PATHOPHYSIOLOGY

OF Hypertension
Presentation Outline Definitio
n
Today' s SYSTOLIC AND DIASTOLIS
Topics
Classification of hypertension

RISK FACTORS

CONTROL OF BLOOD
PRESSURE

Regulation of PR
 NEXT

DEF INI TION :

defined aS either a SuStained SyStolic blood

preSSure of greater than 140 mm Hg or a
SuStained diaStolic blood preSSure of greater
than 90 mm Hg.
HypertenSion reSultS from increaSed
peripheral vaScular arteriolar Smooth muScle
tone.

- In other WordS,HypertenSion iS a State of

- Systolic blood pressure—› is the
blood pressureduring systole or
myocardium contraction.
-diastolic blood pressure —› is the
blood pressureduring diastole or
myocardium relaxation.

| A M
B E N E F ITS
B IO TIN
C
NEXT

01 02 03

SYSTOLIC BP D I A S T O L I C BP

Normal < 120 l< 80

PrehypertenSio 120 - 80 - 89
n
Stage I 139
90 - 99
hypertenSion Stage 140 - —— >
II hypertenSion 159 100
= > 160
 HYPERTENSION
-
Although many patientS have no SymptomS, chronic
hypertenSion can lead to heart diSeaSe and Stroke. It iS alSo an
important riSk factor in the development of chronic kidney
diSeaSe and heart failure. hypertenSion may occur Secondary

| A M
to other diSeaSeS, but more than 9 0 % of patientS have

B E N E F ITS
eSSential hypertenSion, that happenS With no identifiable

B IO TIN
cauSe.
NEXT

C
HYPERTENSION RISK FACTORS

- The family hiStoryof hypertenSion increaSeS the chance to

develop hypertenSion.
- Older ageS, diabeteS, obeSity, Smoking, alcohol
conSumption, StreSSful lifeStyle, and high dietary intake of
Sodium are alSo riSk factorS for hypertenSion.
NEXT
 THERE ARE MULTIPLE ORGANS INVOLVED IN THE CONTROLOF BLOOD PRESSURE, THE
HEART, BLOODVESSELS, KIDNEYS, L IVER,AND LUNGS

-2 major proceSSeS control theSe organS to Work in harmony in controlling

blood preSSure.
1 - The baroreceptorS and the Sympathetic nervouS
SyStem. 2 - And the renin-angiotenSin-aldoSterone
SyStem.

Before We begin you Should knoW that, 3 proceSSeS increaSe the blood
preSSure, increaSing cardiac output, increaSing peripheral reSiStance, or
- So What happenSWhen the
blood preSSure fallS ?
- fall in blood preSSure
cauSeS preSSure-SenSitive neuronS in the aortic arch and carotid SinuSeS, that
are called baroreceptorS, —› to Send feWer impulSeS to cardiovaScular centerS in
the Spinal cord. —›
ThiS promptS a reflex reSponSe of increaSed Sympathetic and decreaSed
paraSympathetic output to the heart and vaSculature, —› reSulting in activation of
fi1 adrenoceptorS in the heart, —› increaSing cardiac output, and activation of 1
adrenoceptorS in the blood veSSelS —› cauSing vaSoconStriction. —›Leading to a
compenSatory riSe in blood preSSure.
- The kidneyS control the blood volume.
Simply, When blood preSSurefallS —› the kidneyS releaSethe
enzyme renin, —› leadingto a SerieS of eventSthat increaSe blood
preSSure
- there are alSo baroreceptorS in the kidneyS, —› they reSpond
to reduced arterial preSSure and to Sympathetic Stimulation of
§1- adrenoceptorS in the kidneySby —› releaSing the

| A M
B E N E F ITS
enzymerenin.
-LoW Sodium intake and greater Sodium loSS alSo increaSe

B IO TIN
C
renin releaSe.
-Renin convertS angiotenSinogen, Which iS SyntheSized in the liver and Secreted in
plaSma,
—› to angiotenSin I, Which iS converted to angiotenSin II in the lungS, in the preSence
of angiotenSin-converting enzyme (ACE).
—› AngiotenSin II iS a potent circulating vaSoconStrictor, conStricting both arterioleS
and veinS, increaSing peripheral reSiStance and blood preSSure.
—› AngiotenSin II alSo StimulateS aldoSterone Secretion —› leading to increaSed renal
Sodium reabSorption and increaSed blood volume, Which contribute to a further increaSe
in blood preSSure.
—› TheSe effectS of angiotenSin II are mediated by Stimulation of angiotenSin II type 1
(AT1) receptorS.
-So We can concludethe categorieS of the drugS that are uSed for
hypertenSion, either they Work aSSympatholyticS to decreaSe the
Sympathetic activity, interfere With renin-angiotenSin SyStem, or
diureticS to decreaSe blood volume.