Ch 15: Blood Flow and the Control of Blood Pressure, Part 2 Keypoints Blood pressure (BP) and Regulation Exchange at capillaries Lymphatic system Cardio-vascular diseases

Review: R = 8L  r4 R = Resistance L = Length of “pipe” = viscosity r = radius

Control of Blood Flow 1. Local control: By paracrines O2 CO2 NO (in erection) In the heart, adenosine serves as a paracrine to dilate coronary arteries Others: histamine, ↓ O2 and ↑ CO2  arteriolar dilation The ↑ flow is hyperemia

Control of blood flow, cont’d 2. Endocrine: ANP and Angiotensin II (Chapt 20) 3. ANS (mostly sympathetic): NE on α receptors  vasoconstriction E on β2 receptors  vasodilation (F or F)

Distribution of Blood

Exchange at the Capillaries Capillaries are anatomically designed for exchange Continuous (leaky junctions) Fenestrated (kidney and intestine) Sinusoids in liver, bone marrow and kidney Capillaries in the brain are less leaky and are surrounded by astrocytes and pericytes  BBB Fig 15-16

Exchange at the Capillaries Capillary blood flow: Greatest total cross sectional area  Lowest Velocity Most cells within 0.1mm of capillary – why? Direct correlation between # of caps and metabolic needs of tissue Three types of exchange of molecules across the barrier:

Methods of Capillary Exchange Paracellular diffusion – between the cells Leaky cell-cell junctions Transendothelial transport (transcytosis) through the cells Endo- and exocytosis, diffusion through the endothelial cell Bulk flow: mass movement of H2O and dissolved solutes as result of hydrostatic or osmotic pressure Filtration – flow direction out of capillaries Absorption – flow direction into capillaries

Two Forces Regulate Capillary Bulk Flow Hydrostatic P: lateral component of fluid flow Colloid Osmotic P: due to solute difference (main solute difference due to proteins inside the capillary) Mostly: Net filtration at arterial end Net re-absorption at venous end Fig 15-18

Lymphatic System Close functional association with three other systems Cardiovascular Digestive Immune

Lymphatic System Functions Return filtered fluid & proteins to circulatory system (anatomical design!) Transfer fat from small intestine to circulatory system (lacteals) Trap and deal with pathogens

Edema Blockage of lymph drainage Capillary filtration > absorption Due to disruption of capillary exchange 2 major causes: Blockage of lymph drainage Cancer & fibrotic growth Pathogens Pregnancy Capillary filtration > absorption Venous pressure  due to right / left heart failure, backs up in to capillaries Plasma protein concentration  due to liver failure or severe malnutrition (Kwashiorkor) reduces colloid osmotic pressure  in interstitial protein

Regulation of Blood Pressure Reflex control: Baroreceptor Reflex = 1o homeostatic control for BP; adjustments for standing Medullary cerebrovascular control center (CVCC) integrates neural control (fig 15-23) Baroreceptors = stretch sensitive receptors in aorta and carotid artery Fig 15-21 Cardiovascular System: Blood Pressure Regulation

Regulation of Blood Pressure, cont’d Arterial chemoreceptors activated by O2 Cerebral cortex emotional responses such as blushing & fainting  vasovagal response Integration with Kidney function Orthostatic hypotension normally triggers Baroreceptor reflex Hormones from heart affect kidney function and vice versa.

Cardiovascular Diseases Account for ~ 1/2 of deaths in US – most common: CAD Uncontrollable & controllable risk factors Gender, age, genetics Cigarette smoking, obesity, high BP, high cholesterol, DM

Cigarette Smoking: Vasoconstriction & BP  Risk for atherosclerosis  Nicotinic cholinergic receptors stimulate sympathetic neurons at precapillary sphincters Vasoconstriction & BP  Risk for atherosclerosis  Carbon monoxide (myocardium extracts most of O2 brought to it under resting conditions)

Atherosclerosis Fig 15-24 Common to several cardiovascular diseases Changes in artery walls start with extracellular lipid deposits Macrophages ingest the EC LDL-cholesterol Called foam cells Fatty streaks just under endothelial lining of larger arteries Macrophage paracrines ↑ smooth muscle cells Smooth muscle cells proliferate  stable plaques vs. vulnerable (easy to rupture) plaques  platelet activation  thrombus Cerebral and coronary thrombi and emboli  Stroke or MI Fig 15-24

Role of Hypertension Essential HT = idiopathic and/or hereditary Creates damage to endothelium Plaques form and occlude lumina ↑ BP  ↑ afterload (R)  cardiac hypertrophy CHF Ca2+ channel blockers hyperpolarize smooth muscle cells  less likely to contract ACE inhibitors block ACE-I → ACE II Vasodilation Diuretics  blood volume β-blockers  catecholamine effects

Running Problem: Essential Hypertension