This document outlines three hormonal mechanisms that can rapidly control arterial pressure: 1. Adrenaline and Nor-adrenaline secreted from the adrenal medulla in response to sympathetic stimulation. Nor-adrenaline causes vasoconstriction increasing blood pressure, while adrenaline increases heart rate. 2. The Renin Angiotensin System where low blood pressure triggers the kidneys to release renin which converts angiotensin I and then II. Angiotensin II causes rapid vasoconstriction and increased norepinephrine release, both of which raise blood pressure. 3. The Vasopressin System where vasopressin is secreted from the pituitary gland, stimulating

1. Hormonal Mechanism for Rapid
Control of Arterial Pressure
Three factors are responsible for hormonal
mechanisms
Adrenaline and Nor-Adrenaline.
Renin Angiotensin System.
Vasopressin System.
1- Adrenaline and Nor-adrenaline.
These are also known as epinephrine and nor-
epinephrine. These are secreted from adrenal
medulla in blood in response to sympathetic
stimulation.

2. Nor-adrenaline is an especially powerful
constrictor hormone, which causes the
constriction of blood vessels which lead to
increased blood pressure.
Adrenaline has less vasoconstrictor
property and also in some cases slight
vasodilation. But the main effect of
adrenaline is that it directly acts on heart
and thus heart rate is increased.

3. So when heart rate is increased, there would be
more cardiac out-put and thus increased systolic
blood pressure.
Diastolic blood pressure may also rise or remain
unchanged.
2- Renin Angiotensin System
Renin is a small protein synthesized and stored
in an inactive form called pro-renin in the Juxta-
glomerular Cells (J G cells) of kidneys.

4. When arterial pressure falls due to intrinsic
reactions in kidneys pro-renin molecules in
the J G cells split and renin is released.
Renin is itself an enzyme and is not a
vasoconstrictor, still it acts enzymatically
on a plasma protein (a globulin) called
renin substrate and 10- amino acid peptide
chain is released called angiotensin1.

5. Angiotensin1 has small vasoconstrictor
properties, and does not cause any
significant functional changes in the
circulatory functions.
Decreased Arterial Pressure
Renin (Kidney)
Renin substrate________Angiotensin1
(plasma protein)

6. Angiotensin11 (angiotensinase)
Renal retention of vasoconstriction
water and salt.
increased Arterial Pressure.

7. After formation of angiotensin1, two
additional (more) amino acids split from it and 8-
amino acids peptide chain, angiotensin11 is
formed. Conversion of angiotensin1 to
angiotensin11 is catalyzed by a converting
enzyme, which is present in the endothelium of
the lung vessel.
Angiotensin11 persists in the blood for 1-2
minutes b/c it is inactivated by several blood and
tissue enzymes called angiotensinase.

8. Still it shows two effects on system
I- Rapid vasoconstriction, it increases
arterial pressure by directly acting on the
blood vessels and causing
vasoconstriction.
It increases blood pressure indirectly also
by increasing the release of Nor-
adrenaline.

9. II- Decrease Excretion of both salt and
water which slowly increases extra cellular
fluid volume, which them increases the
arterial pressure.
3-Vasopressin System.
It also calls as anti diuretic hormone. It is
formed in hypothalamus, from where it is
transported to posterior pituitary gland,
from where it is secreted into the blood.

10. Vasopressin stimulates the kidney tubules to
absorb water from the filtered plasma that
passes through kidneys and thus controls the
amount of urine secreted by kidneys.
Which consequently leads to increase arterial
pressure.
Conc. of circulating vasopressin during severe
hemorrhage can rise high’’ enough to increase
the arterial pressure as much as 60 mm Hg.