The Cardiovascular System In Its Context

6.11.06

Hypertension
• ABC of Hypertension: The Pathophysiology of hypertension, BMJ, 322: 912-916.
• Up to 5% patients with hypertension have it as secondary to some other disease e.g. renal disease.
• Rest have "essential hypertension."

Story so far…
Stroke volume

Cardiac output


Heart rate

• Intrinsic (Starling's law - "more in, more out").
• Extrinsic (principally autonomic.)

Postulated mechanism
• Increased sympathetic activity:
-Leads to increased cardiac output.
-And peripheral vasoconstriction (to protect capillary beds).
• Drop in blood flow triggers rennin-angiotensin system.

Evidence
• Cross transplantation studies show essential hypertension has origins in kidneys.
-Human and animal studies.
• Little evidence "stress" involved.
-But, of course, drugs that decrease sympathetic activity decrease blood pressure.

Control
BRAIN
Volume ANS
Pressure
Chemicals ADH

HEART BODY


Angiotensin

LOCAL BLOOD FLOW

Pressure
• Sensed by baroreceptors - in carotid arteries and aortic arch.
• Increase in pressure causes decrease in sympathetic activity.
• Decrease in pressure causes increase in sympathetic activity.

Volume
• Sensed by atrial volume receptors.
• Decrease in volume causes:
-Increase in ADH secretion.
-Decrease in ANP secretion.

Local blood flow (kidney)
Decreased renal blood flow


Monitored by JGA cells


Renin production


Angiotensin Angiotensin I


Converting enzyme

Angiotensin II

Sodium resorption
Aldosterone
Potassium secretion

Vasoconstriction

Hormones
• Angiotensin II = vasoconstrictor.
• Aldosterone increases vascular sensitivity to angiotensin II.
• ADH increases water resorption.
• ANP decreases sodium secretion.