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PubMed1986

Effects of chlorpropamide on loop of Henle function and plasma renin.

We have suggested that inhibition of renin release by sodium chloride is related to increased absorptive solute transport in the loop of Henle. In the rat, we have shown that reduced chloride transport in the loop is associated with increased renin release. Based on indirect evidence, it has been suggested that chlorpropamide (CPMD) increases loop solute transport. This study directly evaluates the effect of CPMD on loop chloride transport and plasma renin activity (PRA) in the male Sprague-Dawley rat. Loop of Henle chloride reabsorption (measured by recollection micropuncture) and PRA were determined before and after acute infusion of CPMD (N = 8) or vehicle (N = 8). Although delivery to the loop was not significantly changed, CPMD increased (P less than 0.05) absolute loop chloride reabsorption from 1798 pEq/min +/- 200 SE to 2453 pEq/min +/- 206 SE. PRA was decreased (P less than 0.01) from 9.2 ng/ml/hr +/- 1.0 SE to 5.6 ng/ml/hr +/- 0.8 SE following CPMD infusion. Comparable vehicle infusion did not alter loop chloride reabsorption or PRA. Arterial pressure, and whole kidney and single nephron glomerular filtration rates were unchanged following infusion of CPMD or vehicle. These results demonstrate that an increase in loop chloride reabsorption is associated with a decrease in renin release. This observation is consistent with the hypothesis that renin release is inversely related to the magnitude of chloride transport in the thick ascending limb of the loop of Henle.

Animals↗
PubMed1977

Maturation of diluting capacity in loop of Henle of rat superficial nephrons.

The postnatal development of renal diluting capacity was studied by free-flow micropuncture and by microdissection of single superficial loops of Henle in rats kept on a high salt diet. Total renal filtration rate, sodium absorption, total solute excretion, and systemic arterial pressure were monitored during single nephron evaluation at two maturational stages (12-15 days and 27-35 days postnatal). Nephron filtration rates were identical when measured in early distal and late proximal segments of the same nephron. Absolute fluid absorption between these sites increased by a factor of 2.5, whereas loop fractional absorption of the volume load changed from 38.1 +/- 6.9 to 49.8 +/- 4.8% (SD), while proximal volume delivery to the loop increased from 4.33 +/- 1.12 to 7.14 +/- 0.65 nl/min. Simultaneously, the osmolarity of early distal fluid (8.8% of distal length) decreased significantly from 284 + 19.8 to 180.9 +/- 18.2 mosmol/liter during maturation. This study suggests that the ability of the loop of Henle to generate hypotonic fluid is attained only gradually during ontogeny. Volume absorption in the loop of Henle increases disproportionately to the loop volume load.

Absorption↗
PubMed1991

Attenuation of azosemide's action in the loop of Henle of rat kidney by nonsteroidal anti-inflammatory drugs.

The purpose of the present study, which was performed in anaesthetized rats, was to clarify whether the nonsteroidal anti-inflammatory drugs (NSAIDs) indomethacin and meclofenamate interact with the diuretic action of the new loop diuretic azosemide (Luret, CAS-27589-33-9). Since azosemide's diuretic action shows a lower onset and a more prolonged duration as compared to classical loop diuretics it was also tested whether azosemide's tubular action is mediated by an active metabolite. The results demonstrate that azosemide, when infused directly into the lumen of superficial loops of Henle, dose-dependently diminished the loops sodium and chloride reabsorption. A half-maximum effect was observed at an azosemide concentration of 3 x 10(-6) mol/l. These results clearly prove that the diuretic effect of azosemide is exerted by the drug itself and does not require metabolism to an active metabolite. Luminal application of the drug also dose-dependently increased early distal sodium and chloride concentrations, indicating that the drug's tubular action is located in the thick ascending limb of Henle's loop. Indomethacin and meclofenamate blunted the diuretic, natriuretic and chloruretic response to azosemide, and microperfusion experiments on single loops of Henle revealed an attenuation by NSAIDs of azosemide's inhibitory action on the loops sodium and chloride reabsorption. The quantitative extent of this interaction was nearly identical to that observed previously for the NSAID-furosemide interaction.

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↗
PubMed2000

Sodium reabsorption in thick ascending limb of Henle's loop: effect of potassium channel blockade in vivo.

