HORMONE AND CARDIOVASCULAR

SYSTEM

dr. Sri Lestari Sulistyo Rini, MSc

 Introduction
 Various hormones, chemicals
 Start at a low pace,
 Have long-lasting influences on cardiovascular
function.
 Hormones and chemicals are classified into two
groups
 Vasoconstrictors
 Vasodilators
 Posterior Pituitary Hormone
• Anti diuretic hormone or VASOPRESSIN
• Stimulate the contraction of smooth muscle in the
arterioles, small blood vessels that connect the arteries
to capillaries
– blood pressure rises

• Oxytocin
– induces natriuresis and causes a fall in mean
arterial pressure
– oxytocin triggers ANP release in vivo
 Vasopressin
 Also called antidiuretic hormone (ADH),
 formed in the hypothalamus (mainly)
 secreted through the posterior pituitary gland.
 even more powerful than angiotensin as a
vasoconstrictor.
 The high concentration of vasopressin
during hemorrhage can raise the arterial
pressure as much as 40 to 60 mmHg.
 Vasopressin
 The amount of endogenous vasopressin in the
circulation of normal individuals does not
normally affect blood pressure.
 it does not increase blood pressure when small
doses are injected in vivo
 Acts on the brain to cause a decrease in
cardiac output.
 (in the area of postrema, one of the
circumventricular organs)
 Acts on the kidney
 Anterior Pituitary Hormone

• GROWTH HORMONE
– The physiological nature of cardiac growth is
accounted by
• the increment in cardiomyocyte size occurs prevalently
at expense of the short axis.
– This is the basis for the concentric pattern of left ventricular
(LV) hypertrophy,
• improved contractility and relaxation, and a favorable
energetic setting;
• the capillary density of the myocardial tissue
 Anterior Pituitary Hormone

– balanced growth of cardiomyocytes and

nonmyocyte elements, which accounts for the
lack of interstitial fibrosis
– myocardial energetics and mechanics are not
perturbed
– the growth response is not associated with the
gene re-programming that characterizes
pathologic cardiac hypertrophy and heart
failure
 Anterior Pituitary Hormone
• Prolactin
– Increasing blood pressure
– In collaboration with noradrenalin
• INSULIN :
– insulin and leptin cooperate in the modulation
of vascular tone
• through enhancement of endothelial NO
release.
• A major impact on the regulation of the
cardiovascular system, characterized by
endothelial NO dysfunction and metabolic
disorders,
–such as arterial hypertension.
• SEX HORMONE

– The greater incidence of hypertension and

coronary artery disease in men and
postmenopausal women compared with
premenopausal women has been related, in
part, to gender differences in vascular tone and
possible vascular protective effects of the female
sex hormones estrogen and progesterone
• Estrogen, progesterone, and testosterone receptors
have been identified in blood vessels and
cardiomyocytes of human and other mammals and
have been localized in the plasmalemma, cytosol,
and nuclear compartments of various vascular cells,
including the endothelium and the smooth muscle.
• The sex hormone-induced stimulation of the
endothelium-dependent mechanisms of vascular
relaxation and inhibition of the mechanisms of
vascular smooth muscle contraction
• ESTROGEN
– Inflammation plays an important role in the
response to endoluminal vascular injury. Estrogen
(17beta-estradiol, E2) inhibits neointima
formation in animal models
– E2 may limit the neointimal response to
endoluminal vascular injury, at least in part, by
limiting leukocyte entry from
adventitial/periadventitial tissues into injured
vessels early in the injury response.
• Estrogen also has anti-clot function
Avoid the formation of thrombus and thus can
slow down the hardening of arteries
• Microvascular endothelial cells -- cells in the
lining of the smallest blood vessels -- produce
estrogen and express estrogen receptor
• Estrogen may derive part of its known
cardiovascular protective effect by increasing
production of nitric oxide in microvascular
endothelial cells
• Decreasing of Estrogen may induce arrhythmia
 Progesterone
• postmenopausal women, higher blood levels
of progesterone are associated with less of an
increase in blood pressure and less blood
vessel constriction in response to angiotensin
II, one of the naturally occurring substances in
the body which causes the blood vessels to
constrict
• TESTOSTERONE
– Male sex is an acknowledged risk factor for
many forms of cardiovascular disease, and
vascular disease prevalence patterns appear to
be different in men versus women. The vascular
properties of the principal mammalian
androgen, testosterone, are complex and linked
to dose, duration of exposure, presence of
underlying vascular disease, and, possibly,
biological sex
– lower levels of testosterone in men are
associated with higher blood pressure, left
ventricular mass, and left ventricular
hypertrophy.
– Data from isolated vessels and animal models
suggest that pharmacological doses of
testosterone, or its potent intracellular
metabolite dehydrotestosterone, produce
vasodilatation.
– Testosterone's endothelium-dependent effects
are likely mediated at least in part through nitric
oxide (NO) elaboration, whereas mechanisms of
endothelium-independent effects involve 1 or
more types of smooth muscle ion conductance
channels
– Clinical studies indicate that, in men, androgen
replacement may provide beneficial effects when
coronary artery disease is present
• High-dose testosterone significantly increased
the circulating plasma testosterone
concentration, and was associated with a
dramatic increase in brachial artery
vasodilatation
• Males with CAD and associated low serum
levels of testosterone, is the population in
which testosterone replacement therapy may
be clinically advantageous

