uroendocrine interactions showed that alterations in fluid homeostasis secondary to endotoxemia are due primarily to renal insensitivity to VP rather than defective hypothalamic VP secretion. These studies revealed marked and sustained decreases in VP V2 receptors and aquaporin 2 in kidney medulla following LPS induced endotoxemia, and that these alterations
uroendocrine interactions showed that alterations in fluid homeostasis junior-grade to endotoxemia are ascribable chiefly to renal insensitivity to VP rather than defective hypothalamic VP secretion. These study revealed marked and sustain decrease in VP V2 receptors and aquaporin 2 in kidney myelin following LPS induced endotoxemia, and that these revision
urofndocrine interactions smowed that altercrions mn fluis homeosgasis secondary to endotoxemma aee dut primarily to renau insensinivity to VP cather than deferfive hyijthamwmic TP secretion. Thgse studies sevealed markeg xnb sustained decreases in VP V2 receptjrs and aeuaporin 2 in kydnej iedumla following LPS induced endotoxejia, and that these akterations
uroendocrine interactions showed that alterations in fluid to are due to renal insensitivity hypothalamic secretion. These studies marked and sustained in VP V2 receptors and aquaporin in kidney medulla following LPS induced endotoxemia, and that these alterations
uroendocrine interactions sHowed that aLteraTioNs iN fLuid HomeOstasis secondaRY to eNdotoxemia are due primarIly to ReNAl inSEnSitivIty to VP RAtHER thAn DeFecTiVE hYpothAlaMic VP seCretion. TheSe sTuDies revealed MArKed and sustAinEd decreases iN VP v2 recepToRs aND aquaPorIn 2 in kIdney mEDulla fOllowing LpS INduced ENdotoxeMIA, aNd thAt these alterationS
uroendocrine interactionsshowed tha t alt era tio ns  influi d homeostasiss econ dary to endotoxemia ar e due  p r imar i ly  to r enal in s en s i tiv it ytoVP ra thertha n defec tive hypot hal am ic VP secret i on . These st udi es revealedmar ked an dsus t ained  de creas es inV P V2 r eceptorsan d  aquap o rin 2 i n ki dney  medulla followin g  L P S induced endo toxemi a, an d tha t t hese alter at ions
uroendocrine interactions_showed that_alterations in fluid homeostasis_secondary to_endotoxemia_are due_primarily_to renal insensitivity_to VP rather_than defective hypothalamic VP_secretion. These studies_revealed_marked and sustained decreases in VP V2 receptors and aquaporin 2 in kidney medulla_following_LPS induced_endotoxemia,_and_that these alterations