25 8-12 Flashcards
- 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
The good
Water, glucose, amino acids, ions, some hormones, vitamins B & C
The bad
Creatine, urea, uric acid
The ugly
Toxins, poisons, artificial colorings/flavors, drugs
Filtration: Where From/To What Active/passive Selective/nonselective Membrane
Renal corpuscle Blood -->Filtrate Good/bad/ugly Passive Nonselective fenestrated/basement/podocyte
GFR
Glomular filtration rate - the volume of filtrate formed each minute by all the glomeruli of the kidneys.
3 factors affecting GFR:
- NFP - the main controllable factor, altered by changing diameter of the afferent and sometimes efferent arterioles.
- Total surface area for filtration - mesangial cells surrounding capillaries can fine-tune by contracting to adjust surface area available for filtration.
- Filtration membrane permeability - fenestrated, way more permeable than other caps This explains how only 10mm hg NFP can produce huge amounts of filtrate.
Types of autoregulatory intrinsic mechanisms that directly control GFR
Myogenic and Tuboglomerular mechanisms of autoregulation. Directly regulate GFR.
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.
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
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.
When is intrinsic control effective?
When MAP is between 80-180. If below 80, extrinsic takes over.
Sympathetic NS control of GFR
↓ Systemic BP
Inhibits baroreceptors in blood vessels of systemic circulation
Sympathetic NS
2 EFFECTS
- 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
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:
- Hypothlamus/increase thirst
- Hypothalamus/Post Pitt/↑ADH-vasopressin
- Systemic arterioles (afferent)/↑ vasoconstriction
- Adrenal cortex/aldosterone/kidneys/↑ NaCl/ ↑ H2O
End Effect: ↑ BP
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
Aside from Sympathetic and RAAS, how can GFR be influenced extrinsically?
ANP/BNP both can inhibit the release of renin
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)
Two ways reabsorption can happen?
Paracellular - between epithelial cells (leaky tight junctions)
Transcellular - through epithelial cells (most common)
5 steps in transcellular transport
Luminal membrane, cytosol, basolateral membrane, IF, endothelial membrane
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)
Passive tubular reabsorption
Passive reabsorption of negatively charged ions that travel along an electrical gradient created by the active reabsorption of Na+
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)
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
Renal handling of Na+ and H2O by PCT
Na+ - 67%, active/uncontrolled
H2O - 65%, passive/obligatory
Renal handling of Na+ and H2O by LOOP
Na+ - 25%, active/uncontrolled
H2O - 15%, passive/obligatory
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
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.
Two types of cells found in DCT/CD?
Principal cells - responsive to aldosterone/ADH, intercalated cells - help regulate urine ph and blood ph
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
