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Biomedical subjects

A S Rocha

Publications and source records attributed to A S Rocha.

At least 37 records · Page 2Linked to original sources
PubMed1990

Atrial peptide and cGMP effects on NaCl transport in inner medullary collecting duct.

We examined the action of atrial natriuretic factor (ANF) on Na+ and Cl- transport in in vitro microperfused inner medullary collecting ducts (IMCD) isolated from rat kidneys. First we studied the isotopic fluxes at low perfusion rates (7 nl/min). The results showed that ANF added to bath decreased lumen-to-bath flux (Jl----b) of Na+ and increased Na+ bath-to-lumen flux (Jb----l). This was substantiated by a direct demonstration that ANF reduces net Na+ and Cl- absorption. The effect of ANF on Jl----b and Jb----l of Na+ was also observed at high perfusion rates (25 nl/min). The inhibitory effect of ANF was observed even when Na+ Jl----b was stimulated by vasopressin (VP). ANF (6 x 10(-11) M) added to bath increased Cl- Jb----l and generated a negative lumen potential difference (PD). These two effects were inhibited by furosemide and by the replacement of Na+ by choline and Cl- by SO4(2-) in the bath fluid. These observations are compatible with the existence of a Na(+)-Cl(-)-K+ cotransport mechanism stimulated by ANF. Moreover, the effects of guanosine 3',5'-cyclic monophosphate (cGMP) added to the bath on PD, Jl----b, and Jb----l of Na+ were similar to those observed with ANF. Thus, physiological concentrations of ANF inhibit directly Na+ and Cl- absorption in IMCD by two mechanisms, 1) by increasing cotransport Na(+)-Cl(-)-K+ secretion and 2) by inhibiting NaCl absorption both in the absence and in the presence of VP. These effects on NaCl transport appear to be mediated by cGMP.

Animals↗
PubMed1990

Acute renal failure of leptospirosis: nonoliguric and hypokalemic forms.

Acute renal failure induced by leptospirosis was studied in 56 patients. A higher frequency of nonoliguric renal failure was observed with lower morbidity and mortality rates than in oliguric forms. In addition, 45% of the patients in this series were hypokalemic, and no hyperkalemic patients were seen. A prospective study in 11 patients showed an initially elevated urinary fractional potassium excretion that fell simultaneously with the high urinary fractional sodium excretion and the urinary K/Na ratio, suggesting an increased distal potassium secretion due to an increased distal sodium delivery consequent to functional impairment of the proximal reabsorption of sodium.

Acute Kidney Injury↗
PubMed1990

The effect of protein restriction on the severity and recovery from ischemic renal failure.

The effects of chronic dietary protein restriction on ischemic renal failure were evaluated in rats subjected to 90 min of bilateral renal clamping. The rats were kept on either 20% casein (regular) diet or casein-free (protein-free) diet 10 days before and 21 days after renal injury. Rats on regular protein diet showed higher levels of BUN and serum creatinine and had a lower inulin clearance (microliter/min/100 g BW) than animals on protein-free diet (289 +/- 34 vs 582 +/- 103, p less than 0.05) 2 days after ischemia. However, the inulin clearance measured 21 days following ischemia was significantly higher in rats on regular diet (1468 +/- 181) than those maintained on protein-free diet after ischemia (560 +/- 167). When unilateral 90 min ischemia was performed in rats on regular diet, the postischemic kidneys showed an incomplete recovery of the inulin clearance (226 +/- 35) compared to the contralateral kidney (900 +/- 116), 21 days after ischemia; whereas in rats on a protein-free diet the inulin clearance averaged 106 +/- 17 in the postischemic kidney and 345 +/- 41 in the right kidney. When left renal ischemia and contralateral nephrectomy were performed, the inulin clearance was 1149 +/- 74 in rats on regular diet and 534 +/- 60 in rats on protein-free diet, 21 days following renal insult. These results suggest that protein restriction can play a protective role against renal ischemia in an initial phase, but it limits the late recovery from ischemia. The presence of a normal contralateral kidney inhibits the functional recovery of the postischemic kidney and a contralateral nephrectomy produces a compensatory functional hypertrophy of the postischemic kidney, even in rats on a protein-free diet.

