4. Primary Hypertension - Definition
The category of hypertension when the cause is unknown.
There are probably several different genetic causes as well
as a complex interplay of polygenetic and environmental
Includes approximately 90% of cases.
Also referred to as essential hypertension.
Even though the underlying cause usually is not known,
hypertension can usually be very effectively treated.
5. Secondary Hypertension - Definition
The category of hypertension when the cause is secondary
to renal, endocrine, anatomic disorders etc.
Includes approximately 10% of cases.
6. Hypertension - Clinical Significance
1. Heart disease
3. Kidney failure
Effects usually are not apparent until after 10 or more years of
sustained high blood pressure.
7. Treatment Strategies
A. Lifestyle Modifications
low fat diet rich in vegetables and fruit
reduction of excess body weight
limited alcohol consumption
daily aerobic exercise
reduction of sodium uptake
B. Drug Therapy
8. Treatment Strategies
. Additional Risk factors for cardiovascular disease
age older than 60
sex (men and postmenopausal women)
family history of cardiovascular disease
9. Treatment Strategies
Risk Group A
No risk factors
No cardiovascular disease
No Target organ damage
Risk Group B
At least one risk factor not including diabetes mellitus
No cardiovascular disease
No target organ damage
Risk Group C
Target organ damage
10. Treatment Strategy
Blood Pressure Risk group A Risk group B Risk group C
(up to 6 months)
drug therapy drug therapy
11. Blood Pressure Regulation
12. Blood Pressure Regulation
Sympathetic nervous control
13. Drugs Used To Decrease Blood Pressure
Very effective at lowering blood pressure
Usually do not correct the underlying defect
Drug therapy is usually life-long
One of the most common, effective and inexpensive drug classes
for the treatment of hypertension.
Several different classes of diuretics are effective including the
thiazides, loop diuretics and K+
Inhibit renal tubular reabsorption resulting in a reduction of
body salt and water.
The mechanism of long-term blood pressure reduction still
is not completely clear.
16. Drugs Acting on the Angiotensin System
A. Angiotensin Converting Enzyme (ACE) Inhibitors
17. ACE Inhibitors - Mechanism
Inhibit conversion of angiotensin I to angiotensin II
Potentiate actions of bradykinin by inhibiting its degradation
bradykinin degradation products
18. ACE Inhibitors - Characteristics
Little or no increase in heart rate
Reduces ventricular hypertrophy
Side effects: cough, angioedema and rash
Over-all a very safe class of drugs
19. Drugs Acting on the Angiotensin System
B. Angiotensin Receptor Antagonists
Inhibit the action of angiotensin II by antagonizing one of its
Similar effects as the ACE inhibitors
Lack the effect on the kinins which results in a lower
incidence of cough and rash
20. Beta Blockers
Competitively antagonizes the effects of the sympathetic
effectors norepinephrine and epinephrine.
21. Beta Blockers
Blockade of B1-adrenergic receptors in ventricle decreases
contractility and the SA node decreases the rate of contraction.
Blockade of B-Blockers inhibit renin release which also
contributes to a decrease in blood pressure.
22. Beta Blockers
Side effects: Causes bronchoconstriction due to B-2 receptor
Over-all well tolerated
Beta blockers should not be discontinued abruptly
23. Calcium Channel Blockers
Bind to receptors of calcium channels in cardiac and vascular
influx into the smooth muscle cells which reduces
the contraction of the blood vessels and heart rate.
The different calcium channel blockers differ in their relative
effects on vascular and cardiac tissue.
24. Calcium Channel Blockers
Side effects are generally mild.
Can cause a reflex increase in heart rate (tachycardia) in
response to the vasodilation.
Since they act on arterioles, not veins postural hypotension is
Frequently combined with a B-blocker
25. Alpha1-Adrenergic Blockers
Alpha1-adrenergic receptors are found on vascular smooth
muscle where they mediate vasoconstriction.
26. Alpha1-Adrenergic Blockers
Side effects: orthostatic (postural) hypotension and
Blockade of the alpha1-adrenergic receptors results in
vasodilation of both the arterial and venous beds .
27. Alpha1-Adrenergic Blockers
It is usually necessary to take a diuretic with these drugs.
B-blockers are also frequently co-administered with these drugs.
28. Direct-Acting Vasodilators
Directly relaxes the vascular smooth muscle
Several drugs in this category are very quick acting and
are mainly used for hypertensive emergencies
Side effects include reflex tachycardia and edema. As a result
these drugs are frequently combined with a B-blocker and a
29. Direct-Acting Vasodilators
Nitrovasodilators release nitric oxide (NO)
activation of guanylate cyclase
stimulation of a cGMP-dependent kinase and a
decreased cytosolic [Ca+2]
relaxation of vascular smooth muscle
30. Direct-Acting Vasodilators
Several other direct-acting vasodilators that work through
poorly defined mechanisms
Examples of nitrovasodilators include nitroglycerin and sodium
31. Centrally Acting Drugs
Antihypertensive effect results from action in the CNS causing
a reduced sympathetic nerve firing rate.
32. Centrally Acting Drugs
Clonidine activates alpha2 and imidazoline receptors in the
vasomotor center of the medulla which inhibits the sympathetic
Considered a second-line drug or for special cases
(ie methyldopa in pregnant hypertensive patients).
A reduced heart rate and cardiac output account for reduction
in blood pressure.
33. Centrally Acting Drugs
An advantage of these drugs is that they do not cause
Side effects - hypertensive rebound if there is an abrupt
-dry mouth, sedation
34. Additional Considerations
Hypertension during pregnancy poses a risk for both mother
and fetus/ preeclampsia.
Hypertension is a major risk factor for kidney and
cardiovascular problems in patients with diabetes.
Early and cost effective approach is needed by doctors
because complications are life threatning and treatment
may be life long.