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. 2010 Feb 10;298(4):R954–R958. doi: 10.1152/ajpregu.00758.2009

Effect of catecholamines on rat medullary thick ascending limb chloride transport: interaction with angiotensin II

Michel Baum 1,✉
PMCID: PMC2853393  PMID: 20147605

Abstract

Previous studies have shown that in proximal and distal tubule nephron segments, peritubular ANG II stimulates sodium chloride transport. However, ANG II inhibits chloride transport in the medullary thick ascending limb (mTAL). Because ANG II and catecholamines are both stimulated by a decrease in extracellular fluid volume, the purpose of this study was to examine whether there was an interaction between ANG II and catecholamines to mitigate the inhibition in chloride transport by ANG II. In isolated perfused rat mTAL, 10−8 M bath ANG II inhibited transport (from a basal transport rate of 165.6 ± 58.8 to 58.8 ± 29.4 pmol·mm−1·min−1; P < 0.01). Bath norepinephrine stimulated chloride transport (from a basal transport rate of 298.1 ± 31.7 to 425.2 ± 45.8 pmol·mm−1·min−1; P < 0.05) and completely prevented the inhibition in chloride transport by ANG II. The stimulation of chloride transport by norepinephrine was mediated entirely by its β-adrenergic effect; however, both the β- and α-adrenergic agonists isoproterenol and phenylephrine prevent the ANG II-mediated inhibition in chloride transport. In the presence of 10−5 M propranolol, the effect of norepinephrine to prevent the inhibition of chloride transport by ANG II was still present. These data are consistent with an interaction of both α- and β-catecholamines and ANG II on net chloride transport in the mTAL.

Keywords: NKCC2, norepinephrine, isoproterenol

angiotensin ii is one of the factors responsible for increasing sodium absorption in the face of volume depletion. In addition to hemodynamic effects, ANG II has been shown to have a direct epithelial action to regulate sodium absorption along the nephron. Using in vivo micropuncture and in vitro microperfusion, ANG II has been shown to increase sodium chloride and volume absorption in the proximal tubule (3, 8, 20, 26–28, 42, 45). Likewise, sodium transport has been shown to be stimulated in the macula densa by ANG II (5, 24, 36). In an in vivo microperfusion study, ANG II was found to stimulate acidification and sodium absorption in the distal convoluted tubule (44). ANG II increased transcellular chloride transport and sodium transport across the epithelial sodium channel in the cortical collecting tubule (35, 37). Despite the increase in sodium absorption in almost every nephron segment, ANG II was found to decrease chloride transport in the medullary thick ascending limb (mTAL), a nephron segment responsible for a substantive amount of sodium chloride absorption (25).

Both the renin-angiotensin system and the renal nerves are stimulated by similar factors that result in a decrease in effective arteriolar pressure. The interdependence of the renin-angiotensin system and renal nerves can affect renal salt transport, as well as renal hemodynamics in not only a concordant but in a mutually dependent fashion (10, 11). As an example of this interdependence, circulating ANG II facilitated adrenergic transmission at the renal nerve-renal epithelial cell junction (18, 21, 22), so that renal nerve stimulation increased sodium transport in the presence of physiological circulating ANG II and was blunted by administration of captopril (21). We have previously shown that the stimulation in proximal tubule sodium absorption by the intrarenal renal angiotensin system was regulated by and dependent upon renal nerves (40, 41).

Previous studies have shown that β-catecholamines stimulate sodium chloride transport in the mTAL (1, 29, 38). Since proximal and distal nephron segments have an increase in sodium transport with ANG II, the present study reexamined whether ANG II decreases mTAL transport. In addition, this study examined whether there was an interaction of the effect of ANG II and catecholamines on sodium chloride transport in this segment.

METHODS

Animals.

Adult male and female Sprague-Dawley rats weighing between 90 and 210 g were used in these studies. Rats were given intraperitoneal furosemide (2 mg/100 g body wt) ∼5 min prior to receiving intraperitoneal Inactin (10 mg/100 g body wt). After the rats were under anesthesia, the abdomen was opened to expose the left kidney, which was bathed for 1 min in ice-cold PBS. The kidney was then removed and cut into several coronal slices for microdissection (15, 17, 23). These studies were approved by the Institutional Animal Care and Use Committee at the University of Texas Southwestern Medical Center.