Analysis of Variance↗
PubMed1989

Calcium transport across rat inner medullary collecting duct perfused in vitro.

Ca2+ transport by the inner medullary collecting duct (IMCD) of normal rats was studied using the "in vitro" microperfusion technique. Net (Jnet), lumen-to-bath (Jl----b), and bath-to-lumen (Jb----l) fluxes of Ca2+ were measured in the absence of net water absorption using 45Ca as a tracer. In the absence of an electrochemical gradient, an important net absorption of Ca2+ (11.1 +/- 1.6 pmol.cm-2.s-1), similar to the difference between the Jl----b and Jb----l, was observed by direct determination at low (5-6 nl/min) and high (12-17 nl/min) perfusion rates. The Jl----b of Ca2+ was reduced by the addition to the bath fluid of ouabain (10(-3) M) and verapamil (10(-4) M), by the presence of amiloride (10(-5) and 10(-3) M) and verapamil (10(-4) M) in the luminal fluid, or by perfusion with a Na+-free solution. Neither the presence of verapamil (10(-4) M) and ouabain (10(-3) M) in the bath nor the withdrawal of Na+ from bath and perfusion solution was able to modify the Jb----l of Ca2+. Incrementing Ca2+ bath concentration increased proportionally the Jb----l of Ca2+. Therefore Ca2+ outflux is in part dependent on Na+-K+-adenosinetriphosphatase luminal membrane Na+ transport and in part inhibited by verapamil. However, Ca2+ influx is independent of Na+ transport, is not blocked by verapamil, but is increased by Ca2+ transtubular gradient, indicating the presence of a passive diffusion mechanism.

Absorption↗
PubMed1989

Effect of potassium depletion on ischemic renal failure.

The present study was carried out to examine the effect of potassium depletion in rat kidneys subjected to a temporary ischemic event produced by clamping of left renal artery. The postischemic kidneys of rats on a normal diet with adequate potassium intake showed an increase in H2O, Na and K excretion, with no change in inulin clearance whereas significant differences were found in potassium-deprived rats. Potassium depletion was brought about by dietary K deprivation for 10 days. K-depleted rats (serum K = 2.5 +/- 0.1 mEq/l) had a decrease in inulin clearance of the postischemic kidney from 1.01 +/- 0.10 to 0.43 +/- 0.05 ml/min (p less than 0.01), and a greater increase in fractional excretion of H2O, Na and K when compared to normal rats. The postischemic kidney from both normal and hypokalemic rats showed a decrease in Na-K-ATPase of the inner stripe of the outer medulla. These data indicate that short-term ischemia produces polyuria, increases natriuresis and kaliuresis, associated, at least in part, with a decrease in Na-K-ATPase in the inner stripe of the outer medulla (probably the thick ascending limb of Henle) and that K depletion potentiates ischemic renal failure.

Acute Kidney Injury↗
PubMed1982

Morpho-functional patterns of kidney injury in the experimental leptospirosis of the guinea-pig (L. icterohaemorrhagiae).

Thirty-seven guinea-pigs experimentally infected with a virulent strain of L. icterohaemorrhagiae, were submitted to a renal function study as evaluated through the maximal urinary concentration (MUC) test, blood urea nitrogen (BUN) and afterwards had their kidneys examined by light and electron microscopy. Vascular changes were also studied after the administration of colloidal carbon as a marker. Through the MUC test and BUN determination, two groups of tubulo-interstitial lesions can be visualised, one in animals without renal sufficiency, manifested chiefly by cell edema with RE dilation and another, in animals with renal insufficiency, characterised not only by marked cell edema and mitochondrial changes, but also by proximal tubule regenerative aspects without overt tubular necrosis. Interstitial edema and focal nephritis was prominent in both groups, a finding which minimises their role in the pathogenesis of renal failure in experimental leptospirosis. Vascular injury, affecting the vessels of the renal microcirculation chiefly at the cortico-medular junction, was observed in both groups. Its severity and extension ran parallel to the intensity of the tubular injury. This suggests a simultaneous action of a noxious agent liberated by the leptospires over both structures, tubular damage being accentuated by the local circulatory changes.

