Section 3 Quiz 2 Flashcards
two types of cells in collecting tubule
- principal: maintains Na+/K+ ion balance
- intercalated: acid-base regulation
what hormones controls the permeability to water
ADH
final site for processing urine
the medullary collecting duct
high ADH levels
high water reabsorption = reduction of urine volume
most important segment for reabsorption and secretion
proximal tubule
descending LOH
mainly water reabsorption
thick ascending LOH and distal tubule
ion reapsorption, impermeable to water
how are metabolic wastes (creatine and urea) removed?
from blood via the glomerular filtration and then excreted in the urine by failing to be entrely reabsorbed.
high GFR leads to
high filtrate volume -> lower blood volume and BP
filtration efficacy
kidneys need a relative constant GFR to maintain filtration ability
blood presssure
removing fluid from blood modulates blood volume which changes BP
intrinsic control
renal autoregulation -local control in the kidney. maintains GFR
extrinsic control
control by the nervous system and endocrine system. maintains BP by regulating GFR
renal autoregulation
kidney adjusts its own resistance to blood flow to modulate GFR
myogenic mechanism:
tendancy of vascular smooth muscle to contract when stretched. Increase BP = constriction of afferent arterioles = increase Ra = decrease Pg = decrease GFR
tubuloglomerular mechanism:
-directed by macula densa (part of juxtaglomerular apparatus)
-chemoreceptors detects the NaCl in the filtrate in the distal tubule
-high NaCl causes the macula densa to release vasoconstrictor. on afferent arterioles which increases Ra, decreses Pg, and decreases GFR.
-end result: decrease GFR
sympahetic nervous system:
causes constriction of renal arteries which decreases renal blood flow, and descreases GFR
hormonal controls:
-nonepinephrine/epinephrine: systemic vasoconstriction, increase BP, increase Ra, decrease GFR, increase blood volume by decreasing urine output
-endothelin: peptide released by damaged vascular endothelium. vasoconstricts afferent/efferent arterioles to decrease rneal blood flow
-angiotensin II: a hormone that vasocontricts efferent arterioles. increases Re, decreases renal blood flow, decreases flow through peritubular capilaries, increases reabsportion, prevents decrease to blood volume.
renin angiotensin mechanism
regulates BP directed by kidneys
renin
hormone released by jutaglomerular cells due to low BP or low GFR. catalyzes conversion of angiotensin to angiotensin II.
-direct: low BP, reduce stretch in arterioles, activates juxtaglomerular cells directly
-indirect: signaling from macula densa cells to juxtaglomerular cells via chemical messengers
angiotenesin II
-vasoconstrictor thorughout the body which raises mean arterial pressure.
-preferential vasocontriction of efferent arterioles = increase in Re
-decreased renal blood flow, decrease blood flow throughout pertitubular capillaries, increases reabsorption of Na+ and water in tubules, restores blood volume
-prevents further decrease in Pg and GFR and allows kidneys to continue filtering out wastes in times of low BP
-stimuluares reabsorption of Na+ in the tubules, water flollows Na+. blood volume and BP increase
renin-angiotensin mechanism
-stimulates juxtaglomerular cells to release. renin
-renin catlyzes angiotensin to angiotensin II
-angiotensin II increases Re, increases Pg, and increases GFR
macula densa
detects low NaCl and has renin-angiotensin mechanism and tubuloglomerular feedback
tubuloglomerular feedback
-inhibits vasoconctrictors to release
-decrease Ra, increase Pg and GFR