In vitro microperfusion flux studies.

Segments of rat mTAL were dissected free hand and perfused with an ultrafiltrate-like solution that contained (in mM) 115 NaCl, 25 NaHCO3, 4.0 Na2HPO4, 10 Na acetate, 1.8 mM CaCl2, 1 MgSO4, 5 KCl, 8.3 glucose, 5 alanine, 2 lactate, and 2 glutamine at 4 or 5 nl/min. The tubules were bathed in a similar solution containing 6 g/dl of BSA. The osmolality of all solutions was adjusted to 300 mosmol/kg H2O. The bathing solution was heated to 38°C and exchanged at 0.5 ml/min to maintain a constant pH and osmolality.

The rate of chloride transport in the medullary thick ascending limbs (mTAL) was calculated as JCl = (Vl) (Clo − Cll)Po/CloL where V1 is the collection rate, Clo and Cll were the chloride concentrations in the perfusion solution and the collected fluid, respectively, in counts per minute per nanoliter. Po is the perfusate chloride concentration in millimoles and L is the tubular length in mm. The tubule lengths were measured with an eyepiece micrometer. The mean tubular length was 0.5 ± 0.1 mm. The perfusion solution contained 36Cl at a concentration of 10 μCi/ml. A 30-nl constant-volume pipette was used to measure the collection rate. Tubules were perfused at ∼5 nl/min. Tubules were incubated for ∼15 min before initiation of the measurements for chloride absorption and between periods. There were at least three measurements per period, and the mean of the collections in each period was used to represent the chloride absorption. We have previously demonstrated that there is no detectable passive chloride transport in this segment and thus no chloride backflux (9).

The transepithelial potential difference was measured using the perfusion pipette that was inserted into the tubular lumen. The reference electrode was in the bathing solution. The potential difference was measured using a Keithley Electrometer, model no. 6517B (Keithley, Cleveland, OH).

Statistics.

There was variability in the basal transport rate in mTAL with older rats having the highest rate of chloride transport; however, all studies were conducted in a paired fashion, and the results were consistent independent of the basal rate of transport. Paired Student's t-test was used to measure the difference in experimental periods when two periods were compared. Analysis of variance was used to determine statistical significance for studies with more than two groups. Data are expressed as means ± SE.

RESULTS

In the first series of experiments, rat mTAL was perfused in vitro, and chloride transport was measured. We have previously shown that under these conditions, the chloride transport measured was entirely due to active transport (9). I first examined whether 2×10−11M ANG II affected chloride transport in the mTAL. The rate of chloride transport was 148.9 ± 17.7 in the control period and 129.2 ± 14.5 pmol·mm−1·min−1 after the addition of ANG II, confirming that the plasma concentration of ANG II in a euvolemic animal does not affect mTAL transport (25). Similarly, 10−10 M ANG II had no effect on chloride transport (271.1 ± 40.5 in control vs. 242.6 ± 98.1 with 10−10 M ANG II pmol·mm−1·min−1), while 10−9 M ANG II inhibited chloride transport from 317.8 ± 68.6 to 258.7 ± 70.9 pmol·mm−1·min−1 (P < 0.05). The experiments shown in Fig. 1 confirmed previous findings that chloride transport was inhibited significantly by bath 10−8 M ANG II (25). Similarly, 10−8 M ANG II caused a reduction in the transepithelial potential difference from positive 4.6 ± 0.7 to 3.7 ± 0.7 mV, P < 0.01.

Fig. 1.

Fig. 1.

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Effect of ANG II on mTAL chloride transport in the medullary thick ascending limb (mTAL). mTAL was dissected and perfused in vitro. After the control period, 10−8 M ANG II was added to the bathing solution. There was a significant decrease in chloride transport with bath ANG II (*P < 0.01).

