The penetration of inulin, sucrose, mannitol and tritiated water from the interstitial space in muscle into the vascular system

SUMMARY1. The changes in the volumes of cells in slices (thickness 0S3-04 mm) of rat renal outer and inner medulla have been investigated during aerobic incubation for 20 min at 370 C in Krebs phosphate-bicarbonate Ringer modified by the addition of urea or sucrose in order to produce a range of media hypo-and hyperosmolal with respect to the calculated tissue fluid osmolalities in these regions.2. On the assumption that under these conditions the measured inulin space approximates to the true extracellular space (ECS), it was found that osmotic swelling or shrinkage of cells was not accompanied by any significant variation in the absolute size of the ECS.3. Calculated cell volume changes in both regions were minimal when slices were incubated in urea-containing media iso-osmolal with tissue fluids in that region. In sucrose-containing media minimal cell volume changes occurred when media were hypo-osmolal in relation to tissue fluids by a factor of approximately 0-68.4. In all except the most hypo-osmolal media studied, calculated cell volume changes (as percentage of initial volume) were linearly related to the reciprocal of the incubation media osmolalities. The points of interception of the regression lines on the cell volume axis were dependent upon both the region studied and the composition of the incubation medium (urea or sucrose).5. These changes were accompanied by variations in slice solute concentrations. Slice [Na] was greatest, and slice [K] least, following incubation in those media producing the greatest percentage changes in cell volume.6. The volume of distribution of [14C]sucrose within the inner medulla was 61-7 + 2*5 ,ul./100 mg wet weight of tissue (mean + s.E., n = 6) after 10 min incubation. The increase to 708 + 4-2 2l./lO0 mg (n = 6) after 100 min was not significant (041 > P > 0.05). The volume of distribution within the outer medulla rose markedly during this period, from 38'1 to 582 ,ul./100 mg.

Section: -2mentioning

confidence: 99%

Volume adjustment by renal medullary cells in hypo‐ and hyperosmolal solutions containing permeant and impermeant solutes.

Law¹

1975

“…Mannitol is able to move freely across capillary pores (Crone & Garlick, 1970) 3H]glutamine. These were 0-27 + 002 ml g 1 and 033 + 003 ml g' (P <005), respectively.…”

Section: Nature Of Movement Of Amino Acids Into Musclementioning

confidence: 99%

Characteristics of L‐glutamine transport in perfused rat skeletal muscle.

Hundal

Rennie

Watt

1987

111

SUMMARY1. We have investigated glutamine transport in the perfused rat hindlimb using the paired-tracer isotope dilution technique.2. Uptake of L-glutamine was stereospecific, saturable, sodium dependent, insulin sensitive and pH insensitive in the physiological range. The maximum capacity of transport (Vmex) under normal perfusate conditions at 37 0C, 145 mM-Na+ and in the absence of insulin was 1156 + 193 nmol min-' g-1 with transport being half-maximal at a perfusate glutamine concentration of 9-25 + 1-15 mm.3. The kinetics of Na' dependence strongly suggested co-transport of Na+ and glutamine with a stoichiometry of 1:1; furthermore, Na+ activated the carrier without any change in the concentration of glutamine at which transport was halfmaximal, i.e. a 'Vmax effect' rather than a 'Km effect'.4. The characteristics of glutamine transport, especially its substrate specificity and the pattern of competitive and non-competitive inhibition of glutamine transport by other amino acids, suggest that it is mediated by a carrier or carriers for which asparagine and histidine are also suitable substrates.5. The characteristics of muscle glutamine transport are related but distinct from those of system N identified in hepatocytes; we suggest that they are sufficiently distinct to justify the identification of a new variant of mammalian amino acid transport systems which may be identified by the symbol Nm.6. The kinetic characteristics of system Nm are such that glutamine is likely to be the most rapidly exchanging amino acid across the muscle membrane at physiological intra-and extracellular glutamine concentrations. Its hormone and ion sensitivities are likely to be important in the physiological modulation of whole-body glutamine metabolism and also during derangements observed in disease and after injury.

“…To compute the fraction of the remaining tissue 42K content which escapes from the sinus tissue during any sampling interval, the following formula was employed (Crone & Garlick, 1970):…”

Section: Data Reductionmentioning

confidence: 99%

Are acetylcholine‐induced increases in 42K efflux mediated by intracellular cyclic GMP in turtle cardiac pace‐maker tissue?

Fleming¹,

Giles²,

Lederer³

1981

SUMMARY1. 42K efflux has been measured from small strips of turtle sinus venosus tissue in order: (a) to characterize further the pharmacology of the acetylcholine response and (b) to test whether cyclic guanosine 3': 5'-monophosphoric acid (cyclic GMP) is the intracellular mediator of this response.2. The 42K wash-out curves show that the fractional escape rate (FER) of 42K efflux is nearly constant after 60-80 min, indicating that after this time period 42K FER is controlled by barrier-limited diffusion from a single intracellular compartment.3. The threshold of the dose-response relationship for the acetylcholine-induced increase in 42K FER is about 10-8 M and the Km is 2'75 x 10-7 in non-eserinized preparations.4. This acetylcholine response is completely blocked by atropine; but nicotinic blockers produce no detectable reduction of it. 5. Exogenous application of lipid-soluble analogues of cyclic GMP (dibutyryl or 8-bromo-cyclic GMP applied at 2-3 mm for 30 min) failed to mimic the acetylcholineinduced augmentation of 42K FER. 6. Experiments in which sodium nitroprusside (5 x 10-4 M for 30 min) was applied in order to stimulate the guanylate cyclase and hence produce a large, maintained increase in intracellular cyclic GMP failed to show a significant increase in 42K FER.7. When acetylcholine (10-6 M) was applied in the presence of O[Ca2+]o (in an attempt to inhibit the guanylate cyclase) there was no significant reduction in the acetylcholine-induced increases in 42K FER.8. Hence, these three indirect tests indicate that the muscarinic acetylcholineinduced increase in 42K FER in cardiac pace-maker tissue is unlikely to be mediated entirely by changes in the levels of intracellular cyclic GMP.