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Biomedical subjects

A Grandchamp

Publications and source records attributed to A Grandchamp.

At least 19 recordsLinked to original sources
PubMed1980

Pressure natriuresis in isolated kidneys from hypertension-prone and hypertension-resistant rats (Dahl rats).

Dahl described a strain of rats with genetically controlled propensities for hypertension. Chronic excess salt feeding increased blood pressure in sensitive (s) rats, whereas resistant rats (R) remain normotensive. We tested the pressure natriuretic function (urinary sodium excretion versus perfusion pressure) in isolated kidneys perfused with a cellular medium: in sodium-restricted normotensive sensitive (S0) and resistant (R0) animals; in sensitive rats receiving a high-salt diet for 3 weeks (S3): and in both S and R animals exposed to excess sodium for 7 weeks (R7 and S7). The aim of these studies was to determine if a preset alteration of the pressure natriuretic function might be present in S animals prior to the development of hypertension. Systolic blood pressure in S0, S3, and S7 animals were 123 +/- 4, 136 +/- 2, and 162 +/- 4 mm Hg, respectively, whereas that of R0 and R7 were 121 +/- 5 and 126 +/- 5 mm Hg. An increase of the perfusion pressure of isolated kidneys from 105 to 185 mm Hg in stepwise fashion resulted in a pressure natriuresis whose slope was similar in R0 and S0 animals. Of interest was that the pressure natriuretic function slope of kidneys from R0 (low sodium) and R7 (high sodium) rats was as predicted by the Guyton system analysis of normal blood pressure control Micropuncture of the proximal nephrons demonstrated that the origin of the natriuresis resulted from a site beyond the accessible proximal tubule. Results from S7 kidneys contrasted with all others in that the natriuretic response was depressed (P less than 0.01), which resulted from significantly lower filtration rates at higher perfusion pressures. We concluded (1) in normal R rats, the pressure natriuretic function is that predicted by the Guyton hypothesis, (2) Dahl S animals have no preset abnormality of this function until hypertension is present for some time, and (3) a depression of the pressure natriuretic function may aggravate hypertension in S rats once high blood pressure has persisted.

Animals↗
PubMed1980

Fate of vasopressin perfused into nephrons of Wistar and Brattleboro (diabetes insipidus) rats.

1. Iodinated vasopressin was microinjected into early proximal or distal tubules or Wistar and Brattleboro (diabetes insipidus) rats. Sites of infusion were determined by the lissamine green transit time method. 2. Urinary recovery of 125I after proximal and distal injections was 89 +/- SE 1.7% and 94 +/- 1.0% in Wistar rats (corrected for inulin) and 81 +/- 2.0 and 92 +/- 2.0% in Brattleboro rats (uncorrected); injection of hormone into vascular stars resulted in similar 125I recoveries from punctured and contralateral kidneys. 3. Radioactive substances excreted after perfusing proximal and distal sites in Brattleboro animals, and 125I-labelled hormone added to urine from the contralateral kidney, bound similarly to a specific arginine vasopressin antiserum and demonstrated similar radioactive elution profiles after passage through Sephadex G25 columns. 4. Incubation of labelled and unlabelled vasopressin with rat kidney homogenates resulted in similar and complete degradation of the hormone. 5. Results indicate that most of the vasopressin injected into either proximal or distal nephrons enters the urine intact, and no evidence of tubular secretion was found when perfusing vascular stars. Enzymes in rat renal tissue degrade labelled vasopressin, but the ability of the proximal tubule to hydrolyse the 125I-labelled vasopressin is limited, especially when compared with that reported for several linear peptide hormones.

Animals↗
PubMed1976

Effects of nephrectomy on renal salt and water transport in the remaining kidney.

Fluid, sodium, and potassium transport was studied in proximal and distal tubules in rats in which one kidney had been removed two weeks after a suprarenal aortic clamp had been placed to prevent adaptive changes in glomerular filtration rate (GFR) in the experimental kidney. Free-flow micropuncture techniques were used and tubular fluid (TF) samples analyzed for inulin, sodium and potassium. In addition, peritubular total protein concentrations and luminal and peritubular hydrostatic pressures were measured. The following changes were observed 15 hr after unilateral nephrectomy: (1) a significant increase in single nephron GFR; (2) unchanged absolute proximal tubular reabsorption rates of fluid and sodium; (3) increased delivery of fluid into distal tubules; (4) increased distal tubular reabsorption of sodium, but of insufficient magnitude to prevent natriuresis; and (5) an augmentation of distal tubular potassium secretion. Reduction of single nephron GRF to control levels by aortic clamping abolished the natriuresis following nephrectomy.

Animals↗
PubMed1976

Morphological changes in tight junctions of Necturus maculosus proximal tubules undergoing saline diuresis.

