Renal 5: Hypertension, K+, Diuretics

Question 0

How does HYPERVOLEMIA lead to the correction of blood volume and pressure?

Answer 0

1. Hypothalamic osmoreceptors trigger release of ADH: reabsorption of water = Excess volume = natriuresis
2. Baroreceptors (arteries of neck /kidney) respond:
   - Inhibiting RAAS
   - Releasing natriuretic proteins
   - Stimulating Pressure Natriuresis

Question 1

How does HYPOVOLEMIA lead to the correction of blood volume and pressure?

Answer 1

Uses the same mechanisms as when low BP

Question 2

What is the role of the JGA in dealing with hypo- and hypervolemia?

Answer 2

The JGA monitors blood volume/pressure through Na+ detection. In hypERvolemia it reduces reabsorption by inhibiting renin release (and it’s activ of RAAS). It also

In hypOvolemia, the opposite happens - very much like with lie blood pressure: RAAS gets armies, etcetera.

Question 3

What are the 3 underlying mechanisms for type 1 hypertension?

Answer 3

1. Persistent, excess Angiotensin II and sympathetic activity
2. Chronic vasoconstriction due to imbalanced Angio II and NO; subtle renal injury: oxidative stress, SM hypertrophy and vascular lumen reduction; Na+ retention and increased blood volume/pressure.
3. Typical HTN does not show hypervolemia; increased volume/pressure produces natriuresis at higher BP level-rightward shift if natriuresis curve:
   RESULTS in hypertensive kidney and normal salt excretion.

Question 4

How is autoregulation affected in hypertension via NO? Natriuresis?

Answer 4

HTN is assoc with reduced production of NO and an increase in vasoconstrictors such as Angio II

Pressure natriuresis is reset to a higher blood pressure

Question 5

How does dietary salt impact autoregulation and pressure natriuresis?

Answer 5

?

Question 6

Why are people with type I Hypertension not hypervolemic?

Answer 6

Because increased volume/pressure produces natriuresis at a higher BP

(Is this true??)

Question 7

How does renal artery stenosis impact autoregulation and pressure natriuresis?

Answer 7

Reduces blood flow to kidney.
Drop in pressure elicits RAAS.
Renal vasoconstriction by Angio II and symp activ reduce medullary blood flow
AS A RESULT: Greater blood pressure req’d to induce pressure natriuresis to excrete excess salt and water
RIGHTWARD SHIFT OF PRESSURE NATRIURESIS CURVE

Question 8

How does congestive heart failure impact autoregulation and pressure natriuresis?

Answer 8

Reduce RBF in the attempt to correct for hypovolemia, but there is none. Initiates RAAS to reabsorb water and salt, results in increased Blood volume, triggers natriuresis.

Question 9

What tubule cells regulate K+? How do they restore K+ levels?

Answer 9

K+ excretion is hormonally regulated in distal tubule and collecting duct.

alpha-intercalated cells of COLLECTING DUCT actively reabsorb K+ via K+/H+ ATPase

K+ deficiency: K+ reabsorbed while H+ secreted

K+ excess: high concentration of ECF K+ reduces K+ reabsorption

Principal cells of collecting duct ACTIVELY secrete K+ via Na+/K+ATPase in response to aldosterone (which up regs that molecule)
More. Confused

Question 10

What are diuretics and what are they used for?

Answer 10

They increase urine output (promote diuresis). Used to reduce water retention

Question 11

Distinguish diuretics:

1. Osmotic
2. Loop
3. Thiazide
4. K sparing

Answer 11

1. Osmotic diuretics promote water as well as Na+, K+ excretion by osmotic retention of water and solutes in tubule
2. Loop diuretics inhibit Na+, K+, Cl- reabsorption in thick ascending loop; water osmotically held in collecting ducts and excreted
3. Thiazides inhibit Na+/Cl- reabsorption from distal tubules
4. K sparing diuretic inhibits Na+ reabsorption and K+ secretion in collecting tubule by aldosterone. N+ stays in tubule as an osmotic diuretic and K+ is not secreted.