Hypertension
`BY: PROF. SONALI MANWATKAR
Hypertension
Definition: the force exerted by the blood against the walls of the blood
vessels
▪ Adequate to maintain tissue perfusion during activity and rest
▪ Arterial blood pressure: primary function of cardiac output and systemic
vascular resistance
▪ Arterial BP = Cardiac Output (CO) x Systemic vascular resistance (SVR)
▪ Cardiac Output = stroke volume x beats per min
▪ Systemic vascular resistance = force opposing the movement of blood within the
blood vessels
Blood pressure (BP) is a measure of the force that
the circulating blood exerts against the arterial
wall.
1.SYSTOLIC PRESSURE •
▪ Systolic pressure is the maximum pressure exerted
by the blood against the arterial walls.
▪ It results when the ventricles contract ( systole )
2.DIASTOLIC PRESSURE •
▪ Diastolic Pressure is the lowest pressure in the
artery.
▪ It result when the ventricles are relaxed (diastole )
▪ Normal BP: <120/<80
▪ Prehypertension: 120-139/80-89
▪ Hypertension stage1 140-159/90-99
▪ Hypertension stage 2 160/100
▪ Emergency >210/>120
Pathophysiology
Mechanism that regulate BP
Sympathetic Nervous System
Vascular Endothelium
Renal System
Endocrine System
Mechanism that regulate BP
▪ Sympathetic Nervous System (SNS) –
norepinephrine released from sympathetic nerve endings - to
receptors alpha1, alpha2, beta 1 & beta2
▪ Reacts within seconds
▪ Increases Heart Rate - chronotropic
▪ Increased cardiac contractility - inotropic
▪ Produces widespread vasoconstriction in peripheral arterioles
▪ Promotes release of renin from the kidney
Sympathetic Nervous System (SNS)–
▪ Sympathetic Vasomotor Center – located in the medulla – interacts with many areas of
the brain to maintain BP within normal range under various conditions
▪ Exercise – changes to meet oxygen demand
▪ Postural Changes – peripheral vasoconstriction
▪ Baroreceptors: specialized nerve cells the carotid arteries and the aortic arch
▪ Sensitive to BP changes:
▪ Increase: Inhibits SNS – peripheral vessel dilation. Decreased heart rate, and decreased
contractility of the heart + increased parasympathetic activity (vagus nerve) decreased heart
rate
▪ Decrease: Activates SNS – peripheral vessel constriction, increased heart rate, and
increased contractility of the heart
❑Vascular Endothelium
❑ Single cell layer that lines the blood vessels
❑Produce vasoactive substances:
▪ EDRF Endothelium-derive relaxing factor –
▪ Helps maintain low arterial tone at rest
▪ Inhibits growth of the smooth muscle layer
▪ Inhibits platelet aggregation
▪ Vasodilation – prostacyclin
▪ Endothelin (ET) potent vasoconstrictor
Endothelial dysfunction may contribute to atherosclerosis &
primary hypertension
❑Renal System
❑ Control Na+ excretion & extracellular fluid volume
❑ Renal - Renin-angiotensin-aldosterone
❑ Renin converts angiotensinogen to angiotensin I
❑ Angiotensin-converting enzyme (ACE) converts I into angiotsensin II
❑ Immediate: Vasoconstrictor – increased systemic vascular resistance
❑ Prolonged: Stimulates the adrenal cortex to secret Aldosterone – Na+ and Water retention
❑ Renal Medulla - Prostaglandins - vasodilator effect
❑Endocrine System
❑ Stimulates the SNS with
❑ Epinephrine – increases HR and contractility
❑ Activates B2-adrenergic receptors in peripheral arterioles of skeletal muscle = vasodilation
❑ Activates A1-adrenergic receptors in peripheral arterioles of skin and kidneys = vasoconstriction
❑ Adrenal Cortex – Aldosterone – stimulates kidneys to retain Na+
❑ Increased Na+ stimulates posterior pituitary – ADH – reabsorbs ECF/water
✓Increased Aldosterone =
✓Increases sodium reabsorption =
✓Increases water reabsorption =
✓Increases blood volume =
✓Increases cardiac output
Regulatory mechanisms in the health person function in response to the
demands on the body
▪ When Hypertension develops, one or more of these mechanisms are
defective
▪ Sympathetic Nervous System
▪ Vascular Endothelium
▪ Renal System
▪ Endocrine System
ANTIHYPERTENSIVE DRUG CLASSES
Antihypertensive drug classes are as follows:
▪ ACE inhibitors
▪ Angiotensin II receptor antagonists
▪ Diuretics
▪ Calcium channel blockers
▪ β-blockers
▪ α-blockers
▪ α2-blockers
▪ Renin inhibitors
▪ Vasodilators
ACE inhibitors
▪ ACE inhibitors diminishes blood pressure and oxygen demand by dilating blood vessels.
▪ These drugs principle inhibit an angiotensin converting enzyme which is an integral
part of RAAS
Angiotensin II Receptor Antagonists
▪ Angiotensin II receptor antagonist are also known as ARBs or angiotensin receptor
blockers .They are used in place of ACE inhibitors particularly where the persistent
dry cough has become unbearable for the patients.
e.g. Candesartan, lrbesartan, Losartan, Telmisartan
Diuretics
▪ Diuretics are among the most commonly
prescribed drugs, and play an important
role in the treatment of heart failure and
hypertension.
▪ They exert most of their therapeutic
effects through inhibiting the
reabsorption of sodium at different sites
along the nephron of the kidney.
▪ Diminished reabsorption of sodium
results in increased urinary loss of both
sodium and water, leading to a reduction
in plasma volume, and a reduction of
blood pressure.
▪ Thiazide diuretics also exert an additional
vasodilator effect on arterial smooth
muscle by a still poorly understood
mechanism.
Calcium channel blocker
Calcium channel blocker- MOA
▪ Calcium channel blockers (CCBs) are drugs that
bind to and block mainly the L-type calcium
channels present on cardiac and vascular smooth
muscle cells (SMCs).
▪ They prevent calcium ions from entering into
vascular smooth muscles, which results in muscle
relaxation and vasodilation and leads to a
decrease in vascular resistance and, consequently,
diminished arterial BP .
▪ Each subclass of calcium channel blocking agent
binds at a specific location. For example,
dihydropyridines (e.g., amlodipine and nifedipine)
exert vascular selectivity, verapamil has cardiac
selectivity, and diltiazem can act in both the heart
and blood vessels presents the mechanism of
CCB’s action.
