Flashcards in Lect: Long Term Control of BP Deck (17)
low BP in which systolic pressure is below 90mmHg
elevated arterial pressure of 140/90 or higher
Chronic elevation is a major source of
heart failure and stroke
What measures the fast changes in BP
Baroreceptor reflex - cardiac and vascular
What measures intermediate changes?
kidney - PVR
What measures slow changes in BP?
Renal salt and water excretion
many factors go into the acute phase of BP control: stress, baroreceptors
but over many years - chronic - it is the kidneys, volume AND Na that determine what you e BP will regulate at
RAAS system activated by
low BP. It causes water reabsorption and decreases urine volume--> increased BP
Kidney acts directly and indirectly: directly it alters blood volume
Indirect involves RAAS and the juxtaglomerular aparatus
Macula densa is the collective name for a special group of cells in the Distal Tubule.
JG cells make renin, located at the junction of junction of the afferent arteriole, ascendingl limb of PT and DT
Mesangial cells provide anchor and may be involved in response to hypotension. If kidney failure you destroy this and control of BP gets disautoregulated
-stimulates aldosterone secretion
-enhances reabsorption of Na
-stimulates ADH release (volume effect)
patient comes in with very high BP and a very low K level
When someone has a heart attack the most important thing to do is to inhibit RAAS system
ANGII is a growth factor. Over time with elevated levels of ANG II that occurs with fibrosis. Scarring leads to fibrosis and fibrosis leads to dysrhythmias and then sudden death...after a heart attack. So you need to inhibit the RAAS
Determinants of Renin Secretion
1. neural signals (sympathetics to granular cells in JG)
2. INTRA-renal baroreceptors in afferent arterioles
3. Macula densa - more traffic f NaCl detected by these cells causes osmotic swelling and release of an inhibitor of renin
A patient come in with HYPOTENSION--> their glomerular hydrostatic pressure falls as does theIr GFR reducing flow in the LH with a consequent increase in NaCl reabsorption. This causes decreases flow through macula densa NaCl which causes a decrease in afferent arteriolar tone--> allowing more flow into the glomerulus increase GFR.
increases renin release--> ANG II which increases the efferent arteriole resistance--> increasing GFR. Both increasing GFR in the kidney