‘’INTERMEDIATE CONTROL MECHANISM’’

• Presented by: Burhan Umer

• Fluid shift • Stress relaxation• Renin-angiotensin vasoconstrictor

mechanism• Biogenic amines

MECHANISMS:

‘’CAPILLARY FLUID SHIFT MECHANISM’’ WHEN PRESSURE FALLS TOO LOW, FLUID IS ABSORBED FROM THE TISSUES

THROUGH CAPILLARY MEMBRANE AND INTO THE CIRCULATION IT BUILDS UP BLOOD VOLUME AND INCREASES THE PRESSURE IN THE

CIRCULATION.

WHEN PRESSURE RISES TOO HIGH, FLUID IS LOST OUT FROM CIRCULATION INTO THE TISSUES

IT REDUCES BLOOD VOLUME AND DECREASES THE PRESSURE IN THE CIRCULATION.

FLUID SHIFT MECHANISM:

WHEN PRESSURE IN BLOOD VESSELS BECOME TOO HIGH, THEY BECOME STRETCHED AND KEEP ON STRETCHING MORE AND MORE, AS A RESULT THE PRESSURE IN VESSELS FALL TOWARDS NORMAL

THIS MECHANISM SERVES AS AN INTERMEDIATE-TERM PRESSURE ‘’BUFFER’’.

STRESS-RELAXATION MECHANISM:

RENIN ENZYME RELEASED BY KIDNEYS WHEN THE ARTERIAL PRESSURE FALLS TOO LOW.

RENIN ACTS ON A PLASMA PROTIEN ‘’ANGIOTENSINOGEN’’

ANGIOTENSINOGEN RELEASES ANGIOTENSIN I

ANGIOTENSIN I IS CONVERTED TO ANGIOTENSIN II BY ANGIOTENSIN CONVERTING ENZYME (FOUND MOSTLY IN LUNGS)

ANGIOTENSIN II IS A POWERFUL VASOCONSTRICTOR, CONSTRICTON OCCURS IN ARTERIOLES

THE CONSTRICTION INCREASES PERIPHERAL RESISTANCE, THEREBY INCREASING THE ARTERIAL PRESSURE.

RENIN-ANGIOTENSIN VASOCONSTRICTOR

DECREASED ARTERIAL PRESSURE

RENIN (KIDNEY)

RENIN SUBSTRATE (ANGIOTENSINOGEN)

ANGIOTENSIN I

ANGIOTENSIN II

RENAL RETENSION OF SALT AND WATER

VASOCONSTRICTION ANGIOTENSINASE(INACTIVATED)

INCREASED ARTERIAL PRESSURE

VASOCONSTRICTORS:1. EPINEPHRINE via α12. SEROTININ etc.

• VASODILATORS:1. EPINEPHRINE via β22. HISTAMINE3. ANP etc.

BIOGENIC AMINES: