Transcript Cardiovascular hormones - Department of Library Services

Cardiovascular hormones
Dr J Ker
• Previous lecture: Mechanical aspects,
blood pressure, formulas…
• Now: Hormonal aspects of the
cardiovascular system
Hormonal interactions:
• Heart----brain
• Brain----heart
• Heart----kidney
• Kidney----heart
Heart---brain:
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Group of natriuretic peptides.
ANP, BNP,C-type
Produced by atrial and ventricular myocardium
Produced in response to stretch, increased enddiastolic pressure
Physiological action: Acts as diuretic—natriuretic
peptide
Decrease blood pressure
Clinical application:
• Diagnostic test for cardiac failure
• Opioid peptides
• Produced by heart—ventricular
myocardium.
• Released during myocyte damage: MI
• Acts as natural pain killers
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Angiotensin II.
Physiological action of angiotensin II:
Vasoconstriction: Increase blood pressure
Vasoconstriction of efferent arteriole in kidney: Increase
intraglomerular pressure
Stimulate vascular growth—mitogen
Reabsorption of sodium in proximal tubule
Stimulate production of aldosterone
Increase sympathetic outflow
Stimulate thirst: hypothalamus
Heart---kidney:
• Natriuretic peptides
• Angiotensin II
Kidney---heart:
• Renin-angiotensin-aldosterone system:
• 2 pathways to angiotensin II
production:
• Via renin-angiotensin-aldosterone sustem
• Via so-called non-ACE pathways.
Renin-angiotensin-aldosterone
system:
• Renin: An enzyme produced by kidney:
juxtaglomerular apparatus.
• In response to: decrease in BP, increase
in filtered sodium load.
• Acts on: Angiotensinogen. A protein
produced by liver. Converts to
angiotensin I.
Angiotensin converting enzyme
(ACE):
• Enzyme, produced by endothelium (especially
pulmonary endothelium)
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Converts Angiotensin I to angiotensin II
3 Genotypes:
ACE-D/D
ACE-I/I
ACE-D/I
Non-ACE pathways:
• Various tissues: Heart, blood vessels,
uterus, kidney:
• Able to convert AT II to AT II without
renin
• Eg chymase
• Also: Can produce AT II directly
• Clinical implication: Drugs: ACE-inhibitors
vs AT-II receptor blockers
AT-II receptors:
• > 7 known
• 2 of clinical importance:
• AT-II type I: Classic actions of angiotensin II
• AT-II type II: Importance in CV-development,
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fetus
AT-II blockers: Blocks only AT-II type I receptors
Aldosterone:
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Hormone produced by adrenal cortex
Steroid hormone
Production is stimulated by AT-II
Physiological action:
Reabsorption of sodium, excretion of potassium
and hydrogen:
Kidney: Cortical collecting duct
Sweat, saliva, gastric juice
Conn syndrome:
• Tumor of adrenal cortex, producing excess
aldosterone:
• Hypertension
• Hypokalaemia
• Alkalosis
Brain---heart:
• Sympathetic nervous system:
• Acts on adrenal medulla: Increase
catecholamines, increase in stroke volume
and heart rate
• Acts on kidney: Increase production of
renin
• Other hormones: Growth hormone:
Trophic effect on heart
Endothelium:
• An organ
• 2`nd largest organ in body
• Largest=fat
• Why an organ: It produces hormones
• Weight of endothelium +/- 1.5 kg
• Endothelium: 4 groups of functions:
• Maintains balance between
vasoconstriction and vasodilatation:
• NO, bradykinin, ANP: Vasodilatation
• AT-II, thromboxane A2: Vasoconstriction
• Maintains balance between
thrombosis and fibrinolysis:
• Tissue factor (factor III): Thrombosis
• T-PA: Tissue type plasminogen activator:
Fibrinolysis
• Maintains balance between
inflammation and anti-inflammatory
mechanisms.
• Endothelium produces adhesion
molecules: ICAM, PECAM, VECAM etc
• Maintains balance between growth
and apoptosis:
• Angiotensin II: A growth factor, mitogen,
causes hypertrophy of arterial intima