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A sustained elevation of systemic arterial blood pressure Diagnosed when the average of two or more BP measurements made on two or more consecutive clinical visits documents a diastolic pressure of 90 mmHg or greater or a systolic pressure of 140 mmHg or greater
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A sustained elevation of systemic arterial blood pressure Diagnosed when the average of two or more BP measurements made on two or more consecutive clinical visits documents a diastolic pressure of 90 mmHg or greater or a systolic pressure of 140 mmHg or greater
120-139 80-89
Stage 1 hypertension
140-159 90-99
Stage 2 hypertension
≥ 160 ≥ 100
Hypertension is caused by
↑in CO, TPR or both CO = SV X HR TPR = blood viscosity, blood vessel diameter
Primary/Essential/Idiopathic hypertension
No known cause Affects 90%-95% of hypertensive patients
Secondary hypertension
Caused by altered haemodynamics associated with the a primary disease Affects only 5%-8% of hypertensives
Isolated systolic hypertension
elevated systolic pressure accompanied by normal diastolic pressure Manifestation of ↑CO or rigidity of aorta or both
Two important regulatory systems
Sympathetic nervous system, Renin-angiotensin-aldosterone system
Sympathetic nervous system
Beta 1 adrenoceptors on heart Alpha 1 adrenoceptors on the blood vessels
Renin-angiotensin-aldosterone system
Release Ang II Causes hypertension via direct vasoconstriction and facilitates noradrenaline release from sympathetic nerve terminals; Stimulates aldosterone biosynthesis and secretion from the zona glomerulosa of the adrenal cortex; Results in renal vasoconstriction, increases sodium reabsorption from proximal tubular, and inhibits renin secretion; Increases secretion of vasopressin and ACTH from the central nervous system
Angiotensin II leads to
↑ TPR, Renal salt retention, Vascular remodeling, ↑ Thrombosis, ↑ Platelet aggregation, ↑ Growth , ↑ smooth muscle and migration, ↑ Endothelial dysfunction
Antihypertensive drugs
Beta adrenoceptor antagonists Alpha adrenoceptor antagonists Ganglionic blockers Centrally acting antihypertensives Drugs affecting the RAAS (ACE inhibitors Ang II receptor antagonist) Vasodilators
Beta-adrenoceptor antagonists (β-blockers) Mechanism of action in hypertension
reduction of heart rate and myocardial contractility, which decrease cardiac output blockade of renal juxtaglomerular β1-adrenoceptors, which reduces renin secretion peripheral vasodilation, but only with compounds that have a hybrid action, such as carvedilol, nebivolol or pindolol
Alpha-adrenoceptor antagonists (α-blockers)
Blockade of postsynaptic α1-adrenoceptors lowers blood pressure by: reducing tone in arteriolar resistance vessels dilating venous capacitance vessels, which reduces venous return and, therefore, cardiac output Reflex tachycardia with non selective α blockers
Unwanted effects
Postural hypotension caused by venous pooling; this can be particularly troublesome after the first dose Lethargy, headache, dizziness Nausea, rhinitis Urinary frequency or incontinence Palpitations from reflex cardiac stimulation
Ganglion blockers (e.g.trimetaphan)
Ganglion blockers are obsolete except for certain highly specialised indications such as during surgery Mechanism of action Competitive blockade of nicotinic (N1) receptors at autonomic ganglia reduces activity in both the sympathetic and parasympathetic nervous systems Arterial and venous dilation both contribute to the hypotensive effects
Centrally acting antihypertensives Selective imidazoline receptor agonists e.g. moxonidine Mechanism of action
Imidazoline I1 receptors are important for the regulation of sympathetic drive They are concentrated in the rostral ventrolateral medulla, a part of the brainstem vasomotor centre Increased neuronal activity in this area, either through baroreceptor stimulation or by direct stimulation of I1 receptors, will decrease sympathetic outflow The result is a fall in blood pressure with no reflex tachycardia. Unlike other centrally acting drugs (clonidine and methyldopa), moxonidine has little affinity for α2-adrenoceptors