1. Based on previous in vitro studies, inhibition of K(+) recycling in thick ascending limb (TAL) is expected to lower Na(+) reabsorption through (i) reducing the luminal availability of K(+) to reload the Na(+)-2Cl(-)-K(+) cotransporter and (ii) diminishing the lumen positive transepithelial potential difference which drives paracellular cation transport. 2. This issue was investigated in anaesthetized rats employing microperfusion of Henle's loop downstream from late proximal tubular site with K(+)-free artificial tubular fluid in nephrons with superficial glomeruli. 3. The unselective K(+) channel blocker Cs(+) (5 - 40 mM) dose-dependently increased early distal tubular delivery of fluid and Na(+) with a maximum increase of approximately 20 and 185%, respectively, indicating predominant effects on water-impermeable TAL. 4. The modest inhibition of Na(+) reabsorption in response to the 15 mM of Cs(+) but not the enhanced inhibition by 20 mM Cs(+) was prevented by luminal K(+) supplementation. Furthermore, pretreatment with 20 mM Cs(+) did not attenuate the inhibitory effect of furosemide (100 microM) on Na(+)-2Cl(-)-K(+) cotransport. 5. Neither inhibitors of large (charybdotoxin 1 microM) nor low (glibenclamide 250 microM; U37883A 100 microM) conductance K(+) channels altered loop of Henle fluid or Na(+) reabsorption. 6. The intermediate conductance K(+) channel blockers verapamil and quinine (100 microM) modestly increased early distal tubular Na(+) but not fluid delivery, indicating a role for this K(+) channel in Na(+) reabsorption in TAL. As observed for equieffective concentrations of Cs(+) (15 mM), Na(+) reabsorption was preserved by K(+) supplementation. 7. The results indicate that modest inhibition of K(+) channels lowers the luminal availability of K(+) and thus transcellular Na(+) reabsorption in TAL. More complete inhibition lowers paracellular Na(+) transport probably by reducing or even abolishing the lumen positive transepithelial potential difference. Under the latter conditions, transcellular Na(+) transport may be restored by paracellular K(+) backleak.

Adamantane↗
PubMed1996

Role of apoptosis in development of the ascending thin limb of the loop of Henle in rat kidney.

At birth, the rat renal papilla has the structural composition of the mature inner stripe of the outer medulla. All loops of Henle have the configuration of short loops, and there are no ascending thin limbs. This study examines the role of apoptosis in the differentiation of the loop of Henle and the development of the ascending thin limb in the rat kidney. Kidneys of 20-day-old fetuses and 1-, 3-, 5-, 7-, 14-, and 21-day-old pups were preserved for immunohistochemistry and electron microscopy. Using a preembedding immunoperoxidase method, we identified thick ascending limbs by labeling with antibodies to the serotonin receptor, 5-HT1A, and descending thin limbs were identified by labeling with antibodies to aquaporin-1. Three methods were used to identify apoptotic cells as follows: 1) in situ nick end labeling using the ApopTag kit, 2) toluidine blue staining on plastic sections followed by etching, and 3) transmission electron microscopy. At birth, tubules with 5-HT1A immunoreactivity were present throughout the renal papilla, and there were no ascending thin limbs. From 1 to 14 days of age, staining for apoptosis was observed in numerous cells in the 5-HT1A-positive epithelium, beginning at the papillary tip and ascending to the border between outer and inner medulla. This was associated with transformation from a cuboidal to a squamous epithelium and subsequent disappearance of 5-HT1A immunostaining from the transformed cells. Electron microscopy confirmed the presence of apoptotic cells and phagocytosed apoptotic bodies in the thick ascending limb in the renal papilla. We conclude that the ascending thin limb is derived from the 5-HT1A-positive thick ascending limb by apoptotic deletion of thick ascending limb cells and transformation of the remaining tubule cells into the 5-HT1A-negative ascending thin limb.

Animals↗
PubMed1993

Mechanisms of calcium transport across the basolateral membrane of the rabbit cortical thick ascending limb of Henle's loop.