I next examined whether 10−6 M bath norepinephrine affected transport or influenced the effect of bath ANG II. These results are shown in Fig. 2. Bath norepinephrine caused a significant increase in chloride transport. This confirmed previous studies showing that this concentration of norepinephrine increases chloride transport in this nephron segment (38) In addition, when 10−8 M ANG II was added to the bathing solution in the third period in the presence of norepinephrine, the ANG II-mediated decrease in chloride transport was prevented. Norepinephrine caused an increase in the transepithelial potential difference from 9.0 ± 0.5 to 13.8 ± 1.1 mV, P < 0.001 and prevented the decrease in potential difference by ANG II (13.0 ± 0.9 mV P = not significant, ns) I also examined whether 2 × 10−11 ANG II affected chloride transport in the presence of bath 10−6 M norepinephrine. Chloride transport was 325.8 ± 37.4 pmol·mm−1·min−1 in the presence of 10−6 M norepinephrine and 294.5 ± 36.6 pmol·mm−1·min−1 when 2 × 10−11 M ANG II was added to the bathing solution in the presence of norepinephrine (P = ns). Thus, norepinephrine stimulates chloride transport and prevents the decrease in transport by 10−8 M ANG II.

Fig. 2.

Fig. 2.

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Effect of norepinephrine and norepinephrine with ANG II on mTAL transport: mTAL were perfused in vitro. After the control period, 10−6 M norepinephrine (Norepi) was added to the bathing solution. Norepinephrine caused a significant increase in chloride transport: *P < 0.05. 10−8 M ANG II was then added in the presence of norepinephrine, and the inhibition of chloride transport seen in Fig. 1 was abrogated.

The next experiments were designed to determine whether the stimulatory effect of norepinephrine on mTAL chloride transport and its effect to prevent the ANG II-mediated decrease in chloride transport was via an α- or β-effect of catecholamines. The effect of isoproterenol, a β-agonist, on chloride transport was next examined as shown in Fig. 3. Isoproterenol (10−6 M) stimulated chloride transport in the mTAL. These results are shown in Fig. 4. Furthermore, isoproterenol prevented the inhibition in chloride transport mediated by 10−8 M ANG II. Isoproterenol also increased the potential difference from 3.7 ± 1.0 to 5.7 ± 1.3 mV, P < 0.05 and prevented the decrease mediated by ANG II (5.4 ± 1.1 mV, P = ns).

Fig. 3.

Fig. 3.

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Effect of isoproterenol and isoproterenol with ANG II on chloride transport in the mTAL. Isoproterenol (Iso) (10−6 M) increased chloride transport in mTAL. The addition of 10−8 M ANG II had no effect on chloride transport when isoproterenol was in the bathing solution. *P < 0.05 control vs. isoproterenol.

Fig. 4.

Fig. 4.

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Effect of phenylephrine and phenylephrine with ANG II on chloride transport in the mTAL. After the control period 10−6 M phenylephrine (PE) was added to the bathing solution. There was no effect of the pure α-agonist on chloride transport, but PE prevented the decrease in chloride transport with the addition of 10−8 M ANG II to the bathing solution.

In the next series of experiments shown in Fig. 4, the effect of the α-agonist phenylephrine was examined. The addition of 10−6 M phenylephrine to the bathing solution resulted in no change in chloride transport compared with the control period in mTAL. However, phenylephrine also prevented the inhibition of chloride transport mediated by 10−8 M ANG II. Thus, while the stimulation in chloride transport in the mTAL is mediated by a β-effect of catecholamines in this segment, both α- and β-effects of catecholamines prevent the inhibition by ANG II. Phenylephrine had no effect on the potential difference compared with control but prevented the decrease in potential difference by ANG II (3.7 ± 1.1 mV control vs. 4.3 ± 1.5 mV phenylephrine vs. 3.9 ± 0.8 mV phenylephrine plus ANG II, P = ns).

In the last series of experiments shown in Fig. 5, I show that 10−5 M propranolol blocked the increase in chloride transport by 10−6 M norepinephrine. Norepinephrine still prevented the inhibition of chloride transport by 10−8 M ANG II in the presence of propranolol. This is consistent with norepinephrine increasing chloride transport via a β-adrenergic effect and preventing the decrease in chloride transport by a non-β or -α effect. Similarly, norepinephrine did not significantly increase the potential difference in the presence of propranolol (3.6 ± 1.3 mV bath propranolol vs. 4.8 ± 2.7 mV bath propranolol plus norepinephrine, P = ns), but it prevented the inhibition of the potential difference by ANG II (5.0 ± 2.5 mV).

Fig. 5.

Fig. 5.