Animals↗
PubMed1981

Calcium transport in isolated perfused pars recta of proximal tubule.

1. Ca2+ transport was examined in segments of rabbit pars recta isolated from the renal cortex by the technique of in vitro perfusion. 2. The bidirectional Ca2+ flux was determined by adding 45Ca to the bath and to the perfusate sequentially. Five tubules were perfused with Ringer-HCO-3 solution containing 0.5% albumin and bathed in the same solution, which maintained the ionized Ca2+ at the same concentration in the perfusate and bath. The outflux of Ca2+ was 169 +/- 18 pEq cm-1 min-1, while the influx was 53 +/- 13 pEq cm-1 min-1. The difference between these two numbers, the net Ca2+ absorption, is equal to 116 +/- 19 pEq cm-1 min-1. The flux ratio, 3.79 +/- 0.87, was significantly higher than 0.91 +/- 0.01 predicted by the Ussing equation from the transtubular potential difference (PD = -1.3 +/- 0.2 mV). 3. The effect of ouabain and transtubular PD on Ca2+ outflux was studied with rabbit serum ultrafiltrate as perfusate and rabbit serum as the bath. When 10(-5) M ouabain was added to the bath the transtubular PD fell from -2.4 +/- 0.3 mV to -0.65 +/- 0.06mV and fluid absorption decreased from 0.83 +/- 0.15 to 0.42 +/- 0.2 nl min-1 mm-1, whereas Ca2+ outflux remained unchanged (before = 160 +/- 13 pEq cm-1 min-1, after = 167 +/- 7 pq cm-1 min-1). 4. When tubules were perfused with and Na+ -free solution (NaCl replaced by choline chloride), Ca2+ outflux, 170 +/- 170 11 pEq cm-1 min-1, was the same as that obtained with the normal perfusion solution. 5. These results indicate that: a) the pars recta has the capacity for net absorption of significant amounts of Ca2+ that is apparently independent of Na+ efflux; b)Ca2+ transport across the pars recta occurs by a mechanism other than simple diffusion and c), unlike Na+ transport, Ca2+ outflux is not sensitive to ouabain.

Animals↗
PubMed1977

Calcium and phosphate transport in isolated segments of rabbit Henle's loop.

Calcium and phosphate transport was examined in rabbit thin descending, thin ascending, and thick ascending limbs of Henle by in vitro perfusion of isolated tubular segments. Permeability coefficients for these segments with 45Ca and 32PO4 were determined for both lumen-to-bath and bath-to-lumen directions. Both the thin descending and thin ascending limbs were found to be relatively impermeable to both 45Ca and 32PO4. In neither segment were we able to show evidence for net transport of calcium or phosphate. In contrast, the thick ascending limb of Henle showed a decrease in calcium lumen-to-bath concentration from 0.97 +/- 0.02 to 0.88 +/- 0.02 when perfused at 4.8 nl min-1. 45Ca lumen-to-bath and bath-to-lumen fluxes were 19.96 +/- 1.05 and 9.89 +/- 0.02 peq-min-1-cm-1, respectively, and the potential difference was +3.8 +/- 0.3 mV (lumen positive). The observed calcium flux ratio was significantly higher than that predicted by Ussing's equation. When ouabain was added to the bath the potential difference fell to +1.1 +/- 0.3 mV, whereas the calcium efflux was only slightly diminished (29.5 +/- 5.3-23.7 +/- 5.1 peq-cm-1-min-1). Ouabain had no effect on the influx of Ca across the thick ascending limb of Henle. There was no net transport of phosphate across the thick ascending limb. Phosphate permeability was exceedingly low bidirectionally across the thick ascending limb. Our findings indicate: (a) all segments of Henle's loop are relatively impermeable to calcium and phosphate; (b) net transport of phosphate seems to be absent in Henle's loop; (c) net calcium reabsorption, which cannot be explained by passive mechanisms, occurs in the thick ascending limb.