Although net Ca2+ absorption takes place in the thick ascending limb of Henle's loop, detailed mechanisms are unknown. Because it has been reported that the Ca2+ entry step across the luminal membrane is mediated by Ca2+ channels inserted by stimulation with parathyroid hormone, we studied the mechanism of Ca2+ transport across the basolateral membrane of rabbit cortical thick ascending limb (CTAL) perfused in vitro by using microscopic fluorometry of cytosolic Ca2+ ([Ca2+]i) with fura-2. The resting [Ca2+]i in this segment was 49.8 +/- 4.5 nmol/l. Neither Na+ removal from the bathing solution nor addition of ouabain (0.1 mmol/l) to the bath increased [Ca2+]i, indicating that a Na+/Ca2+ exchanger in the basolateral membrane may not contribute in any major way to [Ca2+]i of CTAL. To confirm our technical accuracy, similar protocols were conducted in the connecting tubule, where the existence of a Na+/Ca2+ exchanger has been reported. In this segment, Na+ removal from the bath increased cell Ca2+ from 148.6 +/- 6.4 nmol/l to 647.6 +/- 132.0 nmol/l, confirming the documented fact. [Ca2+]i in the CTAL was markedly increased when 1 mmol/l NaCN was added to the bath in the absence of glucose. Calmodulin inhibitors (trifluoperazine or W-7) increased [Ca2+]i. When the bath pH was made alkaline, [Ca2+]i was also increased. This response was abolished when Ca2+ was eliminated from the bath, indicating that the Ca2+ entry across the basolateral membrane is dependent on bath pH. Increase in [Ca2+]i induced by an alkaline bath was inhibited by increased the bath K+ from 5 nmol/l to 50 mmol/l, suggesting that the Ca2+ entry system is voltage-dependent.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

Separation of renal medullary cells: isolation of cells from the thick ascending limb of Henle's loop.

A homogeneous population of single cells from the thick ascending limb of Henle's loop (TALH) has been isolated from the rabbit kidney medulla. A total medullary cell suspension was prepared by a series of collagenase, hyaluronidase, and trypsin digestions and separated on a Ficoll gradient (2.6-30.7% wt/wt). Morphologically, the cells isolated from the TALH were homogeneous and showed polarity within their plasma membrane structure, with a few blunt microvilli on their apical surface and deep infoldings of the basal-lateral membrane. Biochemically, the TALH cells were highly enriched in calcitonin-sensitive adenylate cyclase and Na, K-ATPase. Alkaline phosphatase and arginine vasopressin-sensitive adenylate cyclase, highly concentrated in proximal tubule and collecting duct, were present only in low concentrations in the TALH cells. Additionally, furosemide, a diuretic inhibiting sodium chloride transport in the TALH in vivo, inhibited oxygen consumption of the TALH cells in a dose-dependent manner. The TALH cells were viable, as judged by morphological appearance, trypan blue exclusion, the response of oxygen consumption to 2,4-dinitrophenol, succinate and ouabain, and the cellular Na, K and ATP levels.

Adenosine Triphosphate↗
PubMed1995

Vasopressin stimulates Cl- transport in ascending thin limb of Henle's loop in hamster.

The effect of arginine vasopressin (AVP) on NaCl transport was investigated in the isolated microperfused hamster ascending thin limb of Henle's loop by measuring transepithelial voltage (Vt) and transmural 22Na+ and 36Cl- fluxes. In the presence of a transmural NaCl concentration gradient (100 mM higher in the lumen), Vt was 8.4 +/- 0.4 mV. Addition of 1 nM AVP to the basolateral solution increased Vt to 9.6 +/- 0.4 mV, which corresponds to an increase in the Cl- to Na+ permselectivity ratio (PCl/PNa) from 2.8 +/- 0.2 to 3.4 +/- 0.2. AVP at physiological concentrations increased Vt in a dose-dependent manner with an ED50 of 5 pM. AVP increased the Cl- efflux coefficient from 99.6 +/- 6.3 to 131.4 +/- 10.6 x 10(-7) cm2/s without affecting the Na+ efflux coefficient. 5-Nitro-2-(3-phenyl-propylamino)-benzoate (0.2 mM), a Cl- channel inhibitor, in the perfusate decreased the basal Cl- efflux coefficient and inhibited the AVP-induced increase in this parameter. The AVP-induced increase in Vt was not affected by [d(CH2)5(1),O-Me-Tyr2,Arg8] vasopressin, a V1 receptor antagonist, but was abolished by [d(CH2)5,D-Ile2,Ile4,Arg8] vasopressin, a V2 receptor antagonist. The selective V2 agonist dDAVP in 1 nM also increased Vt from 8.6 +/- 0.7 to 9.5 +/- 0.6 mV. Dibutyryl cAMP and forskolin both increased Vt, whereas H89, an inhibitor of cAMP-dependent protein kinase, abolished the AVP-induced increase in Vt. These results demonstrate that AVP stimulates Cl- transport in the ascending thin limb of Henle's loop by activating Cl- channels via a signal transduction cascade comprising V2 receptors, adenylate cyclase, and cAMP-dependent protein kinase. The ascending thin limb of Henle's loop thus participates in the formation of concentrated urine as one of the target renal tubular segments of AVP.

Adenylyl Cyclases↗
PubMed1994

Potassium and sodium transport along the loop of Henle: effects of altered dietary potassium intake.

We assessed the effects of changes in potassium (K+) balance on the function of the loop of Henle by a combination of renal clearance and microperfusion experiments. Rat superficial cortical nephrons were perfused in vivo at 20 nl.min-1 from late proximal to early distal tubule with an artificial end-proximal solution containing either 3.8 or 1.8 mM potassium. Rats were fed a control diet, a low-potassium diet for at least three weeks, or a high-potassium diet for 10 to 14 days. When compared with the appropriate end-proximal potassium concentration in the perfusion fluid, potassium absorption along the loop of Henle (JK) increased in potassium-depletion whereas sodium (JNa) and fluid (Jv) absorption decreased. In rats fed a high-potassium diet, absorption of potassium, sodium and fluid was depressed. We propose that changes of external potassium balance affect the transport of electrolytes and fluid along the loop of Henle in vivo by modulating the transport of potassium and sodium primarily in the thick ascending limb. Changes in potassium reabsorption may also be affected by alterations of potassium-recycling.

Animals↗
PubMed2001

Effects of the potassium channel blocker barium on sodium and potassium transport in the rat loop of Henle in vivo.

In vitro evidence suggests that the 'recycling' of K(+) ions through luminal K(+) channels in the thick ascending limb of the loop of Henle (TALH) is essential for the normal operation of the luminal Na(+)-K(+)-2Cl(-) co-transporter. In the present study these channels were investigated in vivo by perfusing superficial loops of Henle in anaesthetised rats with and without the K(+) channel blocker barium. Using a standard perfusate, intraluminal barium (5 mmol l(-1)) reduced sodium reabsorption (J(Na)) from 1887 +/- 50 to 1319 +/- 53 pmol min(-1) (P < 0.001). When the experiment was repeated using a low-Na(+) perfusate, designed to inhibit reabsorption in the pars recta (the initial segment of the loop of Henle), a similar reduction in J(Na) was observed (from 698 +/- 47 to 149 +/- 23 pmol min(-1), P < 0.001), strongly suggesting that the effect of barium is localised to the TALH. The magnitude of the reduction in J(Na) during blockade of K(+) channels confirms the importance of K(+) recycling in facilitating Na(+) reabsorption in the TALH in vivo. However, the reduction in J(Na) was not associated with a fall in the K(+) concentration of the fluid collected at the early distal tubule. When bumetanide, an inhibitor of the Na(+)-K(+)-2Cl(-) co-transporter, was included in the low-Na(+) perfusate, net K(+) secretion was observed. Addition of barium to this perfusate reduced, but did not abolish, the secretion, suggesting that bumetanide-induced K(+) secretion results partly from paracellular transport. Experimental Physiology (2001) 86.4, 469-474.

Animals↗
PubMed1982

Inhibition of calcium absorption in the cortical thick ascending limb of Henle's loop by furosemide.

The effect of luminal furosemide on calcium transport across the cortical thick ascending limb of Henle's loop was studied. Cortical thick ascending limbs were dissected from rabbit kidneys and perfused in vitro. Calcium concentrations in perfused and collected tubule fluids were measured by continuous-flow microcolorimetry. Tubules were perfused at slow flow rates and parathyroid hormone was added to the bathing solution to maximize the difference between perfusate and collectate calcium concentrations. Furosemide simultaneously and reversibly inhibited the lumen-positive transepithelial voltage and calcium absorption. In the presence of furosemide perfusate-minus-collectate calcium concentration difference was smallest under conditions that minimized the residual transepithelial voltage. It was concluded furosemide inhibits calcium absorption in the cortical thick ascending limb of Henle's loop by reducing the lumen-positive transepithelial voltage that drives passive calcium ion transport.

Absorption↗
PubMed1987

Effect of glutaraldehyde on renal tubular function. II. Selective inhibition of Cl- transport in the hamster thin ascending limb of Henle's loop.

