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1. Ventriculo‐cisternal perfusions were performed on rabbits with artificial cerebrospinal fluid containing blue dextran and tritium‐labelled prostaglandin F2α([3H]PGF2α). In order to study the nature of prostaglandin (PG) transfer across the blood—brain barrier, high concentrations of PGF2αor potential PG transport inhibitors were added to the perfusion fluid after the normal rate of [3H]PGF2αclearance was established.

1. Incubation of rabbit choroid plexus, anterior uvea (iris‐ciliary body complex) or slices of kidney cortex in a medium containing tritium‐labelled prostaglandin F(2alpha) ([3H]PGF(2alpha) or E1 ([3H]PGE1) results in a four‐ to thirteenfold concentrative accumulation of 3H activity. 2. Addition of PGF(2alpha, PGF(1) or PGA(1), any one of five PG analogues or a PG precursor, arachidonic acid, at a concentration of 10(‐4) M reduced the active accumulation of [3H]PGs by 47‐97%. Octanoic acid, at the same concentration, had only a moderate effect on the choroid plexus and no significant inhibitory effect on [3H]PFG(2alpha) accumulation by anterior uvea or kidney cortex. 3. Inhibition was also obtained with 2 mM iodoacetate (under anaerobic conditions) and with 10(‐4) M diploretin phosphate, probenecid, iodipamide, indomethacin or dinitrophenol. Perchlorate (10(‐4) M) and iodide (10(‐4) or 10(‐3) M) had no inhibitory effect while 10(‐4) M p‐aminohippuric acid had a significant inhibitory effect on the kidney cortex at a concentration of 10(‐4) M and on the anterior uvea at 10(‐3) M. 4. It is concluded that the apparent carrier mediated PG transport systems of the choroid plexus, anterior uvea and kidney cortex are not related to the iodide transport system, but may represent a subcomponent of the iodipamide transport system of these tissues. 5. These results suggest that the systemic distribution and the rate of renal excretion of PGs could be altered by high concentrations of PGs, pharmacologically less active PG analogues, some inhibitors of organic acid transport, and by some inhibitors of PG synthesis and PG action.

1. Corneal thickness was measured in vivoin normothermic and hibernating (body temperature = 7–10° C) woodchucks and the [Na+], [K+], [Mg2+] and water content of woodchuck and rabbit corneas were determined on freshly isolated tissues.

1. This investigation was undertaken to determine the time course of development of cation transport processes between blood and the extracellular fluid compartments of the central nervous system ( C.N.S.) of the foetal rhesus monkey. The development of concentration gradients withinthe cerebrospinal fluid (c.s.f.) system was also studied in an attempt to gain information on regional variations in transport activities.

1. Rhesus monkey (Macaca mulatta) foetuses were delivered by Caesarean section 3‐10 days before term. Aortic blood and cerebrospinal fluid (c.s.f.) samples were taken, the latter from the cortical subarachnoid space and the cisterna magna. The umbilical cord was clamped and foetal breathing prevented for 14–17 min. Blood and c.s.f. were sampled further during this total asphyxiation and for up to 24 hr thereafter.

1. Slices or bits of rabbit tissues, not exceeding 100 mg, were incubated in tissue culture medium containing tritium‐labelled prostaglandin ([3H]PG). In some experiments, incubation medium also contained saturating concentrations of an unlabelled prostaglandin (PG), or [14C]‐sucrose for determination of extracellular space. At the end of the incubation period, usually 1 hr, the tissues were removed and weighed, and their 3H (and 14C) content were determined along with that of a unit volume of medium.

1. Even when a steady level of 131I−is maintained in the blood for long periods, the uptake by brain and spinal cord is very small, and the possibility that this is due to an active transport of I−from brain‐tissue to blood has been examined.