BIO 241 1st Edition Lecture 10Outline of Last Lecture I. Blood reservoirsII. Capillary exchangeIII. What determines bulk flowIV. Net filtration pressure (arterial end)V. Net filtration pressure (venous end)VI. Review of capillary exchangeVII. HemodynamicsVIII. Blood pressureOutline of Current Lecture II. Systemic vascular resistanceIII. Routing of blood flowIV. Mechanisms of venous returnV. Regulation of blood pressure and flowVI. Neural controlVII. Hormonal control of blood pressureVIII. Local control (autoregulation)Current LectureII. Systemic vascular resistance aka total peripheral resistance is a major function of the arterioles. Increased norepinephrine leads to full vasoconstriction which has the highest resistance. Decreased norepinephrine leads to full vasodilation and has low resistance. Resistance α = __1__ decrease diameter by ½, resistance increases 16 fold. d4 diameter = 1 mm d4 = 14 = 1 resistance = 1diameter = 2 mm d4 = 24 = 16 resistance = 0.0625diameter = 3 mm d4 = 34 = 81 resistance = 0.0123If you decrease the diameter of a vessel by half, you increase the resistance to flow through thatvessel by 16. III. How does blood shunt from one area of the body to another? Well, if you vasodilate somewhere, you have to vasoconstrict somewhere else. Increased activity in skeletal muscle → increased oxygen demand. Vasodilation in skeletal muscle → decreased resistance in vessels. Decreased activity in gut → decreased oxygen demand. Vasoconstriction in gut → increased resistance in vessels. Blood flow always follows path of least resistance, from gut to skeletal muscleIV. There are four mechanisms of venous return. The first is decreasing cross-sectional area which increases velocity and decreases pressure. The venous valves along with blood pressurehelp with venous return because they open and close for regulation. The legs have more valve per area. Skeletal muscle pumps aid in venous return. Blood pools at the feet after sitting a while. This is why after exercise, your feet get skinnier. The final aid is respiratory pumps which is the squeezing of the diaphragm to help breathe. This process decreases volume and increasespressure. V. The cardiovascular center of the medulla consists of three interconnected groups of neurons: cardioacceleratory center, cardioinhibitory center, vasomotor center. Nervous input into the cardiovascular center consists of higher brain centers (cerebral cortex, limbic system, hypothalamus), baroreceptors (monitor arterial blood pressure), chemoreceptors (monitor O2, CO2, and H+ in arterial blood). Nervous output from the cardiovascular center consists of cardioaccelerator nerves (sympathetic - increase HR and contractility), vagus nerve (X) (parasympathetic - decrease HR), vasomotor nerves (sympathetic - vasoconstriction/vasodilation). All of these things, basically sympathetic and parasympathetic, regulate heart rates. VI. Neural control is regulated by three things: the vasomotor center (vasoconstriction/vasodilation of arterioles), baroreflexes and chemoreflexes (carotid sinus and aortic sinus reflexes, right atrial Bainbridge reflex), and the medullary ischemic reflex (loss of oxygen to tissues). Blood pressure decreases, turns off parasympathetic system, increase HR, increase cardiac output, and increase BP. VII. There are a few hormones that control blood pressure. The first is angiotensin II (potent vasoconstrictor → increased resistance → increased BP). The second is aldosterone which promotes sodium retention by kidneys (increased water retention → increased blood volume →increased BP). The third is atrial natriuretic peptide (ANP) which decreases sodium retention by kidneys (decreased water retention → decreased blood volume → decreased BP). The fourth is antidiuretic hormone (ADH) (increases water retention by kidneys → increased blood volume →increased BP). The last is epinephrine and norepinephrine (potent vasoconstrictor → increased resistance → increased HR + increased SV = increased CO → increased BP).VIII. Local control also known as autoregulation is the ability of tissues to regulate their own blood supply. The metabolic theory of autoregulation is inadequate perfusion = decreased O2 → vasodilation and increased wastes (CO2, H+, K+, adenosine) → vasodilation. When adequate perfusion occurs again, vasoconstriction also occurs. Vasoactive chemicals are secreted by platelets, endothelial cells, perivascular tissues with trauma. Histamine, prostaglandins, bradykinin all stimulate