Renal System- semester 2 Flashcards
antidiuretic hormone
regulates h2o balance by how much h20 is reabsorbed by nephrons
causes less urine produced, more h2o reabsorbed
vasocon of bv
also called vasopressin
neuroendocrine cells
release hormones, not neurotransmitters
cell bodies in hypothalamus, axons form posterior pituitary
obligatory urine loss
minimal urine production
result when total body h20 decreases
decrease V of extracellular fluid
decrease BP
increase [] of blood
ADH in collecting duct
ADH binds receptor, info is transmitted
principal cells stimulated by ADH have more aquaporin 2 channels at luminal membrane
-vesicles insert more aquaporin channels into luminal membrane, allowing more h20 in collecting duct cells
ADH and BP relationship
-low total body h2o, decreases MAP
low BP triggers, decrease baroreceptors, activity release of ADH
-then ADH increases number of aquaporin 2 channels in luminal membrane to reabsorb more h2o
most and lease [] urine
1400 mOsm, 100
diuretics
meds increase urine volume
diabetes insipidus
produces large volume of urine b/c nephron tubules doesn’t reabsorb enough h2o
-need to drink a lot of h2o and/or use synthetic ADH
neurogenic diabetes insipidus
caused by damaged hypothalamus or post. pituitary
smaller amounts of ADH or none
nephrogenic diabetes insipidus
receptors for ADH can’t respond to hormones when it is in blood
Low total body Na levels
renin-angiotensin-aldosterone system (RAAS) releases angiotensin 2 and aldosterone
lower blood volume, higher BP
high total body Na levels
atrial natriuretic peptide (ADP) hormone is released
increase blood volume, decrease BP
steps of RAAS pathway
renin is made by juxtaglomerular cells of afferent arterioles when Na level are low
-renin acts on angiotensinogen and breaks it to angiotensin 1
then angiotensin 1 breaks by angiotensin-converting enzyme so it becomes angiotensin 2
function of juxtaglomerular apparatus
macula dense cells detect low Na level
-juxtaglomerular apparatus cells secrete renin in blood when low bp
aldosterone
release in blood by adrenal gland
part of RAAS pathway
stimuli to release is angiotensin 2 or high [] of K
regulates Na and K in convoluted tubule and collecting duct
angiotensin 2
trigger low Na
vasoconstrictor of afferent and efferent arterioles (decrease BF and GFR, more Na in blood)
-stimulate released of aldosterone
actions of angiotensin 2 in epithelial cells
Na/H exchange- increase activity on luminal M
more Na in tubule cells
Na/K ATPase- high primary active transport on basolateral M, increase Na out prox. tubule cells
aldosterone actions in epithelial cells
Na channels: more Na channels move into luminal membrane in tubule cells
Na/K ATPase: increase, Na reabsorbed
K channels: increase K channels to move in luminal M, more secreted
Atrial natriuretic peptide
-stimulus high BP and Na
-ANP decreases Na levels
-released by cardiac atrial cells, have mechanoreceptors (stretch) to detect and release
actions of ANP
-ANP blocks aldosterone from releasing
- ANP vasodilates afferent arterioles, increase GFR, faster filtration, less Na reabsorbed
low plasma Na
RAAS pathway
-angiotensin 2 and aldosterone increase Na reabsorption
high plasma Na
ANP released, more Na excreted
high plasma K
-dangerous
-too lower it, K secreted using aldosterone
ascending loop of henle absorption
only ions
-impermeable to h2o
