Control of Body Fluid Volume And Osmolarity 1/2 Flashcards Preview

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Flashcards in Control of Body Fluid Volume And Osmolarity 1/2 Deck (14)
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How does the kidneys compensate for large changes in renal arterial pressure and keep GFR and blood flow constant?

By changing the afferent and efferent arteriolar resistance
- afferent arteriolar resistance goes up proportionally with renal arterial pressure where as efferent arteriolar pressure and venous resistance goes down


JG cell receptors and control of JG cells

A1 = vasoconstriction

B1 = releases renin

Controls on JG cells:
- sympathetic neurons
- macula densa
- decreased afferent arteriole pressure


Primary actions of the macula densa

1) increased GFR flow and arterial pressure And increased sodium into glomerulus
- causes release of ATP from macula densa to the nearby JG cells to constrict the kidney afferent vessels and decrease renin secretion to allow for more sodium secretion

2) decreased GFR flow and arterial pressure and decreased sodium into glomerulus
- casues release of NO/PGE from macula densa to the nearby JG cells to dilate the kidney afferent vessels and increase renin secretion



1) Decreased effective volume in the body activated JG cells in kidneys

2) JG releases renin which cleaves angiotensinogen -> angiotensin

3) angiotensin-1 goes to the lungs and gets cleaved into angiotensin-2

4) angiotensin-2 goes to the CNS and hypothalamus to increase thirst and releases arginine vasopressin (ADH)

5) angiotensin-2 goes to the adrenal glands and releases aldosterone. Aldosterone goes back to the kidneys and decreases sodium excretion and causes retaining of water

6) angiotensin-2 also goes back to the kidneys and further directly reduces sodium and water excretion


Direct effects of angiotensin-2

Constricts both afferent (slightly) and efferent (by alot)arterioles
- GFR goes up
- filtration fraction goes up
- renal blood flow goes down

Also stimulates sodium:potassium, sodium:H+ and sodium:bicarbonate channels to increase sodium moving into the renal interstitial fluid
- ** a secondary side effect to this is a contraction alkalosis in the body due to increased sodium/H+ exchanger activation


How does angiotensin-2 cause water retention despite decreased renal blood flow and increased GFR?

The filtration fraction (GFR/blood flow) goes up which causes water to enter the bowmans capsule but ions and proteins to enter the capillaries

This separation causes water to actually leave the capsule and enter the capillaries through diffusion via starling forces


Indirect effects of angiotensin-2 on renal function

Decreases blood flow to the vasa recta which induces increased urea and decreased sodium production in the medulla

This produces a gradient for passive NaCl reabsorption by the thin ascending limb of Henle

Ultimately leads to increased Na+ reabsorption


Major actions of aldosterone

1) aldosterone enters principal cells via diffuse and interacts with cytosolic aldosterone receptors

2) these bound receptors interact with nuclear DNA to promote gene expression (protein synthesis) which products from this activate sodium channels (ENaC’s) in the apical membrane and sodium/H+ pumps in the base lateral membrane

3) this ultimately causes increased sodium reabsorption since ENaCs reabsorption sodium from the lumen into the interstitum and the sodium/H+ pumps in the basolateral membrane enhance this effect


What is a secondary effect of ACE that is key to making sure vasoconstriction occurs?

ACE increases Bradykinin breakdown
- bradykinin is a vasodilator in high levels


What is the relationship between plasma AVP/ADH and plasma osmolality?

Positive correlation In normal conditions

Exponential positive in volume contraction

Very slight positive in volume expansion


AVP control/synthesis

Is synthesized in the hypothalamus in the magnocellular neurons within the paraventricular nucleus and supraoptic nucleus

Released in the posterior pituitary to go to the kidneys and act to reabsorption of water to dilute ECF

**this is all inresponse to increase stimulation of osmoreceptors in the OVLT and SFO in the hypothalamus


How does AVP look structurally?

9 aa long with glycine aa getting amidated at position 9 to make mature AVP

1 =. Cystine
2 = tryptophan
3 = phenylalanine
4 = glutamine
5 = asparine
6 = cysteine
7 = proline
8 = arginine
9 = glycine** amide group

Cleaves from proneurophysin-2 molecules


AVP broad effects in the kidney

Increases water permeability along the kidney nephron
- AVP/ADH works by putting aquaporins along the below areas in the nephrons which leads to concentrated urine and increased water in interstitial fluid

**increases ICT/CCT and OMCD/IMCD’s the most within the principle cells in these areas


What happens in the nephrons when high water intake situations are present?

No release of ADH/AVP and causes not much water to leave the nephron

However, NaCl does leave the nephron and goes into the interstital fluid following down its gradient
- leads to really low osmolailty in urine