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Flashcards in 25 8-12 Deck (28):
1

8. Describe the forces (pressures) that promote or counteract glomerular filtration

OUTWARD PRESSURES:
Glomular hydrostatic pressure = HPg 55mm hg

INWARD PRESSURES:
Blood colloid osmotic pressure = OPg 30mm hg
Capsular hydrostatic pressure = HPc 15mm Hg

NFP = HPg55 - (OPg30 + HPc15) = 10mm hg

2

The good

Water, glucose, amino acids, ions, some hormones, vitamins B & C

3

The bad

Creatine, urea, uric acid

4

The ugly

Toxins, poisons, artificial colorings/flavors, drugs

5

Filtration:
Where
From/To
What
Active/passive
Selective/nonselective
Membrane

Renal corpuscle
Blood -->Filtrate
Good/bad/ugly
Passive
Nonselective
fenestrated/basement/podocyte

6

GFR

Glomular filtration rate - the volume of filtrate formed each minute by all the glomeruli of the kidneys.

3 factors affecting GFR:

1. NFP - the main controllable factor, altered by changing diameter of the afferent and sometimes efferent arterioles.

2. Total surface area for filtration - mesangial cells surrounding capillaries can fine-tune by contracting to adjust surface area available for filtration.

3. Filtration membrane permeability - fenestrated, way more permeable than other caps This explains how only 10mm hg NFP can produce huge amounts of filtrate.

7

Types of autoregulatory intrinsic mechanisms that directly control GFR

Myogenic and Tuboglomerular mechanisms of autoregulation. Directly regulate GFR.

8

Types of extrinsic mechanisms that control GFR

Hormonal (renin-angiotensin-aldosterone) mechanism, Neural controls.

Indirectly regulate GFR by maintaining systemic BP which drives filtration in the kidneys.

9

Myogenic control of GFR

↓ Systemic BP
↓ BP in afferent arterioles; ↓ GFR
↓ Stretch of smooth muscle in walls of afferent arterioles
Vasodilation of arterioles
↑ GFR

Property of vascular smooth muscle - contracts when stretched, relaxes when not stretched

10

Tuboglomerular control of GFR

↓ Systemic BP
↓ GFR
↓ Filtrate flow and ↓ NaCl in DCT
Macula Densa cells of juxtaglomerular apparatus of kidneys
2 EFFECTS

Vasodilation of afferent arterioles

OR

Granular cells of juxtaglomerular app release renin (follow with angio/aldo process)

When GFR ↑, there is not enough time for reabsorption and the concentration of NaCl in filtrate remains high. Macula Densa release vasoconstictors that reduce BF into the glomerulus. Conversly, low NaCl concentration inhibits ATP release from macula densa cells causing vasodilation/↑NFP+GFR.

11

When is intrinsic control effective?

When MAP is between 80-180. If below 80, extrinsic takes over.

12

Sympathetic NS control of GFR

↓ Systemic BP
Inhibits baroreceptors in blood vessels of systemic circulation
Sympathetic NS
2 EFFECTS

1. Vasoconstriction of systemic arterioles; ↑ peripheral resistance
↑ Systemic BP

OR

Granular cell of juxtaglomerular app release renin (follow with angio/aldo process)

BOTH end in ↑ Systemic BP

13

RAAS control of GFR

↓ Systemic BP
Granular cells release renin
Results in formation of AngioI from angiotensinogen from liver
ACE from lung causes AngioI --> AngioII

AngioII effects:
1. Hypothlamus/increase thirst
2. Hypothalamus/Post Pitt/↑ADH-vasopressin
3. Systemic arterioles (afferent)/↑ vasoconstriction
4. Adrenal cortex/aldosterone/kidneys/↑ NaCl/ ↑ H2O

End Effect: ↑ BP

14

What three ways can the granular cells be stimulated to release renin?

Direct stimulation/symp NS.

Input from the macula densa - either low BP or vascoconstriction of afferent arterioles ↓ GFR, macula densa sense low NaCl, signal granular cells

Reduced stretch of granular cells - a drop in mean arterial pressure stimulates their mechanoreceptors

15

Aside from Sympathetic and RAAS, how can GFR be influenced extrinsically?

ANP/BNP both can inhibit the release of renin

16

Reabsorption
Where
From/to
Same direction as filtration?
What
Active/passive

PCT (2/3)
Filtrate-->Blood
Opposite
Good (H2O/NaCl)
Both (salt is active, others follow passively)

17

Two ways reabsorption can happen?

Paracellular - between epithelial cells (leaky tight junctions)
Transcellular - through epithelial cells (most common)

18

5 steps in transcellular transport

Luminal membrane,
cytosol,
basolateral membrane,
IF,
endothelial membrane

19

Transport maximum

Tm - max amount of a substance that can be reabsorbed or secreted across tubule epithelium in a given amount of time (depends on the number of transport proteins)

20

Passive tubular reabsorption

Passive reabsorption of negatively charged ions that travel along an electrical gradient created by the active reabsorption of Na+

21

Obligatory water reabsorption

Occurs in water permeable regions of the tubules in response to osmotic gradients created by active transport of Na+ (water follows salt)

22

Secondary active transport

Responsible for absorption of glucose/aminoacids/vitamins/cations - occurs when solutes are cotransported with Na+ when it moves along its concentration gradient

23

Renal handling of Na+ and H2O by PCT

Na+ - 67%, active/uncontrolled

H2O - 65%, passive/obligatory

24

Renal handling of Na+ and H2O by LOOP

Na+ - 25%, active/uncontrolled

H2O - 15%, passive/obligatory

25

Renal handling of Na+ and H2O by DCT/CD (juxtamedullary nephrons)

Na+ - 8%, active/variable (subject to aldosterone)

H2O - 20%, passive/variable (subject to ADH) principal cells

26

Loop of Henle in juxtamedullary nephrons - descending vs. ascending

Descending: permeable to H2O, Impermeable to salt, Permanent aquaporins Ascending: Impermeable to H2O, Permeable to NaCl (passive and active.

27

Two types of cells found in DCT/CD?

Principal cells - responsive to aldosterone/ADH, intercalated cells - help regulate urine ph and blood ph

28

How are sodium and water reabsorption regulated in the DCT/CD?

ADH - inhibits urine output by ↑ aquaporins in principal cell's apical membrane.

Aldosterone - Increases Na+ retention by synthesizing and retaining Na+/K+ channels in apical/principal cells and more basolateral Na+/K= ATPases (almost no salt leaves). Aldosterone ↑ BV/BP because salt follows water.

ANP - lowers blood Na+ by inhibiting Na+ absorption at the CDs