Topic:Control of Blood

pressure

Md.Jabiur Rahaman

Daffodil International University

Dept. Of pharmacy

Control of blood pressure

Mean blood pressure is controlled by changing total peripheral resistance and or cardiac output.

Cardiac output is controlled by sympathetic and para sympathetic nerves which effect: heart rate

force of contraction

TPR controlled by nervous and chemical means to effect constriction/dilatation of arterioles and venules

Regulation of blood pressure

How is pressure “measured”?

Short term

Baroreceptors

Long term

Kidney via renin angiotensin system

Location of

baroreceptors

• Baroreceptors sense stretch and

rate of stretch by generating

action potentials (voltage spikes)

• Located in highly distensible

regions of the circulation to

maximise sensitivity

Baroreceptor output(from single fibres)

Rapid decrease in mean pressure

From: Introduction to Cardiovascular physiology. J.R. Levick. Arnold 4th edition (2003)

Rapid increase in mean pressure

Response to pulse pressure

Two types of baroreceptor

Type A

High sensitivity

High firing rate

Type C

Lower sensitivity

Lower firing rate

Higher threshold (before firing starts)

Therefore can deal with higher pressures than type A which

become “saturated”

From “An Introduction to Cardiovascular Physiology”

J.R. Levick

Baroreceptor reflex

Blood pressure falls

Aortic arch Carotid sinus

Constriction of veins

& arterioles

Increased stroke

volume

Increased heart

rate

Vasoconstriction Cardiac stimulation Cardiac inhibition

Nucleus tractus solitarius

Increased peripheral

resistance

Increased cardiac

output

Increased blood

pressure

Neural integration

Sensors

Effectors

Other stretch receptors

Coronary artery baroreceptors Respond to arterial pressure but more sensitive than

carotid and aortic ones

Veno-atrial mechanoreceptors Respond to changes in central blood volume

Lie down, lift your legs and cause peripheral vasodilatation

Unmyelinated mechanoreceptors Respond to distension of heart

Ventricular ones during systole; atrial ones during inspiration

Other receptors

Heart chemosensors Cause pain in response to ischaemia

K+, lactic acid, bradykinin, prostaglandins

Arterial chemosensors Stimulated in response to

Hypoxaemia, hypercapnia*, acidosis, hyperkalaemia**

Regulate breathing

Lung stretch receptors Cause tachycardia during inspiration

*too much CO2

**too much K+

Overview of short-term control mechanisms

From: Introduction to Cardiovascular physiology. J.R. Levick. Arnold 4th edition (2003)

Long term control of blood pressure

Involves control of blood volume/sodium balance

by the kidneys

Hormonal control

Renin-angiotensin-aldosterone system

Antidiuretic hormone (vasopressin)

Atrial natiuretic peptide

Pressure natriuresis

Arteries

Veins

Reduced renal

blood flow

Juxtaglomerular

apparatus

Renin

Angiotensinogen

Angiotensin I

Angiotensin II

Increased

pre-load

Increased

after-load

vasoconstriction

Increased aldosterone

secretion

Sodium retention

Fluid re-absorption

Increased

blood volume

Renin/angiotensin/ aldosterone system

LV filling pressure)

(LV pressure

beginning of systole)

Atrial natiuretic peptide

Increases salt excretion via kidneys

By reducing water reabsorption in the collecting ducts

relaxes renal arterioles

inhibits sodium reabsorption in the distal tubule

Released in response to stimulation of atrial

receptors

Effect of blood loss

less than 10%, no serious symptoms

e.g. blood transfusion

20 - 30% blood loss not usually life threatening

greater than 30%, severe drop in BP and, often,

death due to impaired cerebral and coronary

perfusion