BP Homeostasis and Hypertension Flashcards
Explain how arterial BP is regulated acutely by the baroreceptor reflex
The baroreceptors are stretch receptors located in the internal carotid arteries and aorta.
They are tonically active, and regulate BP on a moment to moment basis.
Increased BP
- Increases stretch of baroreceptors
- Inhibits the vasoconstrictor center in the medulla
- Induces vasodilation, decreased HR and SV.
Decreased BP
- Decreases stretch of baroreceptor
- Disinhibits the vasoconstrictor center and induces vasoconstriction, increased HR and SV.
There are also different baroreceptors in the atria and pulmonary circulation.
Explain how the kidneys regulate arterial BP with reference to the renin-angiotensin system.
The long term ABP is at the balance point between fluid intake and renal output.
- Increasing arterial pressure causes a corresponding rise in renal urinary output (pressure diuresis). It also causes an increase in sodium ouput (pressure natiuresis).
- Over time, blood volume (and therefore BP) will stabilise when dietary H20 and Na+ output is equal to input.
*If dietary input increases **ABP will also increase. *
The renin-angiotensin system
- Renin is an enzyme produced and released by the kidneys under conditions of reduced ABP
- Renin itself has no direct effect on BP, but is the first step in the RAS cascade.
- Renin cleaves off a peptide (angiotensin I) from the plasma protein angiotensinogen.
- Ang I is converted to Ang II in the pulmonary circulation by angiotensin converting enzyme (ACE)
Angiotensin II causes:
- Aldosterone release from adrenal cortex which increases renal Na+ reabsorbtion (reduced loss of Na+), which increases blood volume and hence BP.
- Directly increases Na+ reabsorption
- Causes vasocontriction (A2 receptors), which increases TPR and thus increases BP.
Explain how salt influences BP.
Na+ stimulates third centers and causes increased fluid ingestion. This results in a higher volume of blood, and hence increase BP.
Na+ also creates an osmotic gradient, so that ore water is drawn back into the blood, and less is excreted by the kidney as urine - this also increases blood volume and hence increases BP.
Na+ also stimulated release of antidiuretic hormone form the pituitary. ADH strongly stimulates water reabsorption by the kidney.
What affects pulse pressure?
- Stroke volume: increasing stroke volume increases PP.
- Compliance: decreasing compliance increases PP.
What determines the mean afterial pressure?
Ohm’s Law states that
Cardiac output = [MAP - RAP] / TPR
We assume RAP is nearly 0, so after rearranging…
Mean arterial pressure = CO x TPR
Because CO = HR x SV
Mean arterial pressure = HR x SV x TPR
Why do we control BP?
- Arterial BP is the gradient for blood flow.
* Ultimately, if you have a good pressure, you can perfuse your heart and brain. - High BP is damaging to vessels.
How can we change the BP?
There are both *short term control mechanisms *and long term mechanisms for BP control.
The variables that can change MAP are found in this equation:
MAP = HR x SV x TPR
HR
- SNS
- PNS
- Circulation catecholamines
Contractility
- SNS
- Circulating catecholamines
Preload
- Venous constriction by SNS
- Blood volume (more on BV later)
TPR
- SNS
- Circulating catecholamines
- Local factors
Short term BP control
-
Sensor
- Directly senses BP. Stretch in the blood vessel walls in sensed by baroreceptor located in various areas.
- Indirectly senses BP (via poor perfusion). Chemoreceptors sense O2 and CO2.
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Control centre
- __The vasomotor centre in the brainstem (medulla)
-
Effector
- Smooth muscle arteries, arterioles: vasoconstriction/dilation changes TPR
- Smooth muscle veins: venoconstriction/dilation, changes venous return (and therefore preload and therefore SV)
- SA node: changes HR
- Ventricular muscle: Changes contractility
- Kidney: SNS activates the RAS
Chemoreceptors
Peripheral chemoreceptors are located in the carotid and aortic bodies.
Central chemoreceptors are located in the brainstem (medulla)
Both are stimulated by a decrease in blood PO2 and an increase in blood PCO2. Stimulation of these chemoreceptors (low O2, or increased CO2) increases rate and depth of respiration btu also causes peripheral vasoconstricion, increased HR and SV.
Long term control of arterial BP
This is achieved by regulation of blood volume, which is determined by the amount of Na+ and water in the blood.
Control of blood volume is carried out by the kidneys.
Increased blood volume increases the central venous pressure and therefore the filling pressure of the heart. Increased blood volume increases the preload, which increases CO, which increases BP.
Long term ABP is at the ‘balance point’ between fluid intake and renal output. Thus, two factors account for the long-term ABP:
- Chronic intake of water and salt (thirst and salt appetite)
- The urine output of water and salt
Affect of RAS on renal function curve
The RAS causes lower output of Na+ and H2O at any given BP. Therefore, it shifts the renal function curve to the right and increases BP.
Aldosterone
Aldosterone is secreted by the adrenal glands and acts on the kidneys to increase Na+ reabsorbtion.
Long term effect of peripheral resistance
Changes in peripheral resistance will only change arterial BP acutely. The kidneys can always return BP to normal, if they are functioning correctly.
However, changes in vascular function may impact the renal circulation and thus indirectly alter blood volume (and thus long-term ABP) by shifting the renal function curve.
