Physiology of cardiovascular system III

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 Endocrine control of cardiovascular function

• Hormones – specially synthesized chemical

substances, that act extracellulary by binding to specific
receptors of target cells.
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Hormonal regulation of cardiovascular
system
pressor systems depressor systems
– ADH (AVP) • Natrium-uretic
– RAAS peptides
– Catecholamines
• urocortins
• Hemopoetins

Local systems
(tissue hormones):

Kinin-kallikrein system
Eikosanoids
NO
Endothelins
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 Vasopressin (ADH)

• Arterial pressure (arterial baroreceptor

reflex) & ↓blood volume (cardiopulmonary
reflex) cause the release of ADH.
• Increased ADH secretion causes increased
fluid reabsorption by the kidneys, helping to
restore blood pressure & blood volume
toward normal.

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Systemic effects of vasopressin (ADH)

Vasopressin (Antidiuretic hormon)

V1 receptors V2 receptors
Smooth muscle of
Epithelium of
arteriols Retention of sodium
vasoconstriction Collecting ducts
(increased permeability and and water
reabsorbtion)

Blood vessel peripheral

resistance Circulatory volume

Arterial pressure

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Osmoreceptors of hypothalamus and
ADH

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Role of ADH in osmolarity control

ADH

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 ADH in presure and circulatory blood
volume control
+ Paraventricular nuclei +
of hypothalamus

Decreased arterial
pressure Increased plazma
Cardiovascular center osmolarity

Reduced baroreceptor
afferentation
Simpathetic ADH
Heart afferentation

Reduced
volumoreceptor Peripheral resistance +
afferentation ANP increases

Arterial pressure
Decreased blood
Samazināts asiņu _ increases
volume
tilpums

kidneys
increased Na and water reabsorbtion
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Renin – Angeotensin – Aldesteron System

renin ACE AT - ases

AT- gen AT I AT II xxx

Secretion of Water and Na+

vasoconstriction
aldesterone reabsorbtion

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RAAS in control of arterial pressure and blood volume

Asins spiediens
un osmolaritāte pazemināti

AT II

+
vasoconstriction
+ +
stimulates JGA

decreased

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Renin-Angiotensin-Aldosterone pathway

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Catecholamines – chemical compounds
derived from the amino
acid tyrosine.
Hormones and transmitters.

Degradation time – few minutes,

Adrenaline
enzymes – (epinephrine)
Monoamine oxidase (MAO)
katehol-O-methil transferase (COMT)

Dopamine

Tyrosine Noradrenaline
(norepinephrine)

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 Adrenal medullary hormones

• Sympathetic stimulation of adrenal medulla cause the

release of norepinephrine (20%) & epinephrine (80%).
• NE causes constriction of essentially all blood vessels &
cause increased activity of heart.
• Epinephrine causes almost same effect but with following
difference
– It has a greater effect on cardiac stimulation than done
by NE
– It causes only weak constriction of smooth muscles of
blood vessels compared to NE
• NE greatly ↑peripheral resistance & elevates BP, whereas
epinephrine raises BP to lesser extent but increases
cardiac output more

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 Reception of Catecholamines

Receptor type Agonist affinity Secondary messengers

α1 NA > A Gq→ + PLC → IP3 → Cai↑

α2 A > NA Gi → - adenilcyclase → cAMF↑

β1,2,3 NA > A Gs → + adenilcyclase →cAMF↓

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Adrenergic receptors in different vascular beds

vasoconstriction vasodilatation

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Reception of Catecholamines

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Regulation of beta-adrenoreceptors
Signal Transduction Pathways for Catecholamine Receptors
Ronald S. Duman and Eric J. Nestler, 2000.

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Reception of Catecholamines

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 Natriuretic peptides

• Atrial natriuretic peptides (ANP); secreted by

atrium cells as a response to stretch

• Brain Natriuretic Peptide (BNP); secreted by

ventricle cells as a response to stretch

• C-type natriuretic peptide (CNP)– local signaling

brain and blood vessels

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 Effects of Natriuretic peptides

• Cardiovascular system
– dilate blood vessels (arterioles veins)
– decreases preload

• Kidneys
– Increase blood supply
– increase filtration rate
– decrease effects of AT II and ADH in collecting ducts

• CNS
– decrease thirst un appetite of salt

• Endocrine system
– depresses secretion of vasopressin in hypothalamus
– depresses renin secretion in JGA macula densa
– depresses secretion of aldesteron in zona glomeruloza 23
 Urocortins
• Urocortins: corticotropin-releasing factor (CRF) -like peptides;
• ~ 40 amino acids-residuals
• Types: Ucn-I, Ucn-II, Ucn-III
• Produced by myocardium cells during physical stress
• Receptors: CRF-R2; G-protein receptors; expressed in myocardium
cells, blood vessel endothelial cells, smooth muscle cells, CNS cells
• Regulatory effects: vasodilatation,
decrease of arterial pressure,
positive inotropic and chronotropic effects,
an increase of coronary blood flow

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