labeled the contractile cardiomyocyte -it obeys all the rules of muscles from before-there is a TSR junction, there are z lines with thin filaments attached and between themthere are thick filaments -the same basic story to cause muscle contraction -muscle contraction is dependent on calcium -the cardiomyocytes have a g-protein coupled receptor which is a receptor for norephephrineadrenergic receptor -the binding of the molecule to this receptor will activate the exchange of GDP to an GTP-once the alpha subunit has the GTP on it, it will activate -the GTP bound to the alpha subunit is used to activate adenylyl cyclase ATPcAMP-here the function is different>the cAMP turns on protein kinase A (phospholoration) phospholarating protein (syrine thryonine kinase)-the fundamental idea is that we are phospholorating proteins >dihydrophyrine receptors >RYR receptors >both of these lead to greater release of Ca2+ from the sarcoplasmic reticulum -the sympathetic intervation of the contraction cells increases the contraction inside the cells, meaning more blood will be squeezed out -we also phospholorate the calcium pumps to increase the rate of calcium removal Ventricular pumps-to provide energy to propel blood through the vasculature -the vasculature is arteries/anterioles carry blood away from the heart -they are surrounded by smooth muscle -they then go into capallaries which are exchange vesicles -the capallaries are composed of a single layer of endothelial cells -the return system was through the veins (the return of blood to the heart) -this is all an entirely closed system -all of the energy that propels the blood through these tubes is from the contraction of the ventricular system Resistance of movement of fluid through a tube -most of the resistance is friction of the fluid with the walls of the tube -imagine 2 tubes >one small, one bigger>they are full of fluid >theres not much resistance in the middle >if we increase the radius from a small amount to much larger, small changes in the radius have a much bigger change on the area then the circumference (we have a big effect on reducing the resistance along the walls) Flow = proportional to the radius (r^4) small changes in the radius make big changes in the
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