Centrally acting α2-adrenoceptor agonists e.g. methyldopa, clonidine
Unwanted effects limit the use of the centrally acting α2-adrenoceptor agonists, although methyldopa is a drug of choice in the treatment of hypertension in pregnancy
Mechanisms of action Centrally acting α2-adrenoceptor agonists
Activates the α2-adrenoceptor at presynaptic autoreceptors in the central nervous system reduce central sympathetic nervous outflow and increase vagal outflow from the vasomotor centre This reduces both peripheral arterial and venous tone Methyldopa acts as a 'false substrate' in the biosynthetic pathway for noradrenaline to produce α-methylnoradrenaline which is a potent α2-adrenoceptor agonist Clonidine is a direct-acting α2-adrenoceptor agonist that is also an agonist at imidazoline I1 receptors
Unwanted effects
Sympathetic blockade: failure of ejaculation, and postural or exertional hypotension unopposed parasympathetic action: diarrhoea Dry mouth CNS effects: sedation and drowsiness; depression Fluid retention Sudden withdrawal of clonidine can produce severe rebound hypertension with tachycardia, sweating and anxiety
Angiotensin-converting enzyme (ACE) inhibitors
Captopril Lisinopril Ramipril Enalapril Fosinopril
Angiotensin II receptor antagonists
Candesartan Losartan Valsartan Telmisartan Irbesartan
ACE inhibitors
Competitive inhibition of ACE reduces generation of angiotensin II and consequently reduces the release of aldosterone There is no reflex tachycardia, probably because of stimulation of the vagus nerve and reduction in the potentiation of the sympathetic nervous system caused by angiotensin II ACE also degrades vasodilator kinins Increased kinins or vasodilator prostaglandins and nitric oxide in the vascular wall may contribute to the hypotensive actions of ACE inhibitors
Unwanted effects
Persistent dry cough Postural hypotension Renal impairment, especially in people with severe bilateral renal artery stenosis Disturbance of taste, nausea, vomiting, dyspepsia or bowel disturbance Rashes
Clinical uses of ACE inhibitors
Treatment of hypertension Treatment of heart failure Secondary prevention after myocardial infarction Diabetic nephropathy in insulin-dependent diabetes
Angiotensin II receptor antagonists
The angiotensin II receptor antagonists are selective for the AT1 receptor subtype found in the heart, blood vessels, kidney, adrenal cortex, lung and brain Actions of angiotensin II via this receptor include vasoconstriction, cell growth and proliferation, aldosterone release, sympathetic stimulation, salt and water retention, and inhibition of renin release They have less effect at the AT2 receptor subtype, which inhibits vascular growth, vasodilates, and increases both renal Na+ excretion and renin release. The overall effect of drugs like candesartan show similarities to those produced by ACE inhibitors, except that kinin degradation is unaffected and inhibition of the effects of angiotensin II on the AT1 receptor is more complete
Unwanted effects
Drugs in this class are usually well tolerated. Their major advantage over ACE inhibitors is the low incidence of cough. Angioedema is also rare headache dizzines arthralgia or myalgia fatigue
Vasodilators in hypertension
Nitrovasodilators Calcium channel blockers Potassium channel openers
Potassium channel openers Minoxidil
It relaxes smooth muscle by selectively increasing the membrane permeability to K+, hyperpolarising the membrane, switching off voltage-dependent Ca2+ channels and inhibiting action potential generation It is used as a drug of last resort in treating severe hypertension unresponsive to other drugs. The adverse effects include hirsutism, and marked water and sodium retention (usually used with a loop diuretics e.g. frusemide)
Potassium channel openers Hydralazine
Hydralazine mainly acts on arteries and arterioles, causing a fall in blood pressure and reflex tachycardia. Its mechanism of action is not entirely clear. It is used to treat patients with hypertension and heart failure

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