In order to further characterize Cl- transport of the thin ascending limb of Henle's loop (TAL), we observed the effects of glutaraldehyde on Na+ and Cl- transport in hamster TAL perfused in vitro. We found that 0.1 mol/l glutaraldehyde added either to the lumen or to the bath caused a rapid irreversible reversal of the NaCl diffusion potential. This was mainly accounted for by an inhibition of Cl- permeability (10(-7) cm2 s-1) from 93.51 +/- 8.39 to 14.89 +/- 3.91 (P less than 0.01, n = 9). By contrast, Na+ permeability changed little from 34.18 +/- 3.27 to 26.56 +/- 2.74 (P less than 0.01, n = 6). Glutaraldehyde treatment abolished the halogen-permselectivity of the TAL as determined by the voltage deflection seen upon ionic substitution. Permeabilities for Cl-, Br-, I-, and SCN- relative to Na+ were changed from 3.16 +/- 0.20, 3.22 +/- 0.19, 2.97 +/- 0.26 and 4.36 +/- 0.36 to 0.38 +/- 0.07, 0.35 +/- 0.06, 0.36 +/- 0.07 and 0.58 +/- 0.05, respectively. The effect of glutaraldehyde on the NaCl diffusion potential was dose-dependent in the range from 10(-5) to 10(-1) M. The effect was reversible at concentrations lower than 10(-3) M. Glutaraldehyde did not affect the NaCl diffusion potential of the long-loop descending limb. These observations constitute additional evidence that the mechanism of Cl- transport across the TAL is different from that of Na+ transport. Glutaraldehyde might inhibit Cl- transport in the TAL by cross-linking amino acid residues of the proteins essential for halogen transport across this segment.

Aldehydes↗
PubMed1987

Effects of anion transport inhibitors and ion substitution on Cl- transport in TAL of Henle's loop.

To identify the mechanism of Cl- transport across the thin ascending limb of Henle's loop (TAL), we examined effects of anion transport inhibitors and ionic substitution in the isolated segments of hamsters using the in vitro microperfusion technique. 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) at 10(-3) M changed the NaCl diffusion voltage (Vt) to the orientation that corresponds to the decrease in the Cl(-)-Na+ permeability ratio when it was added either to the bath or to the lumen. DIDS, added to the bath or to the lumen decreased the lumen-to-bath flux coefficient for 36Cl, KCl-(1----b) (X10(-7) cm2/s), from 74.5 +/- 2.1 to 17.9 +/- 3.6 and from 77.7 +/- 3.6 to 51.1 +/- 5.4, respectively, whereas it had little effect on the flux coefficient for 22Na, KNa+(1----b). Elimination of HCO3- slightly increased rather than decreased both NaCl diffusion potential and KCl-(1----b), indicating that Cl- transport is independent of HCO3- transport. Phloretin at 10(-3) M inhibited both diffusion potential and KCl-(1----b) to a similar extent as DIDS did. KNa+(1----b) was also changed little. The inhibitory effect of phloretin was rapid and reversible. Phloridzin was ineffective. Furosemide added to the bath at 10(-3) M decreased Vt and KCl-(1----b) from 29 +/- 0.9 to 5.3 +/- 0.7 mV and from 75.7 +/- 3.9 to 62.8 +/- 4.1 X 10(-7) cm2/s, respectively; but it was ineffective when added to the lumen. Elimination of Na+ caused only a small decrease in KCl-(1----b) from 119.2 +/- 6.9 to 107.3 +/- 8.5 X 10(-7) cm2/s. Elimination of K+ and addition of Ba2+ did not change KCl-(1----b). From these observations, we conclude that Cl- transport across the TAL is distinct from Na+ and is not coupled with Na+, K+, or HCO3-.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1982

Effects of arginine vasopressin on the thin ascending limb of Henle's loop of hamsters.

Arginine vasopressin (AVP) has been shown to stimulate active Cl transport across the medullary thick ascending limb of Henle's loop (MAL) in association with an increase in adenylate cyclase activity. To determine whether the failure to demonstrate active Cl transport across the thin ascending limb of Henle's loop (TAL) in previous in vitro perfusion studies was due to the absence of AVP in the preparation, we examined the effect of AVP on adenylate cyclase activity and Cl transport in the hamsters TAL. AVP (1 mU/ml) increased adenylate cyclase activity in the hamster TAL (20.7 +/- 5.2 control vs. 46.2 +/- 10.1 fmol . mm-1 . 30 min-1, n = 6, P less than 0.05) but not in the descending limb (27.8 +/- 7.0 control vs. 20.4 +/- 2.7, n = 4, P less than 0.05). When both MAL and TAL were perfused, a lumen-positive transepithelial voltage (Vt) was observed. The Vt was increased by adding 1 or 10 mU/ml AVP to the bath. When only the TAL was perfused, the Vt was not different from zero. Similar results were obtained in mouse renal tubules. In other experiments, AVP did not affect the diffusion potential generated when a transepithelial NaCl gradient was present. AVP or dibutyryl cAMP caused little or no change in efflux of radioactive chloride across the hamster TAL. These findings suggest that electrogenic chloride transport is not demonstrable in the TAL even in the presence of AVP. The physiologic role of AVP-sensitive adenylate cyclase in the TAL remains to be established.

