Lect: Long Term Control of BP Flashcards Preview

Unit 7 - Repro & Renal Physiology > Lect: Long Term Control of BP > Flashcards

Flashcards in Lect: Long Term Control of BP Deck (17)
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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



-potent vasoconstrictor
-stimulates aldosterone secretion



-enhances reabsorption of Na
-stimulates ADH release (volume effect)


Primary hyperaldosteronism

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


ANG II Functions

-vasoconstrictor - increases PVR
-constricts mesangial cells - reduced GFR
-stimulates aldosterone - stimulates proximal Na-H exchange which increases blood volume
(pressure naturesis and diuresis)