BIO 3324 1nd Edition Lecture 15Outline of Last LectureI. ventricular excitationII. eggIII. cardiac cycleIV. eventsV. ejectionVI. capillariesOutline of Current LectureI. venules&veinsII. blood flowIII. bulk flowIV. sympathetic control V. bloodVI. plasmaCurrent lecture:Venules&veins:• Venules– Capillaries drain into venules– Have little tone & resistance– Extensive communication between arterioles & venules via chemical signals to match inflow & outflow• Veins– Large in radius– Little resistance to flow– Serves as a blood reservoirThese notes represent a detailed interpretation of the professor’s lecture. Grade Buddy is best Used as a supplement to your own notes, not as a substitute.• Highly distensible thus can accommodate greater volumes with small incremental pressure• Blood continues to circulate – but holds more blood due to stretching– Blood spends more time in the veins– Transit time is reducedVenous Valves:• Allow blood to move towards the heart & prevent backward flow despite the low pressure in veins• One-way valves• 2-4 cm apart• Counteracts gravitational effectsBlood Pressure:• Smooth muscle and connective tissue– Collagen – provides tensile strength against the high pressure caused by blood leaving from the heart– Elastin – provides elasticity• When blood leaves heart during systole, more blood enters arteries than is leaving (due to R in smaller vessels) therefore arteries expand temporarily• During heart relaxation, arteries passively recoil to ensure continuous blood flow• Force exerted by the blood against a vessel wall– Dependent on vessel distensibility• Highest in arteries and lowest in veins• Systolic pressure – pressure exerted in the arteries when blood is ejected into them during ventricular systole (maximum pressure)• Diastolic pressure – pressure within the arteries when blood is draining into the rest of the vessels during ventricular diastole (minimum pressure)• Pulse pressure – pressure difference between systolic and diastolic pressure• Mean arterial pressure (MAP) – average pressure driving blood forward– Roughly equivalent diastolic pressure + 1/3 pulse pressure• Roughly 2/3 of cardiac cycle is spent in diastole while 1/3 is in systole– Monitored and regulated by the body• Both Pulse pressure and MAP decline with increasing distance from the heart• Sphyngmomanometer (blood pressure cuff)• Korotkoff sounds are used to determine the blood pressure• Expressed as Systolic/Diastolic pressure• Mean arterial pressure is the blood pressure monitored & regulated in the body• Mean arterial pressure ∞ cardiac output x Rarterioles (total peripheral resistance)– CO determined by heart rate & stroke volume– Peripheral resistance determined by the diameter of the arterioles• Also affected by total blood volume and blood distribution in the systemic circulation– ↑ blood volume yields ↑ blood pressure. Adjustments need to be made by both the cardiovascular system and the kidney to maintain homeostatic balance– Blood distribution is determined by the diameter of the veins. Venous constriction forces more blood into arterial circulation (and ↑CO)Influencing arteriolar resistance:• Local control– Matches tissue blood flow to metabolic needs– Accomplished through paracrines and myogenic autoregulation• Sympathetic reflexes– Neural control maintaining mean arterial pressure & blood distribution• Hormones– Regulating resistance through catecholamines & other hormones– Regulation of solute and water balance by the kidneys to influence blood pressureLocal Control of arteriole resistance:• Active Hyperemia – increased blood flow resulting from increased metabolic need– ↓ O2, ↑ CO2, ↑ H+, ↑ K+, ↑ osmolarity– Vasodilation in response to paracrine factors• Reactive hyperemia – increase in blood flow after an occlusion– Occlusion results in ↓ O2 and ↑ CO2 & metabolic wastes– Vasodilation in response to paracrine factors– When occlusion is removed, blood flow remains high to return local chemical compositions to normal• Myogenic Autoregulation – local arteriolar mechanisms that keep tissue blood flow fairly constant despite variations in mean arterial driving pressure– Results from vasoconstriction or vasodilation depending on need– Arteriolar smooth muscles respond to passive stretching• The local chemical changes are detected by endothelial cells of the vessel which release paracrine factors that influence nearby smooth muscle– NO (nitric oxide)• Causes arteriolar vasodilation by inhibiting Ca2+ movement into the smooth muscle– Endothilin• Causes arteriolar vasoconstriction• Other local physical influences– Temperature – indicator of increased metabolic activity– Shear stress – force on vessels caused by friction• Increased shear stress causes the release of NO to promote vasodilationSympathetic control of arteriole resistance:• Both neural and hormonal controls– ↑ sympathetic activity = vasoconstriction– ↓ sympathetic activity = vasodilation• Neural reflex – NorE on smooth muscles– Acts on a1 adrenergic receptors– Results in vasoconstriction– Only exception is brain that doesn’t have a1 receptors• Local controls in skeletal/cardiac muscles are capable of overiding sympathetic control based on metabolic needHormonal control of arteriole resistance:• Adrenal medulla release epinephrine & norepinephrine– The a1 receptors– generalized vasoconstriction• Localized in digestive organs & kidneys– The b2 receptors– reinforce local vasodilation• Increased H2O retention results in increased arteriolar pressure– Vasopressin (anti-diuretic hormone, ADH)• Released from posterior pituitary • Potent vasoconstrictor• Primarily involved in regulating H2O balance promoting H2O retention– Angiotensin II• Part of a larger solute/water regulatory system• Potent vasoconstrictor• Regulates salt balance promoting water retentionBlood flow to organs:• To maintain homeostasis, reconditioning organs receive blood flow in excess of their own need at rest– Reconditioning organs – organs that provide nutrients and remove waste & heat• Blood flow to the other organs is just sufficient to fulfill that organ’s metabolic needs• If activity increases, then blood flow in reconditioning organs can decrease to compensate for the need for more blood in those