Hypertension is defined as a systolic blood pressure greater than or equal to 140 mm Hg or a diastolic blood pressure greater than or equal to 90 mm Hg. Primary (essential) hypertension accounts for 90-95% of cases and has no identifiable cause, while secondary hypertension results from an underlying condition such as renal or endocrine disease. Hypertension develops due to increased total peripheral resistance caused by vasoconstriction from activation of the renin-angiotensin-aldosterone system and sympathetic nervous system, as well as other factors affecting vascular tone and sodium balance.

1. Hypertension
Hypertension

2. Defined as persistently elevated arterial blood pressure (BP).
Elevated systemic blood pressure is usually defined as
 systolic reading greater than or equal to 140 mm Hg
 diastolic reading greater than or equal to 90 mmHg
Classification of hypertension
Primary Secondary
No specific resulting from an identifiable cause, such as renal disease,
Cause Endocrine disease, vascular causes.
can Be identified

3. Etiology
Hypertension is classified as either primary (essential) hypertension or
secondary hypertension according to its cause.
Primary (essential) hypertension in which no specific cause can be
identified.
90–95% of cases of hypertension are "primary hypertension’’.
Predisposing factors for primary hypertension
a. Family history of essential hypertension, stroke, and premature
cardiac
disease.
b. Patient history of intermittent blood pressure elevation

4. d. Obesity
e. Smoking
f. Stress
g. Excess Consumption of Sodium Chloride & saturated fat
h. Certain segments of the population are ‘salt sensitive’
because their blood pressure is affected by salt consumption
i. Sedentary life style
j. Diabetes Mellitus
k. Hyperlipidemia

5. Secondary Hypertension
Secondary hypertension (5-10 %) resulting from an identifiable
cause, such
as renal disease, Endocrine disease, vascular causes.
Certain drugs, either directly or indirectly, can cause hypertension
or exacerbate hypertension by increasing BP.
Causes of secondary hypertension
 Renal disease
 Endocrine disease
Steroid excess – Hyperaldosteronism (conn’s syndrome)
hyperglucocorticoidism (cushing’s syndrome)

6. Others –preeclampsia
 Vascular causes
Renal artery stenosis
Coarctation of the arota
 Drugs
Sympathomimetic amines
Oestrogens (combined oral contraceptive pills)
Ciclosporins
NSAIDs
Erythropoietin
Steroids

7. Pathophysiology
 In general, normal blood pressure is regulated by two
haemodynamic forces- cardiac output and total peripheral vascular
resistance. Increased blood pressure can result from increased
cardiac output and/or increased total peripheral resistance
 In most hypertensive individual cardiac output is not increased and
high
blood pressure arises as a result of increased total peripheral
resistance caused by vasoconstriction of small arterioles.
 Cardiac output is determined by stroke volume and heart rate ;
stroke volume is related to myocardial contractility and to the size
of the vascular compartment. Peripheral resistance is determined

8. BP
CO SVR
HR SV Direct innervations Circulating regulators Local
regulators
PSNS α1- AR Catecholamine NO
SNS AT-II Prostacyclin
Catecholamines AT-II
Contractility Preload o2
SNS H+
Catecholamine Adenosine
Intravascular volume
Venous tone
Thirst
SNS Na /H2o retention
Catecholamine SNS
Aldosterone
ADH

9. Multiple factors may contribute to the development of hypertension,
including:
 Malfunctions in either humoral (i.e., the renin-angiotensin-
aldosterone system [RAAS]) or vasodepressor mechanisms,
abnormal neuronal mechanisms, defects in peripheral
autoregulation, and disturbances in sodium, calcium, and natriuretic
hormone.

10. HUMORAL MECHANISMS
Renin-angiotensin-
aldosterone system
The renin–angiotensin system (RAS) or
the renin–angiotensin–aldosterone system
(RAAS) is a hormone system that regulates
blood pressure and water (fluid) balance.
Renin is an enzyme that is stored in the juxtaglomerular cells,
which are located in the afferent arterioles of the kidney.
• The release of renin is stimulated by renal ischemia, sympathetic
nerve system stimulation and decreased by depressed sodium

11.  fluid depletion and decreased potassium intake.
 Released renin is transported in the blood stream to the liver
& then carries out the conversion of angiotensinogen
released by the liver to angiotensin I.
 Angiotensin I is subsequently converted to angiotensin II by
the enzyme angiotensin converting enzyme found in the
lungs. Angiotensin II is a potent vaso-active peptide that
causes blood vessels to constrict, resulting in increased
blood pressure.
 Angiotensin II also stimulates the secretion of the hormone
aldosterone from the adrenal cortex. Aldosterone causes the
tubules of the kidneys to increase the reabsorption of sodium
and water into the blood. This increases the volume of fluid
in the body, which also increases blood pressure.

12. Activation of the Renin Angiotensin
Aldosterone System (RAAS)

13. NEURONAL REGULATION
The central and autonomic nervous systems are intricately involved
in the regulation of arterial BP.
Sympathetic nervous system . Baroreceptors
 Baroreceptors are nerve endings lying in the walls of large
arteries, especially in the carotid arteries and aortic arch.
Changes in arterial pressure rapidly activate baroreceptors, which
then transmit impulses to the brain stem through the ninth cranial
nerve and vagus nerves. In this reflex system, a decrease in
arterial BP stimulates baroreceptors, causing reflex

14. Multiple factors may contribute to the development of
hypertension,
including:
 a pathologic disturbance in the central nervous system (CNS),
autonomic nerve fibers, adrenergic receptors, or
baroreceptors;
 Abnormalities of renal functions can also contribute to the
development of systemic hypertension. Excessive Na + and
water retention by the kidney is responsible for volume based
hypertension.

15.  A deficiency in the local synthesis of vasodilating substances in
the vascular endothelium, such as prostacyclin, bradykinin, and
nitric oxide, or an increase in production of vasoconstricting
substances such as angiotensin II and endothelin I.
 a high sodium intake and increased circulating natriuretic
hormone inhibition of intracellular sodium transport, resulting in
increased vascular reactivity and a rise in blood pressure; and
 increased intracellular concentration of calcium, leading to
altered vascular smooth muscle function and increased
peripheral vascular resistance