– in women, testosterone may augment existing

hypertension, increase risk for cardiovascular
events, or promote atherogenesis.
– there is a relationship between endogenous
androgen levels and arterial stiffness in older men.
• Minor endocrine gland
– Atriopeptin (atrialnatriuretic factor)
• Helps maintain homoestatic balance of fluids,
electrolytes.
• Lowers blood pressure, blood volume
• Target areas are blood vessel, kidneys and adrenal
glands
 Effects of Thyroid Hormones on the
Cardiovascular System

• Increase heart rate

• Increase force of cardiac contractions
• Increase stroke volume
• Increase Cardiac output
• Up-regulate catecholamine receptors
• Thyroid have chronotropic effect (increase
number and affinity of  adrenergic receptors)
and inotropic effect (enhance response to
circulating catecholamines and increase
proportion of  myosin heavy chain) on the
heart as a target tissue
 Autonomic Pacemaker
Regulation
• Sympathetic and parasympathetic stimulation:
– greatest at SA node (heart rate)
• Membrane potential of pacemaker cells:lower than
other cardiac cells
• Rate of spontaneous depolarization depends on:
– resting membrane potential
– rate of depolarization
• ACh (parasympathetic stimulation):
– slows the heart
• NE (sympathetic stimulation):
– speeds the heart
 Hormonal Effects on Heart Rate
• Increase heart rate (by sympathetic
stimulation of SA node):
– epinephrine (E)
– norepinephrine (NE)
– thyroid hormone
 Vasoconstrictors and Vasodilators

 Vasoconstrictors
 Epinephrine and Norepinephrine
 Angiotensin II
 Vasopressin
 Vasodilators
 EDRF (NO)
 Epinephrine and Norepinephrine

 The adrenal medulla secrete both epinephrine

(80%) and norepinephrine (20%)
 carried by blood flow to everywhere in the
body.
 In the blood, only a little norepinephrine
comes form the endings of the adrenergic
fibers.
 Adrenergic receptors

α1 receptor on vessels Vasoconstriction

Epinephrine
β1 receptor on heart Positive effect
β2 receptor on vessels Vasodilation
Norepinephrine
(skeletal muscle and liver)
 Effect

 On heart in vitro (contractility and

automaticity).
 both increase the force and rate of
contraction of the isolated heart.
 mediated by β1 receptors.
Effect  On peripheral resistance.
 Norepinephrine produces
vasoconstriction in most if
not all organs via α1
receptors
 epinephrine dilates the blood
vessels in skeletal muscle
and the liver via β2
receptors.
 overbalances the
vasoconstriction produced by
epinephrine elsewhere, and
the total peripheral resistance
drops.
 Effect
 On heart in vivo (heart rate and cardiac
output).
 When norepinephrine is infused introvenously
 the systolic and diastolic blood pressure rise.
 The hypertension stimulates the carotid and
aortic baroreceptors,
 producing reflex bradycardia that override the
direct cardioacceleratory effect of
norepinephrine.
 Consequently, the heart rate and cardiac out falls.
 Effect
 On heart in vivo
 Epinephrine causes a
widening of the pulse
pressure
 baroreceptor stimulation is
insufficient to obscure the
direct effect of the
hormone on the heart,
 cardiac rate and output
increase.
 Angiotensin II
 very potent vasoconstrictor
 formed in the plasma through a chain reaction.
 The chain is triggered by a substance, renin, released form
kidneys.
 Renin is released from kidneys in response to renal ischemia,
which may be due to a fall in blood pressure.
Effect of Angiotensin II

 powerful constrictor
 release aldosterone from the
adrenal cortex
 acts on the brain to create the
sensation of thirst.
 inhibit the baroreceotor reflex
and
 increase the release of
norepinephrine from the
sympathetic postganglionic
fiber.
Endothelium – Derived Relaxing Factor
 Metabolism
 Effect of NO
 Relax the vascular smooth muscle directly
 Mediate vascular dilator effect of some hormones
and transmitters (Ach, bradykinin, VIP, substance P)
 Inhibit the tonic excitation of some neurons in the
vasomotor centre.
 Inhibit the norepinephrine release from the
sympathetic postganglionic fiber.

 One or more of these effects are

physiological.
 Long-Term mechanism for Arterial
Pressure Regulation
Renal –body Fluid Mechanism
Terima kasih