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Regulation of
Cardiovascular Activities
Qiang XIA (夏强), PhD
Department of Physiology
Zhejiang University School of Medicine
Tel: 88206417, 88208252
Email: [email protected]
Nervous Regulation
Innervation of the heart
• Cardiac sympathetic nerve
• Cardiac vagus nerve
1.
2.
3.
4.
5.
6.
起源origin
节前纤维preganglionic fiber
外周神经节ganglion
节后纤维postganglionic fiber
支配distribution
递质neurotransmitter
Cardiac sympathetic actions
• Positive chronotropic effect正性变时作用
• Positive dromotropic effect正性变传导作用
• Positive inotropic effect正性变力作用
Cardiac mechanisms of norepinephrine
Mechanisms of norepinephrine
—increase Na+ & Ca2+ permeability
• If , phase 4 spontaneous depolarization,
autorhythmicity 
• Ca2+ influx (ICa,L) , phase 0 amplitude & velocity ,
conductivity 
• Ca2+ influx (ICa,L) , Ca2+ release , [Ca2+ ]i ,
contractility 
(CICR)
Asymmetrical
innervation of
sympathetic nerve
Cardiac parasympathetic actions
• Negative chronotropic effect负性变时作用
• Negative dromotropic effect负性变传导作用
• Negative inotropic effect负性变力作用
Cardiac mechanisms of acetylcholine
Mechanisms of acetylcholine
—increase K+ & decrease Ca2+ permeability
• K+ outward , |MRP| , phase 4 spontaneous
depolarization , autorhythmicity 
• Inhibition of Ca2+ channel, phase 0 amplitude &
velocity , conductivity 
• Ca2+ influx , [Ca2+ ]i , contractility 
Cardiac effect of
parasympathetic
stimulation
Vagal Maneuvers
• Valsalva maneuver
– A maneuver in which a person tries to exhale forcibly with
a closed glottis (the windpipe) so that no air exits through
the mouth or nose as, for example, in strenuous coughing,
straining during a bowel movement, or lifting a heavy
weight. The Valsalva maneuver impedes the return of
venous blood to the heart.
– Named for Antonio Maria Valsalva, a renowned Italian
anatomist, pathologist, physician, and surgeon (1666-1723)
who first described the maneuver.
Physiological response in
Valsalva maneuver
• The normal physiological response consists of 4
phases
Physiological response in
Valsalva maneuver
• The normal physiological response consists of 4 phases
– Initial pressure rise: On application of expiratory force, pressure rises inside the chest forcing
blood out of the pulmonary circulation into the left atrium. This causes a mild rise in stroke
volume.
– Reduced venous return and compensation : Return of systemic blood to the heart is impeded
by the pressure inside the chest. The output of the heart is reduced and stroke volume falls. This
occurs from 5 to about 14 seconds in the illustration. The fall in stroke volume reflexively causes
blood vessels to constrict with some rise in pressure (15 to 20 seconds). This compensation can be
quite marked with pressure returning to near or even above normal, but the cardiac output and
blood flow to the body remains low. During this time the pulse rate increases.
– Pressure release: The pressure on the chest is released, allowing the pulmonary vessels and the
aorta to re-expand causing a further initial slight fall in stroke volume (20 to 23 seconds) due to
decreased left ventricular return and increased aortic volume, respectively. Venous blood can once
more enter the chest and the heart, cardiac output begins to increase.
– Return of cardiac output: Blood return to the heart is enhanced by the effect of entry of blood
which had been dammed back, causing a rapid increase in cardiac output (24 seconds on). The
stroke volume usually rises above normal before returning to a normal level. With return of blood
pressure, the pulse rate returns towards normal.
Interaction of
sympathetic and
parasympathetic
nerves
Predominance of autonomic nerves
Tonus紧张
• Cardiac vagal tone心迷走紧张
• Cardiac sympathetic tone心交感紧张
Innervation of the blood vessels
• Vasoconstrictor nerve缩血管神经
– Sympathetic vasoconstrictor nerve交感缩血管神
经
• Vasodilator nerve舒血管神经
– Sympathetic vasodilator nerve交感舒血管神经
– Parasympathetic vasodilator nerve副交感舒血管
神经
– Dorsal root vasodilator nerve脊髓背根舒血管神
经
Cardiovascular Center
A collection of functionally similar neurons that
help to regulate HR, SV, and blood vessel tone
Vasomotor center
Located bilaterally mainly in the reticular
substance of the medulla and of the lower third
of the pons
– Vasoconstrictor area
– Vasodilator area
– Cardioinhibitor area – dorsal nuclei of the
vagus nerves and ambiguous nucleus
– Sensory area – tractus solitarius
Vasomotor center
Higher cardiovascular centers
– Reticular substance
of the pons
– Mesencephalon
– Diencephalon
– Hypothalamus
– Cerebral cortex
– Cerebellum
Baroreceptor Reflexes
• Arterial baroreceptors
– Carotid sinus receptor
– Aortic arch receptor
• Afferent nerves (Buffer nerves)
• Cardiovascular center: medulla
• Efferent nerves: cardiac sympathetic nerve,
sympathetic constrictor nerve, vagus nerve
• Effector: heart & blood vessels
Baroreceptor neurons
function as sensors in
the homeostatic
maintenance of MAP
by constantly
monitoring pressure
in the aortic arch and
carotid sinuses.
