Control of Blood Pressure
BP is control in two ways:
1. Short-term control – involves the baroreceptor
reflex, chemoreceptors and circulating
hormones.
2. Long-term control – involves regulation of blood
volume by the kidneys and the renin-angiotensin-
aldosterone system.
Baroreceptors
Within the aortic and carotid sinuses
-nerve ending sensitive to stretch (pressure).
1) A rise in BP stimulate baroreceptor, input to
cardiovascular centre CVC respond by
parasympathetic nerve to slow down the heart
activity.
2) At the same time, sympathetic stimulation
inhibited causing vasodilation BP .
Baroreceptors
If pressure within the aortic arch and carotid
sinuses falls, the rate of baroreceptor discharge
also falls.
CVC responds by sympathetic drive to speed up
the heart cause vasoconstriction BP .
Chemoreceptor
These are nerve endings situated in the carotid
and aortic bodies, involved in control respiration.
Changes CO₂, O₂, and the acidity of blood.
These changes detected by chemoreceptor, they
send signals to the CVC, sympathetic drive to
the heart and blood vessel.
Blood O₂ level rise BP up, respiratory up
Higher centres in the brain
Input to the CVC is influenced by emotional – fear,
anxiety, pain and anger that may stimulate
changes in blood pressure.
Long term BP regulation
Slower, longer lasting changes in BP are effected
by the renin-angiotensin-aldosterone system and
the action antidiuretic hormone.
Atrial natriuretic peptide –released by the heart
itself, causes sodium and water loss from the
kidney and reduces BP.
Pressure in the pulmonary circulation
Pulmonary circulation is much lower than
systemic circulation.
If pulmonary capillary pressure exceeds 25mmHg,
fluid is forced out of the bloodstream and into the
airsacs (pulmonary oedema) with very serious
consequences.