Control of Blood Pressure & Blood Flow PDF

Human Anatomy & Physiology II (PSIO202) Control of Blood Pressure & Blood Flow  Objectives 1. Describe and diagram the baroreceptor and chemoreceptor reflex pathways, starting with the stimulus and ending with the physiological result. 2. Describe how hormones...

Human Anatomy & Physiology II (PSIO202) Control of Blood Pressure & Blood Flow  Objectives 1. Describe and diagram the baroreceptor and chemoreceptor reflex pathways, starting with the stimulus and ending with the physiological result. 2. Describe how hormones can either decrease or increase blood pressure. 3. Compare and contrast neural, humoral and local regulation of blood vessel diameter and blood flow.  Levels of Control of Blood Pressure and Blood Flow A. Neural Control – Cardiovascular reflexes B. Hormonal Control – Catecholamines, ADH, angiotensin II, & aldosterone – ANP – Histamine C. Local Control RECALL: Mechanisms of Homeostasis: stimulus Receptors - sense changes in the internal or external environment Control center - processes information gathered from receptors and sends a response to the effectors Effector - adjusts the regulated parameter response RECALL: Mechanisms of Homeostasis: When a change in a variable occurs in a closed system with feedback circuits, the system responds. Two types of feedback circuits: 1. Negative feedback loops changes in monitored parameter cause control mechanism to work to counteract further changes of the parameter in the same direction. Result: changes are triggered to reverse the detected change in the parameter. Result: change triggers reversal of detected change 2. Positive feedback loops AKA “cumulative causation” changes in monitored parameter cause control mechanism to work to cause/amplify changes of the parameter in the same direction. Result: changes are triggered to amplify the detected change in the parameter. Result: change triggers amplification of detected change  A. Neural Control: The Cardiovascular (CV) Center is located in the medulla oblongata includes a collection of gray matter regions (nuclei): – 2 cardiac centers * – the vasomotor center helps regulate HR, SV, and blood vessel diameter receives input from higher brain centers (the cerebral cortex, the limbic system, and the hypothalamus) & from peripheral afferent nerve fibers (baroreceptors, chemoreceptors, and proprioceptors)  A. Neural Control: The CV Center: Input & Output INPUT TO CV CENTER (increased frequency of sensory nerve impulses) From higher brain centers: cerebral cortex, limbic system, and hypothalamus From proprioceptors: monitor joint movements From baroreceptors: monitor blood pressure From chemoreceptors: monitor blood acidity (H+), CO2, and O2 OUTPUT TO EFFECTORS (increased frequency of motor nerve impulses) Vagus nerves Heart: decreased rate (parasympathetic) Cardiac accelerator nerves Heart: increased rate and contractility (sympathetic) Vasomotor nerves Blood vessels: vasoconstriction (sympathetic) Cardiovascular (CV) center  A. Neural Control: Nuclei of the CV Center The CV center is composed of three major functional regions: 1. Cardioacceleratory Center: a collection of sympathetic neurons that increase HR and contractility 2. Cardioinhibitory Center: collection of parasympathetic neurons that decrease heart rate 3. Vasomotor Center: a collection of “vasomotor neurons” that regulate blood vessel diameter via sympathetic nerves that synapse on arteriolar smooth muscle and cause vasoconstriction.  A. Neural Control: Cardiovascular Reflexes Cardiovascular reflexes are produced by afferent signaling of: – Baroreceptors* – Chemoreceptors* – Proprioceptors *by far the most important receptors in CV regulation.  Chemoreceptors located in carotid sinus and in walls of ascending aorta in the carotid sinus signal the medulla via cranial nerve IX in the aortic bodies signal the medulla via cranial nerve X respond to increased hydrogen ion content, increased CO2, and most strongly to hypoxia activate the sympathetic division, leading to increased HR, SV, and vasoconstriction  Baroreceptors High pressure baroreceptors – located in the carotid sinus and aortic arch – enter the CV center via cranial nerves IX & X, respectively Low pressure baroreceptors – located in the walls of the right atrium and vena cavae – enter the CV center via cranial nerve X  Baroreceptor‐Initiation of CV Reflexes Baroreceptors Glossopharyngeal nerves in carotid sinus (cranial nerve IX) Cardiovascular Baroreceptors (CV) center in arch of aorta Vagus nerves Medulla oblongata SA node (cranial nerve X, parasympathetic) AV node Ventricular myocardium Spinal cord Cardiac accelerator nerve (sympathetic) Key: Sensory (afferent) neurons Sympathetic trunk Motor (efferent) neurons ganglion  Baroreceptor‐ Initiated Reflex in Response to Decreasing Blood Pressure  Baroreceptor‐ Initiated Reflex in Response to Elevated Blood Pressure  Figure 20.16 At rest Moderate exercise Total cardiac output 5 L/min. Total cardiac output 17.5 L/min. Other Coronary Other Coronary 350 750 mL/min. 400 200 mL/min. mL/min. (4.3%) mL/min. Cutaneous (4.0%) (7.0%) 1,900 mL/min. (2.3%) Cutaneous (10.9%) 300 mL/min. Muscular (6.0%) Cerebral 1,000 750 mL/min. mL/min. (4.3%) (20.0%) Cerebral 700 Renal mL/min. 600 mL/min. Muscular Digestive (3.4%) (14.0%) 1,350 12,500 Renal mL/min. mL/min. 1,100 (27.0%) Digestive (71.4%) mL/min. 600 mL/min. (22.0%) (3.4%) (a) (b) B. Hormonal Control of Blood Pressure 1. Catecholamines (Epinephrine & NE) – cause arteriole & vein vasoconstriction, and increased HR & SV. 2. Antidiuretic hormone (ADH) – causes intense vasoconstriction and decreased water loss in cases of extremely low BP. 3. Angiotensin II – causes intense vasoconstriction when renal perfusion is inadequate (and BP is too low). 4. Aldosterone – causes water retention and increases blood volume, when BP is too low. 5. Atrial natriuretic peptide—causes vasodilation & water loss when BP is too high. 6. Histamine – causes vasodilation (& increased blood flow).  Hormonal Control of Blood Pressure: Catecholamines Catecholamines (NE and Epinephrine) circulate, and bind directly to cardiac muscle fibers and blood vessel smooth muscle cells The effect is an increase in HR and SV, and constriction of veins and arterioles IMP NOTE: arteries supplying the brain and heart have little smooth muscle and are not subject to vasoconstriction by the sympathetic division or catecholamines; these vessels autoregulate  Hormonal Control of Blood Pressure: Anti‐diuretic hormone (ADH) ADH is produced by the hypothalamus and released from the posterior pituitary when blood loss is severe, and blood pressure is reduced. ADH causes: Kidneys retain more water, which – widespread vasoconstriction decreases urine output – decreased water loss (from skin & urine) Arterioles constrict, which increases blood pressure Sudoriferous (sweat) glands decrease water loss by perspiration from skin  Hormonal Control of Blood Pressure: Angiotensin II one of the most powerful vasoconstrictor substances known usually acts on all arterioles simultaneously when it is released into the blood result is an increase in vascular resistance (when blood pressure is too low) Low BP causes a cascade of effects (the RAA System)… Low BP causes the release of renin by the kidney; angiotensinogen (released by the liver) converts renin into angiotensin I, and the lungs convert AT I into AT II by angiotensin converting enzyme (ACE), which is located in the endothelial cells of the lung.  Hormonal Control of Blood Pressure: 1 Dehydration, Na+ deficiency, or hemorrhage Angiotensin II 2 Decrease in blood volume 14 Blood pressure increases until it returns to normal 4 3 Decrease in Juxtaglomerular blood volume cells of kidneys 15 Vasoconstriction of arterioles 5 Increased renin Liver 6 Angiotensinogen 8 7 Increased angiotensin I ACE 9 Increased angiotensin II Lungs (ACE = angiotensin converting enzyme)  Hormonal Control of Blood Pressure: Aldosterone Angiotensin also controls Blood pressure aldosterone secretion. increases until it returns to normal When AT II levels increase (see previous slide), Vasoconstriction Increased blood aldosterone is secreted by of arterioles volume the adrenal cortex. Adrenal cortex Increased Aldosterone increases salt K+ in extracellular and water reabsorption; fluid this raises blood volume, In kidneys, increased Na+ and water reabsorption which raises BP. Increased Increased and increased secretion angiotensin II aldosterone of K+ and H+ into urine Powerfully stimulates the thirst center as well.  Hormonal Control of Blood Pressure: Atrial natriuretic peptide (ANP) & Histamine ANP is released by cells of the atria when BP is high. causes vasodilation and promotes loss of water and salt by the kidneys… collectively, this reduces blood volume and vasoconstriction, and acts to lower blood pressure Histamine is released by mast cells. causes vasodilation by relaxing blood vessel smooth muscle especially important in increasing the rate of blood flow to inflamed or damaged tissue  C. Local Control of Blood Pressure: Overall Regulation of “Organ Blood Flow” Neural regulation of flow refers to changes in flow due to vasoconstriction Humoral flow control refers to changes in vessel diameter due to circulating hormones BUT Major regulatory factor is tissue metabolic activity Metabolic, or “local” regulation, is blood vessel dilation due to substances released by tissue cells Control of Blood Pressure: Integrated Responses to Low Blood Pressure Blood volume and blood pressure Receptors Baroreceptors in Baroreceptors kidneys (juxta‐ in arch of aorta Increased glomerular and carotid secretion cells) sinus Inputs of renin Decreased rate of nerve impulses Control center Control center Control center Return to Hypothalamus & homeostasis when Cardiovascular center responses bring Angiotensinogen posterior pituitary in medulla oblongata blood volume and in blood blood pressure back to normal Angiotensin II in blood ADH Increased sympathetic stimulation and hormones from adrenal medulla Outputs ADH in blood Effectors Adrenal cortex Kidneys Blood Heart rate & liberates conserve vessels contractility aldosterone salt & water constrict increase Increased  systemic vascular resistance Increased blood blood volume pressure  PRACTICE: Map out how BP homeostasis is achieved using the framework below. stimulus Receptors - sense changes in the internal or external environment Control center - processes information gathered from receptors and sends a response to the effectors Effector - adjusts the regulated parameter response