Characteristics of baroreceptors:
Sensitive to stretching of the vessel walls
Proportional firing rate to increased
stretching
Responding to pressures ranging from 60180 mmHg
Receptors within the aortic arch are less
sensitive than the carotid sinus receptors
The action potential frequency in baroreceptor neurons is
represented here as being directly proportional to MAP.
i.e., MAP is
above
homeostatic
set point
i.e., reduce cardiac output
Baroreceptor neurons deliver MAP information to the
medulla oblongata’s cardiovascular control center (CVCC);
the CVCC determines autonomic output to the heart.
Reflex pathway
Typical carotid sinus reflex
Physiological Significance
Maintaining relatively
constant arterial
pressure, reducing the
variation in arterial
pressure
Humoral Regulation
• Vasoconstrictor agents
• Vasodilator agents
Renin-angiotensin system
Juxtaglomerular
cell
Renin
Physiological effects of angiotensin II
– Constricts resistance vessels
– Acts upon the adrenal cortex to release aldosterone
– Stimulates the release of vasopressin
– Facilitates norepinephrine release from sympathetic nerve
endings
– Stimulates thirst centers within the brain
Epinephrine & Norepinephrine
• Sources
Epinephrine---adrenal medulla
Norepinephrine----
adrenal medulla
sympathetic nerves
Catecholamines
Norepinephrine
Epinephrine
Effects
Receptor
Heart
Vessels
Epinephrine
Norepinephrine
a-adrenoceptor
++
+++
b-adrenoceptor
++
+
heart rate
+
cardiac output
+++
+ (in vitro) － (in vivo)
±
constriction (skin, visceral) +
+++
－
+++
relaxation (SM, liver)
total peripheral resistance ±
Blood pressure systolic
+++
+++
+++
diastolic
±
++
MAP
+
++
Clinical application
positive inotropic
agent
pressor agent
Vasopressin (antidiuretic hormone, ADH)
Endothelium-derived vasoactive substances
•Vasodilator factors
PGI2--prostacyclin
EDRF, NO--endothelium-derived relaxing factor, nitric oxide
EDHF--endothelium-dependent hyperpolarizing factor
•Vasoconstrictor factors
Endothelin
Atrial natriuretic peptide (ANP)
•Produces natriuresis and diuresis
•Decreases renin release
•Reduces total peripheral resistance via vasodilatation
•Decreases heart rate, cardiac output
Autoregulation
Definition:
Intrinsic ability of an organ to maintain a constant
blood flow despite changes in perfusion pressure,
independent of any neural or humoral influences
Myogenic mechanism
• The myogenic mechanism is how arteries and arterioles react
to an increase or decrease of blood pressure to keep the blood
flow within the blood vessel constant
• The smooth muscle of the blood vessels reacts to the stretching
of the muscle by opening ion channels, which cause the muscle
to depolarize, leading to muscle contraction. This significantly
reduces the volume of blood able to pass through the lumen,
which reduces blood flow through the blood vessel.
Alternatively when the smooth muscle in the blood vessel
relaxes, the ion channels close, resulting in vasodilation of the
blood vessel; this increases the rate of flow through the lumen.
From: http://www.umm.uni-heidelberg.de/inst/cbtm/kphys/research-schubert.html
Universität Heidelberg > Fakultäten > Medizinische Fakultät Mannheim > CBTM: Kardiovaskuläre Physiologie >
From: AJP - Heart October 2008 vol. 295 no. 4 H1505-H1513
Metabolic mechanism
• Any intervention that results in an inadequate
oxygen (nutrient) supply for the metabolic
requirements of the tissues results in the formation
of vasodilator substances which increase blood
flow to the tissues
Metabolic mechanism
Metarteriole
Precapillary
Sphincter
Capillary
Relaxation of smooth muscle
Lack of oxygen?
Formation of vasodilators?
Combination of both??
Increased Blood
Flow
Metabolic mechanism
• Hypoxia
• Tissue metabolites and ions
– Adenosine
– Potassium ions
– Carbon dioxide
– Hydrogen ion
– Lactic acid
– Inorganic phosphate
• Mary rose quickly from her bed to answer the
door. This change in body position resulted in:
– A. Increased dilation of peripheral blood
vessels
– B. Decreased firing of the carotid baroreceptors
– C. Increased parasympathetic stimulation of the
SA node
– D. Unchanged venous return
• Total peripheral resistance decreases in a runner
during strenuous exercise due to:
– A. increased parasympathetic nervous
stimulation of the working skeletal muscle
– B. increased vasoconstriction of the large veins
of the body
– C. increased metabolites in the IS surrounding
the muscle
• If two liters of blood are lost from the body,
arterial hypotension occurs. This can lead to the
movement of fluid from the tissues into the
capillaries in response to:
– A. Higher capillary hydrostatic pressure
– B. Lower capillary hydrostatic pressure
– C. Higher capillary oncotic pressure
– D. Lower capillary oncotic pressure
• Does MAP (increase, decrease or remain
unchanged) during anaerobic exercise such as
weight lifting?
– A. Increases
– B. Decreases
– C. Remains unchanged
The End.