8- Long Term Regulation of Arterial Blood Pressure Flashcards
what is a key component involved in regulation of blood pressure?
- regulation of body fluids
- regulation of body fluids is multifactorial process involving nerves, hormones, physical factors, but is primarily handled by the kidney (look at “neural-humoral factors” graph)
sympathetic activity with respect to kidney to help maintain mass balance with water and Na
(hormones/systems involved)
ADH/antidiuretic hormone/vasopressin
renin-angiotensin-aldosterone system
atrial natriuretic peptide (if the other two decrease, this increases)
Proportionate feedback controllers
- finite feedback gain
- adapt for acute short-term responses
Analysis of long-term arterial pressure regulation by pressure-diuresis
- renal output is equated with salt and water intake
- over days, water and salt output must equal intake
- “equilibrium point” is where the intake is equal to the output
- if pressure rises, body loses fluid until pressure falls all the way back to the equilibrium point (if pressure increases then you’re gonna filter blood faster)
pressure diuresis
getting rid of water
natriuresis
getting rid of sodium
how do kidneys help you come back to equilibrium
-pee more to help you come back to equilibrium (pee more to lower arterial pressure)
arterial pressure equilibrium point
100
reduced renal mass model
What they do
- mimics loss of renal excretory ability that occurs in renal disease (cut part of kidneys)
- kidneys have huge excess capacity to filter blood and regulate sodium and water in the body so in order to induce hypertension significant reductions in renal mass must be combined with a high sodium intake
What it showed
-diminished excretory ability (NaCl vs Mean arterial pressure curve shifts right and down)
what does salt do to bp
increases it, especially when kidney function is already decreased
what happens in the early phase of reduced renal mass?
- hypertension arterial pressure is elevated because CO i shigh (AP = CO x TPR)
- later, CO returns to normal but now bp is high because of elevated TPR
- this transition occurs because of functional (auto-regulation) and structural (vascular remodeling) changes in vasculature
- all the blood is constricting their own blood vessels so they dont get too much blood, which increases blood going back to the heart but that causes a decrease in stroke volume cause not as much blood is able to go through
how hypertension develops
- renal function reduced
- increased extracellular fluid volume
- increased blood volume
- increased mean circulatory filling pressure
- increased venous return of blood to heart
- increased cardiac output
- autoregulation causes an increase in total peripheral resistance
- increased arterial pressure
autoregulation and hypertension
Auto-regulation can serve as a multiplier if the effect of volume expansion. When blood flow increases pressure rises since AP= CO x TPR. Since the rise in cardiac output also causes an increase in TPR because of auto-regulation, arterial pressure goes up even more
renin-angiotensin (-aldosterone) system
- Angiotensin: retains salt
simplified: angiotensinogen -> angiotensin I -> angiotensin II -> aldosterone
1. Angiotensinogen (made in the liver) circulates in the blood where it is cleaved by renin (released from the kidney)
2. Produces Angiotensin I (ANG I). ANG I has minimal biological activity but it circulates in the blood until it encounters angiotensin converting enzyme (ACE) on the surface of endothelial cells where this enzyme produces ANG II from ANG I.
3. ANGII is a highly potent vasoconstrictor, stimulates the release of aldosterone and together are involved in reabsorption of sodium and water in the kidney
ANG II
causes kidney to reabsorb Na and water (less excretion)
-regulated by Na intake (more Na = less ANG II)
what happens in a low pressure system to renin and angiotensin?
they are released to save more Na and water