Adenylyl Cyclases↗
PubMed1994

Lithium reabsorption in perfused loops of Henle: effects of perfusion rate and bumetanide.

The contribution of the loop segments to lithium reabsorption in sodium-replete, anesthetized Sprague-Dawley rats was examined by perfusing superficial loops of Henle between late proximal convolutions and early distal tubules. Preliminary experiments in which lithium was initially present only inside or outside the perfused loop confirmed substantial permeability of one or more of the loop segments to lithium. In subsequent experiments, in which lithium was infused intravenously and included in the perfusate so that the perfusate-to-plasma lithium concentration ratio was close to that found in late proximal tubules during lithium clearance studies, lithium reabsorption was inversely related to the perfusion rate: values for fractional lithium reabsorption (FRLi) at perfusion rates of 10, 20, and 30 nl/min were 58 +/- 3, 17 +/- 2, and 2 +/- 2%, respectively. Bumetanide (10(-6) M) markedly inhibited FRLi but also reduced water reabsorption, suggesting an effect on the pars recta at this dose; 10(-7) M bumetanide, which was without effect on water reabsorption, had only a small effect on FRLi at a perfusion rate of 10 nl/min but reduced FRLi by approximately 70% at 20 nl/min. We argue that the remarkable flow dependency of lithium reabsorption, together with its bumetanide sensitivity, provides evidence for significant voltage-driven lithium reabsorption in the thick ascending limb of Henle.

Absorption↗
PubMed1986

Lack of direct action of alpha-human atrial natriuretic polypeptide on the in vitro perfused segments of Henle's loop isolated from rabbit kidney.

We examined direct effects of alpha-human atrial natriuretic polypeptide (alpha-hANP) on water and NaCl transport across the segments of Henle's loop by the in vitro microperfusion technique. In the medullary and the cortical thick ascending limb, 10(-6) M alpha-hANP did not affect the transmural voltage (Vt) and the lumen to bath 36Cl flux whether it was added to the perfusate or to the bath. In the thin ascending limb, 10(-6) M alpha-hANP did not affect the lumen to bath 36Cl flux. The peptide may not affect permselectivity of the thin ascending limb, since it did not influence the diffusion potential generated in the presence of a NaCl gradient. In the descending limb, 10(-6) M alpha-hANP did not affect osmotic water permeability, whether it was added to the perfusate or to the bathing fluid. From these observations, we conclude that alpha-hANP does not show direct effects on water and NaCl transport in the segments of Henle's loop at least under our experimental conditions. Therefore, natriuresis by alpha-hANP may be caused either by an action on nephron segments other than Henle's loop or by an action on renal vasculatures.

Animals↗
PubMed1996

Evidence of calcium phosphate supersaturation in the loop of Henle.

We have used published rat micropuncture data to construct a matrix of ion concentrations along the rat nephron. With an iterative computer model of known ion interactions, we calculated relative supersaturation ratios in all nephron segments. The collecting ducts and urine showed expected supersaturation with stone-forming salts. Fluid in the thin segment of the loop of Henle may be supersaturated with calcium carbonate and calcium phosphate under certain conditions. Because calculations cannot predict the actual course of crystallization, we made solutions to mimic, in vitro, presumed conditions in the loop of Henle. The solid phases that formed were analyzed by X-ray powder diffraction, electron microprobe, and infrared spectroscopy. All samples were identified as poorly crystallized or immature apatite. The descending limb of Henle's loop creates a unique condition as it extracts water but not sodium, bicarbonate, calcium, or phosphate, giving a calcium concentration at the bend of 3 mM, pH 7.4, and a phosphate concentration that varies from 0.8 to 48 mM, depending on parathyroid hormone and dietary phosphate. We conclude that conditions in the thin segment potentially could create a solid calcium phosphate phase, which may initiate nucleation of calcium oxalate salts in the collecting ducts, potentiating nephrolithiasis and nephrocalcinosis.

Animals↗