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Regulation of Blood Flow and Pressure

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Presentation on theme: "Regulation of Blood Flow and Pressure"— Presentation transcript:

1 Regulation of Blood Flow and Pressure

2 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 1st couple of lectures.

3 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.

4 Local Control of Blood Flow
Each tissue regulates its own local blood flow based on its needs, which include: - Deliver O2, glucose, amino acids, and fatty acids. - Remove CO2 and H+ ions. - Maintain proper [ion]s. - Transport hormones and other nutrients.

5 Normal Blood Flow to Organs and Tissues

6 Changes in Blood Flow During Exercise

7 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.

8 Relationship Between Metabolism and Blood Flow

9 Vascular Theory for Local Control of Blood Flow
Vasodilator  Theory - As   metabolism and  O2  consumption  increase,  vasodilators are produced  and  released  from the  tissue.  These  act  on   precapillary  sphincters,   metarterioles  and  arterioles.   Some  vasodilators  are: Adenosine,  CO2,  ATP   compounds,  histamine,  K+  ions  and  H+ ions. Many  think  adenosine  is  the  most important

10 Nutrient-Lack Theory for Local Control of Blood Flow
Nutrient Lack or O2 Lack   Theory – O2 and other   nutrients are required to keep smooth muscle  contracted,  so when  these  area  low, the   precapillary  sphincters,   metarterioles  and  arterioles  dilate. In  contrast,  when  nutrients (O2)  are high,  smooth muscle contracts  and the precapillary  sphincters,metarterioles and arterioles constrict. Both the Vasodilation and Nutrient-Lack Theories likely contribute to local control of blood flow.

11 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.

12 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.

13 Nitric Oxide Increased blood flow in arterioles causes the release of NO (endothelium relaxing factor). This causes small arteries upstream to relax.

14 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.

15 Humoral Control of Circulation
Controlled by substances secreted or absorbed into the body fluids. - Vasoconstriction - Vasodilation

16 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 H2O reabsorption. Endothelin A – released from damaged vessels.

17 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.

18 Ions and Other Chemical Factors
Ca2+ ions – vasoconstriction. K+ ions – vasodilation. Mg2+ ions – vasodilation (often inhibits the actions of Ca2+ ions). H+ ions – increase cause vasodilation, decrease causes constriction. Anions – acetate and citrate cause vasodilation. CO2 – vasodilation, particularly important in the brain.

19 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.

20 Sympathetic Control

21 Rapid Increase in Arterial Pressure
3 Ways in which sympathetic nervous system increases arterial pressure: Constrict arterioles. Constrict veins and other large vessels. Increase heart rate and contractility.

22 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.

23 Cardiovascular Changes During Mild Exercise

24 Cardiovascular Changes During Mild Exercise

25 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 O2. CNS ischemic responses.

26 Baroreceptors Regulate arterial pressure by increasing firing when stretched (high pressure) and conversely, slowing firing when relaxed (low pressure).

27 Baroreceptors During High Arterial Pressure

28 Baroreceptors During Low Arterial Pressure

29 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.

30 Baroreceptor Reflex (continued)

31 Chemoreceptors Very similar to baroreceptors, except that they respond to chemical changes. - At low O2 or high CO2 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.

32 CNS Ischemic Response If blood flow is decreased to the vasomotor center in the lower brainstem and CO2 accumulates, the CNS ischemic response is initiated. Very strong sympathetic stimulator causing major vasoconstriction and cardiac acceleration. Sometimes called the “last ditch stand”.

33 Long-term Regulation of Arterial Pressure by the Kidneys
The kidneys control the level of H2O 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 H2O (pressure diuresis) and salt (pressure natiuresis).

34 Renal Urinary Output Curve

35 Renin-Angiotensin System

36 Renin-Angiotensin System in Maintaining Arterial Pressure During Salt Intake

37 Summary of Arterial Pressure Regulation

38 Regulation of Cardiovascular System Overview-

39 Regulation of Cardiovascular System Overview-

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42 Control of Cardiovascular Function – Hormones Decreased Blood Pressure

43 Control of Cardiovascular Function – Hormones Increased Blood Pressure


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