Control of Blood Pressure PDF

Life Sciences & Medicine Control of blood Prof. James Clark pressure School of Cardiovascular and Metabolic Medicine and Sciences PHYSIOLOGY AND ANATOMY OF SYSTEMS Learning Out...

Life Sciences & Medicine Control of blood Prof. James Clark pressure School of Cardiovascular and Metabolic Medicine and Sciences PHYSIOLOGY AND ANATOMY OF SYSTEMS Learning Outcomes  Briefly explain the key mechanisms governing pressure and flow waves in the arteries system  Describe the mechanism of the baroreceptor reflex, and explain its role in the short-term stabilisation of mean arterial blood pressure  Explain how the kidneys regulate mean blood pressure in the long term by controlling Na+ excretion and extracellular fluid volume.  Describe pressure natriuresis and its role in controlling renal excretion of Na+ and water Blood pressure - a brief review The term blood pressure (BP) as it is normally used refers to SBP the pressure in the large arteries. The BP oscillates with the cardiac cycle DBP systolic blood pressure (SBP) diastolic blood pressure (DBP) Blood pressure measurement - a brief review BP is generally measured at the level of the heart of one arm using a sphygmomanometer ‘Normal’ systolic and diastolic pressures measured this way are ~120/80 mmHg Mean BP is calculated as the time-weighted average of the systolic and diastolic blood pressures or 2/3 x DBP + 1/3 x SBP BP recorded in arteries below the heart is higher and is lower in arteries above the heart (e.g., mean BP is ~60mmHg in the neck and 180 mmHg in the foot). Pressure and flow in the Blood from the heart hits the blood arteries in the aorta and causes pressure and flow waves which are propagated down the vascular system. The pressure wave becomes larger as it moves down the arterial tree (due to greater arterial stiffness). It then progressively dies out as it moves into the arterioles and the microcirculation Flow is progressively smoothed out as blood moves into the arterioles and the microcirculation Blood flow is pulsatile in the aorta and arteries Pulse and pressure waves are moving at ~5 m/s Blood cell moves at ~ 32 cm/s Average aortic length is ~33 cm What happens to the ABP and blood flow during the cardiac cycle during systole? Energy stored in elastic walls Systole ~25% SV pushed forward into the ~75% SV is transiently stored smaller arteries in the aorta and large arteries TPR* Skin Muscle Brain Gut etc TPR* = total peripheral resistance = mainly the resistance arteries and arterioles What happens to the ABP and blood flow during the diastole? Stored energy maintains Diastole flow during diastole Arterial recoil pushes blood forward into the smaller arteries During diastole, the stored pressure falls as flow TPR* continues through the tissues. The minimum Skin Muscle Brain Gut etc pressure reached before the next systole is the diastolic pressure. TPR* = total peripheral resistance = mainly the resistance arteries and arterioles Relationships between pressure, flow, and resistance DPressure = flow x resistance ABP = arterial blood pressure Pressure falls steeply across segments of high resistance CVP = central venous pressure ~77mmHg ~25mmHg 120/80 ~5-10mmHg (mean ~95) mmHg Left 0 - 5mmHg heart P1 = ABP R1 R3 arteries veins P2 = CVP Rtotal = R1 + R2 + R3 R2 resistance arteries arterioles Pressures in the CVS Large Great Capillaries veins Pulmonary circulation arteries 120 Segment resistance 80 Pressure mmHg Velocity cm/sec 40 resistance arteries Venules and veins Arteries and 40 Capillaries 0 0 LV Resistance Venules RV arteries & arterioles Control of blood pressure Fluid balance Posture Exercise Sleep Stress 140 Arterial pressure (mmHg) systolic 100 60 diastolic 20 Sleep 09:00 12:00 15:00 18:00 21:00 24:0 03:00 06:00 09:00 Time (hrs) 0 The arterial baroreflex In the late 19th century, it was shown that stimulation of the aortic nerve caused bradycardia and hypotension The same reflex was observed by Hering in 1923 (right), when stimulating the carotid Carotid nerve stimulation sinus nerve Although BP is constantly changing, the extent is limited by the baroreceptor reflex. The Arterial Baroreflex helps maintain a (relatively) constant pressure, allowing the body to regulate blood flow to some organs while maintaining a constant flow to other organs R1: muscle BP R2: heart R3: brain BP set point can alter to allow the body to cope with stress (e.g., BP increasing during exercise, allowing the cardiac output to increase) Acute regulation of BP: Baroreceptor reflex Baroreceptors contain fine nerve endings sensitive to stretch (mechanoreceptors)  pressure causes  firing: most sensitive when mean BP is between 80-150mmHg Sensitivity also increased by a large pulse pressure – Baroreceptors are more sensitive to rapid changes in pressure Receptors show adaptation – If the new pressure is sustained, the reflex becomes partially reset after a few hours Baroreceptors The baroreflex responds rapidly to changes in MAP and pulse baroreceptors Caro erves pressure in the short-term n tid s inus communicates via sympathetic/parasympathetic NS ve n er tic r Ao Effectors for control of cardiac output Heart rate and contractility (i.e., heart) Venous return (i.e., veins) Blood volume (i.e., kidneys) arterioles SA node medulla & heart muscle Effectors for control of total peripheral resistance (arterioles) SNS/PNS veins kidney Determinants of mean arterial BP Baroreceptor reflex Arterial tone Total peripheral resistance Afterload (force against which the heart pumps) CO x TPR = BP Baroreceptor ANS Heart rate x Stroke volume = Cardiac output reflex (Starling) ANS CVP-Preload Cardiac contractility (degree of cardiac stretch) Venous tone Venous capacitance Blood volume Baroreceptor reflex  Blood volume Negative Restoration of MAP feedback  MAP CO  Firing of  TPR baroreceptors SV HR b1  Venous return medulla Constriction  Parasympathetic of veins a1 + drive  Sympathetic drive a1 Systemic arteriole constriction NOTE: These changes go in the opposite direction in response to an increase in MAP Other Determinants of mean arterial BP – RAAS system Baroreceptor reflex Renin-angiotensin-aldosterone Arterial tone Total peripheral resistance system = RAAS Afterload (force against which the heart pumps) CO x TPR = BP Baroreceptor RAAS + ANS Heart rate x Stroke volume = Cardiac output reflex (Starling) ANS CVP-Preload Cardiac contractility (degree of cardiac stretch) + RAAS ↑ or ↓ Na+ Venous tone Venous capacitance Blood volume excretion kidneys Regulation of mean arterial blood pressure by the renin angiotensin aldosterone system Various stimuli Angiotensinogen (in blood) Renin (enzyme) from JG cells In kidney Angiotensin I (in blood) Angiotensin Converting Renal H2O Enzyme (ACE) reabsorption Angiotensin II (in blood) Vasoconstriction ADH Release Aldosterone Renal Na+ (from adrenal gland) reabsorption Long-term determinants of mean arterial BP Stable body Na+ content Arterial tone Total peripheral resistance Stable extracellular fluid volume Afterload (force against which the heart pumps) CO x TPR = BP Stable plasma/blood volume Heart rate x Stroke volume = Cardiac output (Starling) natriuresis Stable mean arterial blood pressure Pressure CVP-Preload Cardiac contractility (degree of cardiac stretch) RAAS ↑ or ↓ Na+ Venous tone Venous capacitance Blood volume kidneys excretion Pressure Naturesis ↑ Renal Perfusion ↑ Medullary blood ↓Ang II flow Pressure ↑Nitric Oxide ↑Prostaglandins ↑Renal kinins ↑ Renal interstitial hydrostatic pressure ↑ Mean Arterial Pressure ↓ Tubular sodium reabsorption ↑ Water excretion ↑ Sodium excretion (Diuresis) (Naturesis)  Long-term regulation of arterial blood pressure Stabilisation of BP in the long term is mainly due to maintenance of a constant ECF volume (ECF includes the plasma) This ECF volume is controlled by the Na2+ concentration of the ECF. Diseases of civilisation, such as hypertension and type 2 diabetes, may be explained by the thrifty genotype hypothesis Evolution has shaped organisms to crave and conserve nutritional resources while times are good, so they can survive through periods of scarcity. Humanity emerged in the hot and dry savannahs of Africa, where the ability to conserve salt (Na+) was necessary. For most people salt is never scarce, but we are still programmed by evolution to crave it. Most of us are continually eating too much salt. Regulation of long-term blood ↓ Na+ consumption pressure ↓ plasma [Na+] Blood volume changes in response to variable ingestion of salt and/or ↓ plasma osmolality water. reverses ↓ ADH release What would happen if you started ↓ water consumption eating very little salt? ↑ water excretion ↓ blood volume blood volume ↓ BP increases RAAS ↑ ↓ natriuresis Pressure natriuresis ↓ ↓ diuresis Effects of blood volume on Na+ excretion ↓ CVP ↓Blood volume ↓ atrial stretch ↓ activation of ↓BP cardiopulmonary receptors ↑SNS outflow ↓ Atrial natriuretic ↑RAAS to the kidney peptide (ANP) release ↓ Pressure natriuresis ↓Renal Na+ excretion restores Is renal excretion of Na+ the only factor which stabilised BP over the long term? Maybe not. Activation of the SNS can increase blood pressure even when the kidneys are denervated 1. Changes in BP don’t always affect Na+ excretion 2. Changes in Na+ excretion can occur without changes in BP 3. The baroreceptor reflex doesn’t turn off completely after a short time Alternative models of BP control, which propose that regulation of vascular tone (e.g., by the SNS) can also contribute to the long term control of BP. Why does this matter? If Na+ excretion is the only determinant of blood pressure, vasodilators shouldn’t be able to lower blood pressure. However, many effective anti-hypertensive drugs are vasodilators.  Learning outcomes  Briefly explain the key mechanisms governing pressure and flow waves in the arteries system  Describe the mechanism of the baroreceptor reflex, and explain its role in the short-term stabilisation of mean arterial blood pressure  Explain how the kidneys regulate mean blood pressure in the long term by controlling Na+ excretion and extracellular fluid volume.  Describe pressure natriuresis and its role in controlling renal excretion of Na+ and water Recommended reading Silverthorne’s Human Physiology: An Integrated Approach, Global Edition, pp 517-521, 528-530, 665-677 Ward’s Physiology at a Glance Chapters 25 and 38 See also Kidney Function IV lecture by Dr Sarah Thomas in Semester B