Animals↗
PubMed1973

Sodium chloride and water transport in the medullary thick ascending limb of Henle. Evidence for active chloride transport.

Transport of NaCl and water was examined in the rabbit medullary thick ascending limb of Henle (ALH) by perfusing isolated segments of these nephrons in vitro. Osmotic water permeability was evaluated by perfusing tubules against imposed osmotic gradients. In these experiments the net transport of fluid remained at zero when segments of thick ALH were perfused with isotonic ultrafiltrate in a bath of rabbit serum in which the serum osmolality was increased by the addition of either 239+/-8 mosmol/liter of raffinose or 232+/-17 mosmol of NaCl indicating that the thick ascending limb of Henle is impermeant to osmotic flow of water. When these tubules were perfused at slow rates with isosmolal ultrafiltrate of same rabbit serum as used for the bath, the effluent osmolality was consistently lowered to concentrations less than the perfusate and the bath. That this decrease in collected fluid osmolality represented salt transport was demonstrated in a separate set of experiments in which it was shown that the sodium and chloride concentrations decreased to 0.79+/-0.02 and 0.77+/-0.02 respectively when compared with the perfusion fluid concentrations. In each instance the simultaneously determined transtubular potential difference (PD) revealed the lumen to be positive with the magnitude dependent on the perfusion rate. At flow rates above 2 nl.min(-1), the mean transtubular PD was stable and equal to 6.70+/-0.34 mv. At stop-flow conditions this PD became more positive. Ouabain and cooling reversibly decreased the magnitude of this PD. The transtubular PD remained positive, 3.3+/-0.2 mV, when complete substitution of Na by choline was carried out in both the perfusion fluid and the bathing media. These results are interpreted to indicate that the active transport process is primarily an electrogenic chloride mechanism. The isotopic permeability coefficient for Na was 6.27+/-0.38 x 10(-5) cm.s(-1) indicating that the thick ALH is approximately as permeable to Na as the proximal convoluted tubule. The chloride permeability coefficient for the thick ALH was 1.06+/-0.12 x 10(-5) cm.s(-1) which is significantly less than the chloride permeability of the proximal tubule. These data demonstrate that the medullary thick ascending limb of Henle is water impermeable while having the capacity for active outward solute transport as a consequence of an electrogenic chloride pump. The combination of these characteristics allows this segment to generate a dilute tubular fluid and participate as the principal energy source for the overall operation of the countercurrent multiplication system.

Animals↗
PubMedDate not supplied

Comparisons of models of cortical necrosis with segmental infarction.

Sodium and water excretion were studied by standard clearance techniques in three experimental models where renal mass was reduced by superficial cortical necrosis (CN) or ischemic segmental infarction (SI). During hydropenia either CN or SI were able to conserve and regulate sodium to a very similar degree. After expansion of extracellular volume, CN reabsorbed less sodium and water than SI. In free-water clearance (CH2O) experiments, the 'apparent distal' sodium delivery was higher in CN than in SI, suggesting a decreased sodium and water reabsorption in the proximal tubules of juxtamedullary nephrons (JM). Both kidneys had similar CH2O when factored for inulin clearance but when CH2O was corrected for 'apparent distal' sodium delivery it was lower in CN than in SI, demonstrating an incapacity of JM to dilute urine. CN also showed less capacity to reabsorb free water than SI. Thus, the use of CN and SI within the same animal was useful to study functional differences between superficial and juxtamedullary nephrons. The present study also suggests that the kidney with superficial CN was unable to perform maximal urine dilution and concentration.

Absorption↗