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Effects of high potassium concentrations on para-aminohippurate (PAH) transport by isolated, perfused snake (Thamnophis spp.) distal-proximal renal tubules were studied. Increasing the potassium concentration in bath from 3 mM TO 10 mM OR 40 MM led to about 50% decrease in net PAH transport from bath to lumen in less than 10 min, but transport still occurred against concentration gradient. Cell water PAH concentration was not significantly depressed in 10 mMpotassium and was nearly double control level in 40 mM potassium. Apparent luminal membrane permeability to PAH, calculated from perfusion studies, averaged about 3.5 x 10(-5) cm sec(-1) in 3 mM potassium, 1.15 x 10(-5) cm sec(-1) in 10 mM potassium, and 0.48 x 10(-5) cm sec(-1) in 40 mM potassium. Apparent peritubular membrane permeability, determined from PAH efflux from tubules with oil-filled lumens averaged about 0.5 x 10(-5) cm sec(-1) in 3 mM potassium, 0.29 x 10(-5) cm sec(-1) in 10 mM potassium, and 0.17 x 10(-5) cm sec(-1) in 40 mM potassium. These data suggest that high potassium concentrations depress transepithelial PAH transport primarily by reducing luminal and peritubular membrane permeabilities. Effect of high potassium on PAH transport was reversed within 20 min after restoration of control potassium concentration.

Accumulation of p-aminohippurate (PAH) and N-methylnicotinamide (NMN) by renal cortical slices was used to estimate transport capacity for organic anions and cations, respectively. In a previous study, renal organic anion transport appeared to be selectively depressed in animals rendered obese by high fat feeding. However, the effects of obesity could not be discretely separated from the effects of the 30% fat diet used to produce the obesity. Genetically obese hyperglycemic mice provided a model to determine the effect of obesity on renal transport systems without the complication due to diet. Accumulation of both PAH and NMN was depressed in renal cortical slices from genetically obese mice. Addition of plasma from thin or obese animals increased PAH accumulation by slices from thin animals. Accumulation by slices from obese animals was unaffected by addition of plasma. Oxygen consumption with acetate in the medium was less in kidneys from obese mice than kidneys from thin mice. Thus, in addition to inhibition of transport capacity, renal cortex of genetically obese mice has a biochemical defect that prevents response to stimulators. It is concluded that several renal functions are depressed in the genetically obese hyperglycemic mouse. Whether the depressed function results from the obesity or is concomitant with the gene for obesity is as yet undertermined.

Using radioimmunoassay techniques, arteria (A) and renal venous (RV) plasma renin activities were measured in sodium pentobarbital-anesthetized dogs during clearance and stop-flow periods. Changes in RV-A renin were used to estimate changes in renin secretion. RV-A renin increased during stop flow from its average value during clearance periods, whether 10% mannitol in 0.15 M NaCl or 10% mannitol in 0.1 M Na2SO4 was being administered intravenously. However, RV-A renin during mannitol + NaCl stop-flow periods was significantly greater than during mannitol + Na2SO4 stop-flow periods. Distal tubular fluid Na concentrations as indicated by stop-flow analysis were higher during the latter. These observations suggest that a macula densa stimulus, Na concentration, and/or load, may control renin secretion during ureteral occlusion.

The sites of origin of renal lymph were studied by analysis of simultaneously collected samples of lymph and plasma. The samples included renal hilar (HL) and capsular lymph (CL), thoracic duct lymph (TD), renal venous (RVP) and arterial plasma (AP), and were analyzed for Na+, Cl-, K+, urea, glucose, inulin, and PAH concentrations. The glucose concentrations of HL (76 mg/100 ml, SE +/- 1.9), and CL (92 mg/100 ml, SE +/- 2.5) were significantly different (P less than 0.01) from that of RVP (86 mg/100 ml, SE +/- 2.2). Concentrations of both inulin and PAH in CL and HL fell between the AP and RVP values. The concentration of inulin in CL (CL/RVP = 1.27) exceeded that in HL (HL/RVP = 1.10), but no such difference was detected for PAH. The Na+ (152 meq/liter) and Cl- (129 meq/liter) concentrations in HL were significantly (P less than 0.01) higher than those in CL (Na+ = 148 meq/liter; Cl- = 120 meq/liter), in TD (Na+ = 146 meq/liter; Cl- = 121 meq/liter), and in RVP (Na+ = 144 meq/liter; Cl- = 114 meq/liter. These differences remained highly significant when the electrolyte concentrations were converted to milliequivalents per kilogram H2O. In contrast, no significant differences were detected between the concentrations of urea in the various fluids sampled. It is concluded that CL and HL do not drain a perfectly homogeneous intrarenal pool, and that they do not equilibrate with RVP or AP within the kidney. The results also indicate that CL and HL derive a small component from tubular reabsorbate; that for CL stemming from the cortex, and that for HL from the deeper cortex and outer medulla.

Section freeze-dry radioautography has been used to examine the intrarenal distribution of a water-soluble organic acid (para-aminohippuric acid (PAH-3H)) under constant-infusion, steady-state conditions in mouse and rat kidney in vivo. The technique described here has the following advantages: (a) Sectioning and freeze-drying are accomplished in a closed cryostat at temperatures below -40 degrees C; (b) Handling of the section is facilitated by mounting of the section-to-be on adhesive-coated Saran Wrap prior to cutting; (c) Unembedded freeze-dried sections are attached to photographic film at ambient temperature in the dark room; (d) Fixation follows completion of radioautographic exposure and precedes photographic development; (e) Permanent close contact is maintained between tissue and film. Morphologic preservation compared favorably with that obtained by optimal fixation techniques, which, however, permit diffusion. Cellular accumulation of PAH-3H during secretion was demonstrated in the proximal tubule under steady-state conditions in vivo. The cellular concentration of PAH-3H was uniform throughout the length of the proximal tubule in mouse and rat kidney.