Regulation of Na and H20 Flashcards
Factors that promote Na+ reabsorption
Activation of renal sympathetic nerves
Activation of renin/angiotensin system
Secretion of aldosterone
Factors that promote Na+ excretion:
Release of atrial, brain natriuretic peptides (ANP, BNP)
Release of urodilatin
Intrarenal prostaglandins
Factors that promote renin secretion
Renal sympathetic stimulation (due to fall in perfusion pressure through the cardiopulmonary baroreceptors): directly stimulates renin secretion via β1 receptor activation in the JG apparatus
Tubuloglomerular feedback: dec. NaCl delivery to macula densa = inc. renin secretion
Intrarenal baroreceptor (wall of afferent arteriole): afferent arteriolar vasoconstriction = dec pressure at granular cells = inc. renin secretion
What effect would loop diuretics have on renin secretion?
diuress casue can’t conc/ urine= hypoperfusion renin secretion goes up =may aggravate HTN
Angiotensin II stimulates
Systemic arteriolar constriction
Renal arteriolar constriction: efferent > afferent.
How would this affect GFR & RBF?
-Maintain GFR mostly, RBF goes down
Na+ reabsorption: PCT (via ↑ Na-H exchanger activity) > TAL, CCD
Thirst
ADH secretion from posterior pituitary
Aldosterone secretion from adrenal cortex
Constrict renal mesangial cells (dec. Filtration)
RAAS responds to
decreased BP, RBF or release of catecholamines
Results in dec NA excreaton and inc Na reabsorption
Aldosterone’s actions
in late distal convoluted tubule, collecting duct (principal cells)
Stimulates sodium reabsorption
Results in: lumen-negative potential difference
Electroneutrality maintained by: passive Cl- reabsorption & K+/H+ secretion
Stimulates potassium secretion
Stimulates H+ secretion (↑ H +-ATPase activity in intercalated cells of CCD)
Secreted any time you have hyperK ATCH or vol depletion
What would happen to K & H excretion in a patient with hyperaldosteronism?
hypoK & metabolic alkalosis
ANP
increases Na+, H2O excretion
increases GFR: Afferent arteriolar dilation, efferent arteriolar constriction
ANP inhibits Na+ reabsorption in medullary collecting duct
ANP suppresses renin secretion
ANP suppresses aldosterone secretion
ANP is a systemic vasodilator
ANP suppresses AVP secretion, actions
Urodilatin
Endogenous renal natriuretic peptide
Secreted by DCT, collecting duct in response to increased arterial pressure and ECF volume
Urodilatin suppresses Na+ and water reabsorption by medullary collecting duct
Unlike ANP and BNP, urodilatin has no effect on systemic circulation
Intrarenal prostaglandins (e.g. PGE2)
Increase GFR by dilating renal arterioles
Suppress Na+ reabsorption in thick ascending limb, cortical collecting duct-
what effect will this have on the solute concentration in the renal medullary tissue?
Net effect: increased urinary Na+ excretion
NSAIDs oppose = renal failure
Two major stimuli for ADH release:
hyperosmolality
volume depletion
Hypothalamic osmoreceptors are more important than hepatic osmoreceptors