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Endocrine E3
Endocrine E3 Regulation of Salt & Water Balance
Question | Answer |
---|---|
what system regulates sodium and water | endocrine |
how is osmolality of the ECF monitored and adjusted | regulating water excretion by the kidney in response to ADH |
Na+ is the major ________ in ECF, maintenance of vascular volume depends on what | electrolyte, maintenance sodium balance |
renal mechanisms of Na+ balance are regulated by | 1)renin-angiotensin-aldosterone system 2)atrial natriuretic peptide |
hormonal mechanisms also regulate | salt and water intake and vascular tone |
all renal reabsorption is due to what | 1)passive Na+ reabsorption into tubular cells following a concentration gradient at luminal surface 2)active Na+ removal from tubular cells due to Na+/K+ ATPase(pump) at basolateral surface keeps tubular intracellular Na+ low |
Na+ coupled transport also reabsorbs | 1)glucose 2)amino acids 3)phosphate 4)HCO3- 5)H20 |
hormones that regulate NaCl/H20 | 1)antidiurectic hormone 2)renin-angiotensin-aldosterone 3)atrial natriuretic peptide |
what signals the kidney to conserve H20 | ADH |
when is ADH released in the kidney to conserve H20 | 1)plasma osmolality is increases(>280 mOsm/Kg) 2)plasma volume is decreased at least 10-15% |
powerful vasoconstrictor targeting the arteriolar smooth muscle | ADH |
ADH via V2 receptor causes insertion of _______ making the collecting duct permeable to ______ | aquaporins, H20 |
osmole receptors are found where | in the circumventricular organs near the 3rd ventricle |
what is the most potent osmolyte | NaCl |
what stimulates ADH during dehydration | 1)increased osmolality 2)decreased volume(pressure) |
what happens if there is a decrease in both osmolality and a decrease in volume | osmolality is kept constant if volume depletion is small but if volume loss is large osmolality is sacrificed to maintain integrity of circulation |
1)decreased ADH production(central) or decreased response of kidney to ADH(nephrogenic) 2)large amounts of dilute urine 3)concentrated body fluids if intake is not increased | diabetes insipidis |
1)increased ADH secretion as plasma osmolality is low 2)death can occur due to dilution of plasma electrolytes due to excessive reabsorption of free H20 | syndrome of inappropriate ADH |
what is renin synthesized and secreted by | juxtaglomerular cells in walls of afferent renal arterioles |
what is renin release stimulated by (3) | 1)SNS activation associated with decreased blood pressure sensed by baroreceptors 2)decreased tension on afferent arterioles in glomerulus 3)decreased pressure in glomerulus, decreased rate of NaCl delivery to macula densa |
renin catalyses the formation of ___________ from _____________ | angiotensin I, angiotensinogen(liver) |
angiotensin I is converted to angiotensin II by converting what enzyme | ACE |
where is angiotensin I converted to angiotensin II | pulmonary endothelium as blood perfuses the pulmonary capillaries |
angiotensin II is produced locally in what different tissue | 1)blood vessels 2)adipose 3)brain |
angiotensinogen, renin, and ACE may act as a ________ to stimulate prostaglandins or act as what | paracrine, local growth factor |
what is the primary signal for release of aldosterone | angiotensin II |
what acts in vasoconstriction in the kidney decreasing renal blood flow & glomerular filtration | angiotensin II |
what increases cardiac contractility | angiotensin II |
what redistributes blood flow: increase brain, heart, skeletal muscle, decrease skin, viscera | angiotensin II |
what is the most potent pressor substance known | angiotensin II |
angiotensin II may act as growth factor for what | cardiac and smooth muscle |
what are the actions of angiotensin II in the CNS | stimulates thirst, appetite for Na+, secretion of ADH |
ADH receptors are found where | in hypothalmic cells(subfornical organ & organum vasculosum) which project to supraoptic & paraventricular N. and vasomotor centers |
what is renin-angiotensin-aldosterone regulated by | negative feedback, regulated by blood volume which increases as a result of sodium retention |
what promotes the excretion of sodium in the urine | atrial natriuretic peptide |
what is atrial natriuretic peptide syntehsized and secreted from | atrial myocyctes, 28aa in response to stretch(increased atrial pressure) |
another form of brain natiuretic peptide is synthesized and secreted by | atrial and ventricles isolated from the brain |
CNP is found in | CNS and endothelial cells |
ANP/BNP binds to | natriuretic peptide receptor-A(NPR-A) |
natriuretic peptide receptor-B (NPR-B) binds to | CNP |
natriuretic peptide receptor-C (NPR-C) binds to | ANP/BNP/CNP |
ANP half life is ________ and BNP half life is _______ | 3 minutes, 20 minutes |
both ANP and BNP do what | stimulate formation of cyclic GMP which modify functions |
what are the 3 mechanisms used to modify cellular functions | 1)phosphorylation of regulatory proteins 2)cyclic nucleotide phosphodiesterases 3)direct ion channel regulation |
physiologic actions of ANP | 1)prevent volume overloading 2)lower blood volume & decrease blood pressure |
what is the physiologic action of ANP on the cardiovascular system | vasodilation of vascular smooth muscle |
what is the physiologic action of AnP on the kidney | 1)increase Na+ & H2O excretion by increase glomerular filtration & decrease Na+ & H2O reabsorption 2)decrease renin secretion by decreasing angiotensin II |
what are physiologic actions of ANP on the hypthalamus | 1)decrease ADH secretion 2)decrease vasomotor activity 3)inhibits thirst 4)decreases Na+ appetite |
what is the physiologic action of ANP on the pituitary gland | inhibits release of ACTH (decreases adrenal support) |
what is the physiologic action of ANP on the adrenal gland | decrease aldosterone secretion |
what is the physiologic action of ANP on the sympathetic nervous system | may decrease norepinephrine release from SNS & decrease epinephrine release from adrenal medulla |
what are the 4 derangements of fluid balance discussed in class | 1)hemorrhage 2)dehydration 3)salt loading 4)salt depletion |
what happens during a hemorrhage | 1)immediate response is massive vasoconstriction mediated by SNS 2)slower in onset stimulated by renin-angiotensin-aldosterone 3)stimulation of ADH 4)inhibition of ANP |
what happens during dehydration | 1)H2O loss > solute loss leads to increase in both ECF and ICF osmolality 2)ADH primary way to correct because it promotes H2O reabsorption without reabsorbing solute 3)inhibition of ANP |
what happens during salt loading | promotes the excretion of increased Na+ in the urine |
what happens during salt depletion | minimizes excretion of Na+ in the urine |
when salt loading 350 mm/day/5days what are the levels | 1)plasma Na+ 140mm 2)hematocrit 38% 3)ADH, ANP, urine Na+ all increase 4)plasma renin activity, aldosterone decrease 5)plasma protein concentration stays constant 6)volume expansion |
when salt depletion 10mm/day/5days what are the levels | 1)plasma Na+ 140mm 2)hematocrit 41% 3)ADH, ANP, urine Na+ decrease 4)plasma renin activity, aldosterone increase 5)plasma protein concentration stays constant 6)volume contraction |