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BIOC33/34 Lec 9.docx

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Biological Sciences
Stephen Reid

BIOC34 Lec 9  Finishing up cardiovascular system  Adrenergic regulation o Catecholamine action o In humans, catecholamines circulating are good regulatory systems for heart and blood pressure o Decrease in blood pressure is sensed by baroR in carotid arteries and aortic arch o Catecholamine regulation   2 reflexes: • Increase in sympathetic activity releasing Ad and Nad onto nerves and heart  increases in HR and SV • Catecholamines release from adrenal glands (cortex- synthesis of steroid)  adrenal gland is in control of splanchnic nerve o Large increases ofAd when BP is low; NAd is not as prevalent (it’s main function is as a neurotransmitter - works on heart and blood vessels to cause constriction or vasodilation) o With low BP, actions are to constrict BP and increase TPR o But it can depend on severity of decrease and amounts of hormones that are released  Adrenergic Regulation of BP (TPR) o When looking at catecholamine hormones, when NAd andAd are released, can act on 2 major pop’n of R: alpha and beta  Alpha 1,2 beta 1,2 o Activate second messenger systems - whenAd or NAd work on alpha-R it leads to vasoconstriction and when working on beta-R - vasodilation  1. NAd from Sympathetic Nerves (neural) o When NAd is released as a NT from sympathetic nerves  outcome = vasoconstriction. This is because alpha adrenoceptors are located mostly on smooth muscle being innervated by sympathetic nerves  NAd finds itself interacting more with alpha R  Alpha-R on blood vessels tend to be found around sympathetic nerve terminal endings • Promote vasoconstriction when stimulated  2. Ad and NAd from theAdrenal Gland (endocrine) o When adrenal gland releases small amounts of NAd, they are brought to blood instead of going to synaptic region  Interact with alpha and beta receptors  Binding to alpha-R = vasoconstriction  Binding to beta-R = vasodilation o At low concentrations there is preferential binding ofAd and NAd to beta-R - beta-R have a higher affinity for catecholamines than alpha-R  Causes vasodilation  At high [adrenaline] o At high concentrations, get binding of adrenaline to BOTH alpha and beta receptors o Ultimate effect depends on the organ of the tissue being looked at - in some tissues, there is a higher number of B-receptors as opposed toA-receptors o In cardiac and skeletal muscle: #B-receptors > #a-receptors  Adrenaline promotes vasodilation o In almost all other tissues, # a-receptors > # B -receptors and get vasoconstriction  Vasopressin o Anti-diuretic hormone (ADH) o Neurohormone synthesized and released from brain - from paraventricular nucleus and stored in pituitary gland o This is a case where there are other pop’n of baroreceptors (in the heart, venous system) in addition to aortic arch and carotid artery  When stimulated, release vasopressin o 2 major effects:  Work on blood vessels causing vasoconstriction  (major role = water retention) Works on kidneys - filters the plasma frequently, kidney reabsorbs water back into blood or releases as urine - whether or not kidney is reabsorbing water or releasing is due to anti- diuretic hormone o Hormone system that alcohol works on - alcohol inhibits R that vasopressin works on. Kidney does not reabsorb water  Renin-angiotensin (3) o This system involves cascade of actions leading to production of angiotensinogen I which produces a peptide called angiotensin II  Angiotensinogen gets converted to angiotensin I - angiotensin I is similar to II but not as potent  Conversion to angiotensin I is done by renin - released by cells in kidney • Low BP causes renin to be released  As angiotensin I gets circulated, it is exposed in lungs to enzyme bound to small capillaries called ACE (angiotensin converting enzyme) - cleaves off small peptide turning angiotensin I to angiotensin II o With low BP - 3 main factors that angiotensin works on:  Causes BV to constrict - powerful vasoconstrictor; most powerful on humans • Causes an increase in BP  Works on pituitary gland to release ADH (anti-diuretic hormone) - vasoconstricts blood vessels and works on kidneys  Triggers adrenal gland cortex to release aldosterone - aldosterone triggers kidney to reabsorb Na - reabsorbing Na also reabsorbs water by osmosis  Summary of BP regulation o When looking at it from diagrams, everything boils down to CO and resistance o Diagram 2  Boils down to changing HR, CO and TPR - 3 major determinants of BP along with blood volume  Low BP sensed by kidneys to release renin to get angiotensin II to constrict BV leading to increases in TPR and works on adrenal cortex to release aldosterone  Hormones affecting blood volume - release of hormones from pituitary glands  19:30  Respiratory System o Pulmonary mechanics - the nervous, muscular and mechanical effects, changes in pressure on breath by breath basis o Long volumes/capacities - important; lead to lung function tests and these tests can tell if lung is working properly  Restrictive lung disease - problems inflating the lungs and inspiring  Alveolar ventilation - alveoli are the primary area of ventilation • Minute ventilation = overall breathing o Huge amounts can cause very low levels of alveolar ventilation • Reach a point where breathing so fast, taking large amounts of air but are not reaching alveoli o Gas transfer - oxygen and CO2 transports are done by the red blood cells and are linked to processes of taking CO2 from metabolically active tissue o Control of breathing - control systems starting in the brain; in medulla oblongata there is region called the preboxy complex?  functions as a pacemaker but is not an actual pacemaker, it is a complicated neural network  Lungs o Organ of ventilation o Gas exchange occurs here o Right and left lungs are slightly different  Left lung is slightly reduced in size because of cardiac notch - accommodates the heart • Larger capacity here  Right lung is slightly shorter than left lung due to position of diaphragm and liver  Function both the same  Respiratory Tract o Air enters from larynx to trachea and to lungs o Trachea is very rigid unlike esophagus  Trachea has large rings of cartilage  important - keep trachea from collapsing  Sleep apnea - obstructive - airway gets blocked because there is a loss in neck muscle tone during sleep and bigger people can create pressure on trachea and cause it to collapse  10% of sleep apnea cases are non-obstructive - due to abnormalities in brain regarding breathing o Opening to trachea = glottis - muscular valve that opens and closes  Cover flipping over this = epiglottis  This cover flaps down when we swallow so we do not get food or liquid into lungs o Major respiratory muscle in humans = diaphragm  Muscles in between the ribs and ab muscles are involved  Respiratory tract: the conducting zone o Air is constantly going in through series of branching into trachea tubes o Branching into primary and then secondary (go into lobes). Further branching at the end of tubes is called terminal bronchi o Throughout this course of tubing, these are conduits for air to move down into lung - no gas exchange taking place with air and blood in this tube system o These tubes are too thick for gas exchange  This branching is called the conducting zone  In addition to conducting air, it is important for warming and humidifying air  Important temperature regulation and water conservation o Refer to conducting zone as anatomical dead space - no gas exchange but air is moving through it o Respiratory dead space - gas exchange but no air is moving  Respiratory Tract: the respiratory zone & alveoli o Will reach respiratory zone o Small terminal bronchi leading to respiratory bronchi - continuation of bronchi but walls are getting thinner and gas exchange can occur here o Respiratory bronchi have alveolar sacs - predominant site of gas exchange  Millions of alveoli in the lungs  Respiratory tract: the respi
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