Tight junctions between epithelial cells are believed to control the paracellular diffusion of substances across epithelia. Epithelia in which tight junctions are poorly developed display a higher paracellular electrical conductance, while those with extensive tight junctions show lower conductance values. We described here a particular epithelium, that of the proximal tubules of the Necturus kidney, in which the development of the tight junctions varies in parallel with a change of paracellular electrical conductance. In control conditions, tight junctions between epithelial cells of the proximal tubules are more developed than in tubules undergoing saline diuresis, a situation which increases the conductance across the paracellular shunt pathway.

Animals↗
PubMed1975

Role of luminal hydrostatic pressure in proximal tubular fluid reabsorption in the rat.

The effect of small changes in intraluminal hydrostatic pressure (P) on the tubular radius (r) and the net fluid reabsorption per unit of surface area of the tubular wall (Js) has been studied in the proximal tubule of the rat kidney. The split-drop method was used to simultaneously determine Js and r. Two standardized split-drop techniques A and B allow selective change in P. P was 31.6 +/- 1.3 mmHg in technique A and 15.5 +/- 1.5 in technique B. The pressure difference significantly affected the tubular radius; r was 21.9 +/- 0.4 and 18.6 +/- 0.5 mum in the split drop A and B, respectively. In contrast, net transepithelial fluid reabsorption Js was unchanged. Js amounted to 2.72 +/- 0.20, and 2.78 +/- 0.33 10(-5) cm3 cm-2 s-1 in split drop A and B. The absence of variations in Js could result from two opposite effects of pressure. P might enhance Js by increased ultrafiltration. However, the rise in r might decrease the density of the intraepithelial transport paths per unit area of tubular wall and therefore might decrease Js.

Absorption↗
PubMed1974

Pressure control of sodium reabsorption and intercellular backflux across proximal kidney tubule.

The magnitude of changes in luminal hydrostatic pressure (DeltaP(L)), peritubular capillary hydrostatic pressure (DeltaP(PT)), and peritubular capillary colloid osmotic pressure (Deltapi) was determined in the Necturus kidney during volume expansion (VE). The specific effects of separate changes of each pressure parameter on proximal net sodium transport (J(Na)) were studied in isolated perfused kidneys. The combined effect of DeltaP(L), DeltaP(PT), and Deltapi, of a magnitude similar to that induced by volume expansion, decreases J(Na) by 26% in the perfused kidney. A major portion of the natriuresis in VE is due to changes in intrarenal pressures. The effect of Deltapi on the permeability characteristics of Necturus proximal tubule was studied. With increasing Deltapi, the ionic conductance of the paracellular shunt pathway decreased, since transepithelial input and specific resistance rose significantly, whereas cellular membrane resistance remained unchanged. Transepithelial permeability coefficients for sodium chloride and raffinose changed inversely proportional to transepithelial resistance, indicating an alteration of a paracellular permeation route. Net passive sodium backflux and active transport flux components were calculated. Increased net sodium transport with rising Deltapi is accompanied by a significant drop in passive back diffusion, without an increment in the active flux component. Change in passive sodium ion back diffusion thus appears to be a key physiological factor in the control of transepithelial sodium transport.

Animals↗
PubMed1971

Relationship between renin and intrarenal hemodynamics in hemorrhagic hypotension.

In order to investigate the possible role of the renin-angiotensin system in the regulation of intrarenal hemodynamics in hemorrhagic hypotension (HH), seven mongrel dogs have been studied under the following conditions: (a) Control, (b) HH (mean arterial pressure 70 mm Hg), and (c) HH + alpha adrenergic blockade by phenoxybenzamine (HH + POB). The following parameters were obtained for the right kidney: Intrarenal distribution of blood flow and local blood flow rates ((133)Xe washout technique); total renal blood flow (RBF) on the basis of the clearance and extraction ratio of PAH and the arterial hematocrit; plasma renin concentrations in the renal artery and vein by the method of Boucher and his associates; and renin release into the renal circulation. Alpha adrenergic blockade reverted the typical redistribution of intrarenal blood flow observed under HH. In hemorrhage, arterial and venous renin concentrations increased by a factor of 3.4 and 4.8 respectively. A further small increase was observed during HH + POB with the respective factors increasing to 4.8 and 5.3, as compared with control values. The renin release into the circulation increased by a factor of 1.2 in HH and 4.0 in HH + POB. Whereas in HH there seemed to be a relationship between increased renin concentrations or renin release, and the redistribution of blood flow, no such correlation was found during alpha-adrenergic blockade. From these observations it is concluded that renin alone is unable to maintain the typical redistribution of RBF seen during hemorrhage. Circumstantial evidence points to a permissive role of the renin-angiotensin system in the pathogenesis of the patchy cortical hypoperfusion caused by sympathoadrenergic mechanisms during hemorrhagic hypotension.

Angiotensin II↗