Hepatic portal vein infusion of glucose on sodium excretion in the rat.

Anesthetized rats were prepared with catheters in the hepatic portal (HPV) and femoral (FEM) veins and in the bladder or ureters. In some experiments the left kidney was denervated. HPV infusion of 1 M glucose at 2 ml/h for 20 min increased Na excretion by the kidney when given as a second infusion. Bilateral cervical vagotomy eliminated the increase in Na excretion during glucose infusion and uncovered a delayed decrease in Na and K excretion. Renal denervation attenuated the increase in Na excretion to HPV glucose. FEM infusion of glucose had variable effects, increasing Na excretion only after vagotomy. The results are interpreted to suggest that central and vagal receptors tend to enhance Na excretionwhereas splanchnic nerve afferents and humoral mediator(s) have the opposite effect.

Hepatic portal vein infusion of glucose and sodium solutions on the control of saline drinking in the rat.

1. Rats were prepared under anaesthesia with non-occlusive catheters in hepatic portal vein (HP) and inferior vena cava (VC) and maintained under standard conditions. 2. Each rat received a series (3 day intervals) of 30 min infusions of different solutions or sham into HP or VC. Oral intake of 0.15 M-NaCl and water were measured for 30 min. Significant change in drinking behaviour was assumed when the response to HP infusion differed from both sham and VC infusion. 3. Saline drinking was inhibited by HP infusion of 1 M- or 2M-NaCl, an effect blocked by right vagotomy or by addition of 16 mM-KCl to the infusate. 4. Saline drinking was increased and water drinking decreased by HP infusion of 2 M-glucose but not sucrose or fructose. 5. Saline drinking was decreased by HP infusion of deoxy-D-glucose to inhibit glucose utilization or ouabain to inhibit (Na4-K+) ATPase. 6. Results are consistent with the presence of afferent nerve terminals in hepatic portal vessels which are sensitive to change in NaCl or glucose concentration and which, in response thereto, alter drinking behaviour. The effects of NaCl and glucose on the discharge rate of the nerve terminals may be interpreted in terms of changing activity or electrogenicity of a Na pump but changes in membrane conductance or Na influx cannot be ruled out.

Effect of fructose and mannitol on dog renal cortical adenine nucleotide content, in vivo.

The renal cortex of anesthetized dogs was found to contain per gram lyophilized dry weight 9.5+/-0.6 micronmol ATP, 3.2+/-0.5 MICRONMOL ADP, 0.68+/-0.3 MICRONMOL AMP, and 22.5+/-4.4 micronmol Pi. These amounts were unchanged by the administration of moderate amounts of saline or hypertonic mannitol in load doses of about 20mmol/kg. Fructose in doses of 5 mmol/kg was found to cause a marked decrease in cortical ATP content. In doses of 20 mmol/kg fructose not only caused a decrease in ATP, but in total adenine nucleotides and Pi content as well. These results are consistent with the mode of action proposed for fructose, in rat kidney.

Renal sodium reabsorption after acute renal denervation in the rabbit.

1. Separate effects on the functions of left and right kidneys were examined after left-sided renal handling and acute denervation. Studies were done on pentobarbital-anaesthetized rabbits using clearance techniques to evaluate renal haemodynamics and water and electrolyte excretion.2. When compared with its counterpart, the handled kidney exhibited some decrease in function for at least 20 min. Recovery of most functions occurred in 40-60 min.3. The effects of denervation on renal functions were observed when the effects of handling had subsided. Renal plasma flow (R.P.F.) and glomerular filtration rate (G.F.R.) were not significantly changed, whereas the decrease in Na, K and water excretion, which was usually observed for no ascertained reason in the innervated kidney, was prevented.4. The magnitude of the denervation natriuresis was greater in these rabbits than in dogs studied previously; other functions studied were comparable in the two species.5. The results from thirty-five experiments are interpreted to indicate that denervation decreases Na reabsorption independently of G.F.R., perhaps by a direct effect on tubular transport, but more probably by a redistribution of filtration to nephrons of lesser reabsorptive capacity.