Transcript Regulation of Blood Flow and Pressure

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 1st couple of
lectures.
Learning Objectives
• Know the mechanisms that control local blood flow, both
acute and long‐term.
• Know the substances that mediate humoral
vasoconstriction and vasodilation.
• 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 O2, glucose, amino acids, and fatty
acids.
- Remove CO2 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 O2 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, CO2, 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 O2
Lack Theory – O2 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
(O2) are high, smooth mus
cle contracts and the
precapillary sphincters,
metarterioles and
Both the
Vasodilation and Nutrient-Lack Theories likely contribute to local control
arterioles
constrict.
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 of vascularity 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 H2O reabsorption.
• Endothelin A – released from damaged vessels.
Humoral Vasodilation
• 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
• 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.
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.
Sympathetic Control
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
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 O2.
• 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 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.
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”.
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).
Renal Urinary Output Curve
Renin-Angiotensin System
Renin-Angiotensin System in Maintaining
Arterial Pressure During Salt Intake
Summary of Arterial Pressure Regulation
Regulation of Cardiovascular System
Overview-
Regulation of Cardiovascular System
Overview-
Control of Cardiovascular Function – Hormones
Decreased Blood Pressure
Control of Cardiovascular Function – Hormones
Increased Blood Pressure
Cardiovascular
Practice Questions
1. Which valve on the left side of the heart opens after
isovolumic contraction?
2. If the R-R intervaal in an ECG is 0.40 sec, what is the
patient’s BPM? What is the R-R interval in a normal heart?
3. If the SA node discharges at 0.00 sec in a normal heart,
when will the AP arrive at the Purkinje fibers?
4. If the QRS voltage is 2 mV in lead I and 5 mV in lead II,
what is the QRS voltage in lead III?
5. Which phase of the cardiac cycle follows immediately
after the T wave?
6. The ECG of a patient in the ER has 80 P waves/min and 45
QRS waves/ min. Explain briefly what could cause this.
7. In the peripheral vascular system, if the conductance is 0.5
(PRU)-1 and the ΔP is 100 mm Hg, what is the blood flow
(use the correct units)?