Very usefull ppt

1. ANGIOTENSIN

2. • Angiotensin is a hormone that helps regulate
your blood pressure by constricting
(narrowing) blood vessels and triggering water
and salt (sodium) intake.
• There are four different forms of angiotensin,
and they’re denoted by Roman numerals:
angiotensin I– IV. Angiotensin II is the main
and active form of the hormone.

3. • While angiotensin II has a complex series of effects on body,
the primary results are higher blood volume, increased blood
pressure and increased sodium (salt) levels. Angiotensin II
binds to several receptors throughout body, affecting many
different systems and functions, including:
• Stimulating the release of aldosterone from your adrenal
glands, which causes body to retain sodium and lose
potassium through your urine.
• Increasing blood pressure by constricting (narrowing) blood
vessels.
• Triggering the sensation of thirst through hypothalamus.
• Triggering the desire for salt (sodium) through hypothalamus.
• Stimulating the release of antidiuretic hormone (ADH, or
vasopressin) from pituitary gland, which causes kidneys to
reabsorb water.

4. • What controls angiotensin levels?
• Angiotensin is part of an elaborate group of
linked hormones, enzymes, proteins and
reactions called the renin-angiotensin-
aldosterone system that helps regulate blood
pressure.
• To start the system or cycle, when blood
pressure falls, kidneys release the enzyme renin
into your bloodstream.
• Renin splits angiotensinogen, a protein made in
your liver and releases the pieces. One piece is
the hormone angiotensin I.

5. • Angiotensin I, which is inactive (doesn’t cause
any effects), flows through bloodstream and is
split by angiotensin-converting enzyme (ACE) in
lungs and kidneys. One of those pieces is
angiotensin II, an active hormone.
• Angiotensin II causes the muscular walls of
small arteries (arterioles) to constrict (narrow),
increasing blood pressure. Angiotensin II also
triggers your adrenal glands to release
aldosterone and pituitary gland to release
antidiuretic hormone (ADH, or vasopressin).

6. • What happens when angiotensin levels are
low?
• Lower-than-normal angiotensin II levels
(angiotensin deficiency) can cause the
following issues:
• Low blood pressure (hypotension).
• Elevated potassium levels (hyperkalemia).
• Low sodium levels (hyponatremia).
• Fluid (water) loss through urine (pee).

9. BRADYKININ
• Bradykinin is a potent inflammatory peptide
messenger, and as a kinin is part of the kallikrein-
kinin system which has wide ranging effects on the
body.
• Bradykinin is generated from high-molecular-
weight kininogen by the enzyme kallikrein. It is also
released from mast cells during asthma attacks and
within the gut as a gastrointestinal vasodilator.
•

10. • Roles in the Body
• Bradykinin is released from damaged tissue following injury or with
inflammation. Mast cells also release bradykinin.
• Nociceptive system: Bradykinin both activates and sensitises sensory
neurons. it is a very potent pain-producing substance. Following the release
with injury or inflammation, it excites a high percentage or nociceptors and
sensitises them to other noxious stimuli. The sensitisation occurs through
activation of B1 and B2 receptors.
• Rheumatological system: The des-Arg kinin derivates induce collagen
synthesis, fibroblast proliferation, and cytokine release from macrophages.
• Vascular system: bradykinin acts as a vasodilator (through local production
of NO and prostaglandins), increases vessel permeability, and stimulates the
formation of prostacyclin. It has a role in the pathophysiology of C1 esterase
inhibitor deficiency.
• Renal system: It increases renal flow through vasodilation and inhibits
inhibits sodium reabsorption leading to natriuresis. This leads to reduced
blood pressure.
• Respiratory system: It has bronchoconstrictor effects and plays a role in
asthma and rhinitis.
• Gastrointestinal system: causes smooth muscle contraction, and is involved
in visceral nociception.

11. Physiology of bradykinin

12. • Kinins are the active peptides of the kallikrein-kinin
system . Kinins are released either by tissue or the
plasma.
• Tissue kallikrein-kinin system: Tissue kallikrein acts
to form kallidin from kininogens, which are inactive
precursors. Tissue kallikrein is inhibited by
kallikrein-binding protein or kallistatin.
• Plasma kallikrein-kinin system: Plasma kallikrein is
released from prekallikrein by activated factor XII.
Prekallikrein reciprocally activates FXII. Plasma
kallikrein forms bradykinin from the kininogens.
Plasma kallikrein is inhibited by compliment 1
inhibitor protein.

13. • Bradykinin and Kallidin (also known as Lys-
bradykinin) are vasoactive, and cause the
classical signs of inflammation. Kallidin is similar
to bradykinin in its effects, and can be converted
to bradykinin by aminopeptidase. They mediate
their effects through kinin receptor B2.
• When bradykinin activates B2, there is direct
stimulation of nociceptors (C & Aδ fibres). Kinins
cause sensitisation of sensory fibres to thermal,
chemical, and mechanical stimuli.

14. SUBSTANCE - P
• Substance P (SP) is a neuropeptide that is part of the
tachykinin family. It is made up of 11 amino acids and
acts as a neurotransmitter and neuromodulator. SP is
expressed in the central nervous system (CNS),
peripheral nervous system, and immune cells.
•
Substance P (SP) is a neuropeptide that is released
from sensory nerve endings and is widely present in
nerve fibers. It acts on bones and related tissues by
binding to receptors, thereby regulating bone
metabolism, cartilage metabolism, and fracture
healing.