Endocrinology of Blood Pressure Control
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Transcript of Endocrinology of Blood Pressure Control
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ENDOCRINOLOGY OF BLOOD
PRESSURE CONTROL
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The control of blood pressure (BP) is complex,
involving neural, cardiac, hormonal and many
other mechanisms.
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BP is dependent upon cardiac output and
peripheral resistance.
Although cardiac output can be increased in
endocrine disease (e.g. hyperthyroidism), the
main role of hormonal mechanisms is control
of peripheral resistance and of circulating
blood volume
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The oral contraceptive pill is a common
endocrine cause of mild hypertension.
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Endocrine causes of hypertension
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The renin-angiotensin-aldosterone
axis
Angiotensinogen, an alpha2-globulin of
hepatic origin, circulates in plasma. The
enzyme, renin, is secreted by the kidney in
response to decreased renal perfusion
pressure or flow; it cleaves the decapeptide
angiotensin I from angiotensinogen.
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Angiotensin I is inactive but is further cleaved
by angiotensin-converting enzyme (ACE;
present in lung and vascular endothelium)
into the active peptide, angiotensin II, which
has two major actions (mediated by two types
of receptor, AT1 and AT2).
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The AT1 subtype which is found in the heart,
blood vessels, kidney, adrenal cortex, lung and
brain mediates the vasoconstrictor effect. AT2
is probably involved in vascular growth.
Angiotension II:
causes rapid, powerful vasoconstriction
stimulates the adrenal zona glomerulosa toincrease aldosterone production (over hours or
days).
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As BP increases and sodium is retained, the
stimuli to renin secretion are reduced.
Dietary sodium excess also suppresses renin
secretion, whereas sodium deprivation or
urinary sodium loss will increase it.
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The renin-angiotensin system can be blocked
at several points with renin inhibitors,
angiotensin-converting enzyme inhibitors
(ACEI) and angiotensin II receptor antagonists
(A-IIRA).
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The latter two are useful agents in treatment
of hypertension and heart failure but have
differences in action: ACEIs also block kinin
production while A-IIRAs are specific for the
AT-II receptor
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Atrial and brain natriuretic
factors/peptides (ANP and BNP)
Atrial natriuretic peptides, a family of varying
length forms, are secreted from atrial granules
in response to atrial stretch. They produce
marked effects on the kidney, increasingsodium and water excretion and glomerular
filtration rate and lowering BP, plasma renin
activity and plasma aldosterone
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Brain natriuretic peptide is found in the
ventricle as well as the brain and has
moderate sequence homology with ANP;
normally its circulating level is much less thanfor ANP but may exceed it in congestive
cardiac failure
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ANP and BNP appear to play a significant role
in cardiovascular and fluid homeostasis, but
there is no evidence of primary defects in
their secretion causing disease
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RENIN (AND ANGIOTENSIN)
DEPENDENT HYPERTENSION
Many forms of unilateral and bilateral renal
diseases are associated with hypertension.
The classic example is renal artery stenosis:
the major hypertensive effects of this andother situations such as renin-secreting
tumours are directly or indirectly due to
angiotensin II.
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Angiotensin II receptor antagonists (e.g.
losartan, valsartan, candesartan and
irbesartan) are effective in hypertension and
congestive cardiac failure, similar toangiotensin-converting enzyme inhibitors
(ACEI). They produce much the same clinical
effects, though with fewer side-effects (e.g. nocough and less hyperkalaemia).
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THE ADRENAL MEDULLA
The major catecholamines, noradrenaline
(norepinephrine) and adrenaline
(epinephrine) are produced in the adrenal
medulla, although most noradrenaline isderived from sympathetic neuronal release.
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Phaeochromocytoma
Phaeochromocytomas, tumours of the
sympathetic nervous system, are very rare
(less than 1 in 1000 cases of hypertension).
Ninety per cent arise in the adrenal, while
10% occur elsewhere in the sympathetic chain
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Pathology
Oval groups of cells occur in clusters and stain
for chromogranin A. Twenty-five percent are
multiple and 10% malignant, the latter being
more frequent in the extra-adrenal tumours.
Malignancy cannot be determined on simple
histological examination alone.
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Clinical features
Symptoms Anxiety or panic attacks
Palpitations
Tremor
Sweating Headache
Flushing
Nausea and/or vomiting
Weight loss
Constipation or diarrhoea
Raynaud's phenomenon
Chest pain
Polyuria/nocturia
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Signs
Hypertension - intermittent or constant
Tachycardia plus arrhythmias
Bradycardia
Orthostatic hypotension
Pallor or flushing
Glycosuria
Fever (Signs of hypertensive damage)
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The clinical features are those of
catecholamine excess and are frequently, but
not necessarily, intermittent. The diagnosis
should particularly be considered whencardiovascular instability has been
demonstrated, and in severe hypertension in
pregnancy.
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Diagnosis
Measurement of urinary catecholamines and
metabolites
Resting plasma catecholamines
CT scans
MRI
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Treatment
Tumours should be removed if this is possible;
5-year survival is about 95% when not
malignant. Medical preoperative and
perioperative treatment is vital and includescomplete alpha- and beta-blockade with
phenoxybenzamine (20-80 mg daily initially in
divided doses), then propranolol (120-240 mgdaily), plus transfusion of whole blood to re-
expand the contracted plasma volume