Presentation on theme: "Regulation of Blood Flow and Pressure. Outline Local control of blood flow. Nervous control of blood flow. Cardiovascular changes in exercise. Reflexes."— Presentation transcript:
Regulation of Blood Flow and Pressure
Outline Local control of blood flow. Nervous control of blood flow. Cardiovascular changes in exercise. Reflexes that control arterial pressure. Long-term regulation of arterial pressure by the kidneys. Practice CV questions for the 1 st couple of lectures.
Learning Objectives Know the mechanisms that control local blood flow, both acute and long ‐ term. Know the substances that mediatehumoral vasoconstriction andvasodilation. Understand how the autonomic nervous system regulates circulation. Know how the cardiovascular system changes during exercise. Understand the reflex mechanisms that control arterial pressure. Know how the kidneys function in the long ‐ term regulation of arterial pressure. Know how the renin ‐ angiotensin system regulates arterial pressure. Know the time courses for the mechanisms that control arterial pressure.
Local Control of Blood Flow Each tissue regulates its own local blood flow based on its needs, which include: - Deliver O 2, glucose, amino acids, and fatty acids. - Remove CO 2 and H + ions. - Maintain proper [ion]s. - Transport hormones and other nutrients.
Normal Blood Flow to Organs and Tissues
Changes in Blood Flow During Exercise
Local and Humoral Control of Blood Flow Local Control - Acute control rapid (seconds to minutes) changes in vasodilation or vasoconstriction. - Long-term local control - change in the physical size or numbers of blood vessels, occurs over days to months. Humoral Control - Substances secreted or absorbed into the body fluids that cause vasoconstriction or vasodilation, e.g., hormones, peptides and ions.
Relationship Between Metabolism and Blood Flow
Vascular Theory for Local Control of Blood Flow Vasodilator Theory - As metabolism and O 2 consumption incr ease, vasodilators are produced and released fr om the tissue. These act on precapillary sphincters, m etarterioles and arterioles. Some vasodilators are: Adenosine, CO 2, ATP co mpounds, histamine, K + i ons and H + ions. Many think adenosine is the most important
Nutrient-Lack Theory for Local Control of Blood Flow Nutrient Lack or O 2 Lack Theory – O 2 and other nutrients are required to keep smooth muscle contracted, so when these area low, the precapillary sphincter s, metarterioles and arte rioles dilate. In contrast, when nutrien ts (O 2 ) are high, smooth mus cle contracts and the precapillary sphincters,me tarterioles and arterioles constrict. Both the Vasodilation and Nutrient-Lack Theories likely contribute to local control of blood flow.
Reactive and Active Hyperemia These are examples of vasodilation and nutrient-lack theory (metabolic control). Reactive hyperemia is an increase of blood flow after the flow to a tissue has been blocked (think of nutrient-lack theory). Active hyperemia is an increase in blood flow in response to increased activity.
Myogenic Theory Another example of local control of blood flow. Arterial Pressure causes increased blood flow less than a min BF normalizes even though arterial Pressure stays high. The Myogenic theory for this is that stretching of small blood vessels causes the smooth muscle of the vessel wall to contract. Conversely, at low pressures, the muscles relax.
Nitric Oxide Increased blood flow in arterioles causes the release of NO (endothelium relaxing factor). This causes small arteries upstream to relax.
Long-term Local Regulation of Blood Flow Works by changing the vascularity (number and size of arterioles and capillaries) to match the needs of a tissue. Degree ofvascularity is determined by the maximum blood flow needed. Important peptides that increase vascularity are vascular endothelial growth factor (VEGF), fibroblast growth factor, and angiogenin.
Humoral Control of Circulation Controlled by substances secreted or absorbed into the body fluids. - Vasoconstriction - Vasodilation
Humoral Vasoconstriction Sympathetic and adrenal release of norepinephrine and epinephrine. Angiotensin II (more on this when we discuss renal mechanisms). Vasopressin (ADH) – very potent vasoconstrictor secreted by the posterior pituitary. Also increases renal H 2 O reabsorption. Endothelin A – released from damaged vessels.
HumoralVasodilation Bradykinin – powerful arteriolar dilation and increased permeability of the capillaries. Histamine – released from damaged or inflamed tissue; also during an allergic reaction. Also cases arteriolar dilation and increased permeability of the capillaries.
Ions and Other Chemical Factors Ca 2+ ions – vasoconstriction. K + ions – vasodilation. Mg 2+ ions – vasodilation (often inhibits the actions of Ca 2+ ions). H + ions – increase cause vasodilation, decrease causes constriction. Anions – acetate and citrate cause vasodilation. CO 2 – vasodilation, particularly important in the brain.
Nervous Regulation of Circulation More global control, such as: - Redistribution of blood flow - Regulating heart rate - Rapid control of arterial pressure Autonomic nervous system provides the main nervous control of CV function. - For circulation, sympathetic is the main regulator.
Rapid Increase in Arterial Pressure 3 Ways in which sympathetic nervous system increases arterial pressure: 1.Constrict arterioles. 2.Constrict veins and other large vessels. 3.Increase heart rate and contractility.
Sympathetic Neurotransmitters and Hormones Sympathetic nerve endings release almost entirely norepinephrine (alpha adrenergic receptors). Sympathetic stimulate the adrenal medulla to release norepinephrine and epinephrine. In some tissues (skeletal muscle), epinephrine causes vasodilation through beta adrenergic receptors.
Cardiovascular Changes During Mild Exercise
Reflex Mechanisms Controlling Arterial Pressure Baroreceptors – stretch receptors in large systemic arteries (particularly the carotid a.) and aorta. Carotid and aortic chemoreceptors – respond to low O 2. CNS ischemic responses.
Baroreceptors Regulate arterial pressure by increasing firing when stretched (high pressure) and conversely, slowing firing when relaxed (low pressure).
Baroreceptors During High Arterial Pressure
Baroreceptors During Low Arterial Pressure
Baroreceptor Reflex An increase in pressure causes the receptors (aortic arch and carotid sinuses) to stretch, increasing frequency of APs. Baroreceptors send APs to vasomotor control and cardiac control centers in the medulla. Baroreceptor reflex activated with changes in BP. More sensitive to decrease in pressure and sudden changes in pressure.
Baroreceptor Reflex (continued)
Chemoreceptors Very similar to baroreceptors, except that they respond to chemical changes. - At low O 2 or high CO 2 or H + (as occurs during low pressure because of decreased blood flow), chemoreceptors are stimulated. - Chemoreceptors excite the vasomotor center, which elevates the arterial pressure.
CNS Ischemic Response If blood flow is decreased to the vasomotor center in the lower brainstem and CO 2 accumulates, the CNS ischemic response is initiated. Very strong sympathetic stimulator causing major vasoconstriction and cardiac acceleration. Sometimes called the “last ditch stand”.
Long-term Regulation of Arterial Pressure by the Kidneys The kidneys control the level of H 2 O and NaCl in the body, thus controlling the volume of the extracellular fluid and blood. By controlling blood volume, the kidneys control arterial pressure. Increased arterial pressure results in increased renal output of H 2 O (pressure diuresis) and salt (pressure natiuresis).
Renal Urinary Output Curve
Renin-Angiotensin System in Maintaining Arterial Pressure During Salt Intake
Summary of Arterial Pressure Regulation
Regulation of Cardiovascular System Overview-
Control of Cardiovascular Function – Hormones Decreased Blood Pressure
Control of Cardiovascular Function – Hormones Increased Blood Pressure