AVP V-1 receptor-mediated decrease in Cl- efflux and increase in dark cellnumber in choroid plexus epithelium

The cerebrospinal fluid (CSF)-generating choroid plexus (CP) has many Vr bi nding sites for arginine vasopressin (AVP). AVP decreases CSF formation rat e and choroidal blood flow but little is known about how AVP alters ion tra nsport across the blood-CSF barrier. Adult rat lateral ventricle CP was loa ded with Cl-36(-), exposed to AVP for 20 min, and then placed in isotope-fr ee artificial CSF to measure release of Cl-36(-). Effect of AVP at 10(-12) to 10(-7) M on the Cl- efflux rate coefficient (in s(-1)) was quantified. M aximal inhibition (by 20%) of Cl- extrusion at 10(-9) M AVP was prevented b y the V-1 receptor antagonist [beta-mercapto-beta,beta-cyclopentamethylenep roprionyl(1),O-Me-Tyr(2),Arg(8)]vasopressin. AVP also increased by more tha n twofold the number of dark and possibly dehydrated but otherwise morpholo gically normal choroid epithelial cells in adult CP. The V-1 receptor antag onist prevented this AVP-induced increment in dark cell frequency. In infan t rats (1 wk) with incomplete CSF secretory ability, 10(-9) M AVP altered n either Cl- efflux nor dark cell frequency. The ability of AVP to elicit fun ctional and structural changes in adult, but not infant, CP epithelium is d iscussed in regard to ion transport, CSF secretion, intracranial pressure, and hydrocephalus.