Week 1: Sodium and volume homeostasis Flashcards Preview

Renal > Week 1: Sodium and volume homeostasis > Flashcards

Flashcards in Week 1: Sodium and volume homeostasis Deck (13):
1

Analyze the relationship between Na intake, plasma [Na], and plasma volume. describe how extracellular volume is sensed in the body.

-sodium is primary determinant of ECF and plasma blood volume since it is main cation in ECF
-If NaCl in body increases, plasma volume increases with no change in osmolality
-varying salt in diet affects plasma volume, high Na+ diet expands plasma volume but doesn't change interstitial fluid volume or body weight
-ISF compartment can store Na non osmotically on negatively charged matrix molecules in skin and/or move into muscle in exchange for K+
-plasma volume sensed by stretch receptors

2

Describe sensors in renin angiotensin system. Summarize the major pathways that carry information to modulate renin release.

SENSORs
1. renal afferent arteriolar baroreceptors "myogenic"
-senses stretch
2. macula densa NKCC senses low [NaCl] "Macula densa transport"
3. extrarenal baroreceptors to CNS? increases SNS input to JGA "neurogenic"
These sensors induce renin release from JG cells

3

Localize renal granular cells that produce renin. What controls release of renin?

Juxtaglomerular apparatus: region consisting of macula densa, extraglomerular mesangium, and juxtaglomerular cells
-JG cells: specialized afferent arteriolar SMCs that make and store renin
-Renin is stored in granules in JG cells, released in response to increase in cAMP (from MD or SNS input) or decrease in cell [Ca2+] set off by less volume/stress

4

Compare and contrast the effects of AngII on vascular, endocrine, and renal targets.

1. CV: systemic vasoconstriction of arterioles
2. Endocrine
-increase ADH release, aldosterone, thirst
3. Renal
-regulation of GFR: constricts efferent arterioles and glomerular mesangial cells to help maintain GFR in face of decreased RBF
-increase Na+ transporter #s: NHE3, NKCC, NCC, and collecting duct (ENaC)
-aldosterone also amplifies previous by increasing NaCl reabsorption and K+,H+ secretion in distal tubule (NCC) and collection duct (ENaC)

5

Describe local RAS.

-activation can amplify Na+ reabsorption locally, without further systemic vasoconstriction
0may be good therapeutic target in HTN

6

Identify the location of aldosterone synthesis, and the factors that stimulate aldosterone synthesis and release.

-made in zona glomerulosa of adrenal gland
-synthesis stimulated by: increase AngII, increase plasma [K+], ACTH, low Na+ diet (indirectly)
-synthesis inhibited by: ANP

7

What is the mechanism of action of aldosterone. Explain the importance of both mineralocorticoid receptors and 11 B-OH steroid dehydrogenase for aldosterone action.

-mineralocorticoid receptors (MR_ are activated by steroid binding-->moves to nucleus, binds to DNA regulatory regions (MRE)-->alters transcription rates
-stimulates synthesis of serine/threonin kinase (Sgk), which acts on Na channels, causing less degradation of Na channels
-MR is also activated by glucocorticoids. Need 11 B-OH-SD to metabolize glucocorticodes to a form that doesn't bind MR, otherwise will have MR saturation and increased aldosterone

8

ID the regions of the nephron where aldosterone acts. Explain the renal actions of aldosterone on Na, K, and H transport and excretion.

-distal tubule: activates NaCl co transporters
-CCD: increases apical and basolateral Na transporter activity-->increasing K+ and H+ secretion
-Na reabsorption drives secretion of K+ and H+ into lumen of collecting duct
-Sgk increase apical ENaC by decreased degradation and increased activation, increases pump activity also
-slower action: increases # of channels, Na/K ATPases, NCC by transcription

9

Summarize the renal responses to decreased ECF volume and the signals that trigger the responses.

-decreased ECF volume leads to:
-thirst, increased SNS, increased ADH, decreased ANP, increased Renin and therefore AngII
-AngII: increased NaCl reabsorption in PT, and in DT and CDD (also via aldosterone)-->decreased NaCl excretion
-AngII also increases thirst
-SNS activity also increases renin production

10

Describe where ANP is made, the stimulus that provides its secretion, and list the targets and actions of ANP.

-ANP made in atria and stored in atrial granules
-released in response to atrial stretch which increases cellular Ca2+ and stimulates fusion of vesicles and release of contents to blood
-it activates guanylate cyclase-> increased cGMP, which inhibits IMCD NaCl reabsorption via amiloride sensitive channels
TARGETS
1. CV: vasodilation
2. Endocrine: decreased renin, aldosterone, ADH
3. renal: increased GFR by decreased afferent arteriole resistance, and decreased Na reabsorption in IMCD

11

Summarize the renal responses to increased ECF volume and decrease the signals that trigger the response.

-decreased SNS, ADH, renin and AngII
-increased ANP
-leads to decreased NaCl reabsorption in PT, DT, CDD
-increased NaCl excretion

12

Why can't ANP correct edema in CHF?

-ANP released due to increased atrial stretch from increased ECF volume
-not enough Na gets to IMCD for ANP to have diuretic effect
-anti-natriuretic hormones induced work to increase Na reabsorption along nephron before the IMCD

13

Signals that stimulate renin release

1. Myogenic: decrease bp means less cell Ca, activates renin
-increase BP, stress and increase cell Ca inhibits Renin (via inhibition of AC5/6)
2. Decrease NaCl transport by MD
-due to decrease ECF vol. or decreased GFR
-signals to afferent arteriole via prostaglandins, increase cAMP-->release renin
3. Neurogenic
-decrease extrarenal baroreceptor stretch-->CNS-->increase sympathetic tone to afferent arteriole-->stimulates cAMP-->renin release
4. Metabolic: high glucose levels and renin release?
5. Hormones: AngII via AT1R raises cell Ca2+ and inhibits renin release. ANP via cGMP inhibits renin release