الفهرس 
INTRODUCTION &AIM OF ’TI-lE WORKOnly 14 pages are availabe for public view
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Abstract
The Renin-Angiotensin- Aldosterone System (RAAS)
The Enzyme renin is secreted f!·om epithelioid cells of afferent renal
arterioles. These are adjoined to nwcula den sa cells of ascending limbs of
nephrons sensing sodium delivery to distal tubular parts and
subsequently modulating renin release. Angiotensin I is cleaved in
plasma by renin from angiotensinogen, a high molecular weight
glycoprotein synthesized in the liver.
Angiotensin II, in turn, is generated by converting enzyme through
cleavage of 2 amino acids from angiotcnsi n l.
Converting enzyme is ubiquitously present. and therefore conversiOn
of angiotensin I to an angiotensin II occms in all perfused tissues but the
main conversion takes place in lungs.
Angiotensin 11, the effector pcpt.idP of t.he renin-angiotensinaldosterone
system, is a potent. v<~soconslriclor preferentially acting on
arterial vessels. It promotes sodium reabsorption in proximal tubular
parts of nephrons and stimulates aldosl.t•ront’ release from cortical cells of
adrenal glands. The presence of aldosterone permits reabsorption of
sodium in distal tubular parts lherl’b_v resulting in potassium secretion.
Angiotensin II also causes t.hc n•lc·ast• of pituitary hormones and
possibly facilitates sympathetic neurotransmission. The actions of the
renin-angiotensin-aldosterone system are aimed at preserving sufficient
fluid to maintain circulation and tissue perfusion. The renin-angiotensinaldosterone
system is physiologically activated in case of fluid or salt loss
or decreases in blood pressure, and is pathophysiologically involved in
circulatot·y disorders such as hypertension and congestive heart failure.r:~
- ,) ’ -
Reversing the actions of angiotensin II with an ACE inhibitor, which
occupies active sites of converting enzyme explains almost all observed
pharmacodynamic effects.
Relationship between plasma renin concentration and other
biochemical Ineasureinents :
There is positive correlation between plasma renin concentration and
the plasma urea level. Also there is a close inverse relationship between
plasma sodium and plasma renin in both treated and untreated patients.
A weak positive correlation is found between plasma potassium and
renin concentration in untreated patients but there is no significant
relationship in the treated patients.
A high plasma remn IS usually associated with a low tC02 in the
untreated patients but no simple relationship could be detected with
treated patients. A weak and statistically insignificant inverse
relationship is found between plasma renin concentration and arterial
blood pressure.
In the early stage of heart failure, increased atrial pressure result in
the release of atrial natriuretic factor, which modulates the effects of the
sympathetic nervous system and the renin angiotensin system.
In advanced heart failure the effects of the vasoconstrictor forces
become dominant and exceed the ability of atrial natriuretic factor to
modulate these forces i.e. circulatory homeostasis.
A major area of use for converting enzyme inhibitors is heart failure.
They are set to replace the more conventional approach of using
vasodilating agents in addition to diuretics.Angiotensin converting enzyme inhibitor has been shown in many
trials to relieve symptoms of CIIF’ and to improve cardiac hemodynamics,
functional capacity and exercise tolenmce.