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Effect 10−6 M norepinephrine and norepinephrine in the presence of ANG II on chloride transport in the presence of 10−5 M propranolol in the mTAL. To determine whether norepinephrine was acting via an α- or β-agonist to increase chloride transport, 10−5 M propranolol, a β-blocker was studied. Propranolol prevented the increase in chloride transport by 10−6 M norepinephrine. In the presence of propranolol and norepinephrine, the inhibitory effect of 10−8 M ANG II was blocked.

DISCUSSION

The present study confirms that ANG II by itself inhibits mTAL chloride transport. However, both α- and β-catecholamines prevent the inhibition of chloride transport by ANG II. Finally, norepinephrine stimulates chloride transport in the mTAL, an effect due entirely to its β-catecholamine effect.

While studies in the proximal tubule and distal convoluted tubule and collecting duct have all shown that ANG II stimulates sodium chloride transport consistent with its known regulatory role to limit sodium losses in the face of volume depletion (3, 5, 8, 20, 24–28, 35–37, 42, 45), the effect of ANG II on transport in the mTAL has not been clear. ANG II at 10−8 M has been shown previously to inhibit both chloride and bicarbonate transport in the mTAL perfused in vitro when added to the bathing solution (16, 25). Studies have also examined the effect of ANG II on loop of Henle sodium absorption in vivo, where ANG II resulted in an increase in proximal tubule reabsorption but had no effect on loop of Henle sodium absorption (12). However, when renal perfusion pressure was normalized to control values during ANG II infusion, there was an increase in proximal and loop of Henle reabsorption with ANG II infusion (12). While it is possible that sodium absorption in the proximal straight tubule was stimulated to such an extent that net sodium absorption in the entire loop was either not affected or stimulated in spite of an inhibition in mTAL transport, the magnitude of the inhibition in mTAL chloride transport seen in these in vitro microperfusion studies in the absence of catecholamines makes an inhibition in chloride transport in the mTAL in vivo unlikely. It should be noted that in vivo micropuncture studies were performed in innervated kidneys, which could account for the discrepancy between in vivo and in vitro effects of ANG II. Furthermore, there may be other factors besides renal nerves that are present in vivo that may affect the action of ANG II on the thick ascending limb.

The present study showed that norepinephrine prevents the decrease in chloride transport seen with ANG II in the mTAL. There are several other studies that have shown an interaction between hormones that can affect net transport. For example, there is no effect of atrial natriuretic peptide on sodium transport in the proximal tubule (4, 7). However, in the presence of either ANG II or norepinephrine, atrial natriuretic peptide inhibits proximal tubule transport (13, 14, 19). The intrarenal renin-angiotensin system regulates proximal tubule transport (39), an effect abrogated by renal denervation (40). Likewise, dopamine has no effect on proximal convoluted tubule transport but blunts the stimulation in proximal tubule sodium absorption caused by norepinephrine (2).

In this study and in previous studies by other investigators, plasma levels of ANG II had no effect on chloride transport in the mTAL (25). However, this is unlikely the concentration of ANG II in the medulla, as the kidney can generate ANG II independent of the systemic production (6, 31, 43). Interstitial ANG II levels are ∼3 nmol/l (32, 33) and can be augmented by chronic infusion of ANG II to twice this concentration (34). Furthermore, ANG II levels in the medulla are 3- to 4-fold greater than that in the cortex (30). Thus, the concentration of ANG II used in these and other studies is likely the physiologically relevant concentration (16, 25).

The present study shows that both norepinephrine and isoproterenol stimulate chloride transport in the mTAL, while the α-agonist phenylephrine had no effect. The stimulatory effect of norepinephrine was blocked by propranolol consistent with a β-adrenergic effect of norepinephrine to stimulate chloride transport. Previous studies have demonstrated that isoproterenol, at a concentration used in this study, stimulates transport in mouse and rat mTAL (1, 29, 38). Phenylephrine was also previously found to not affect chloride transport (38). The present studies extend these previous findings to demonstrate that both α- and β-agonists block the inhibition of ANG II in the mTAL. The fact that only β-agonist stimulates transport in this segment indicates that α- and β-catecholamines act via different signal transduction pathways. Thus, it is surprising that both the α-agonist phenylephrine and the β-agonist isoproterenol prevent the effect of ANG II to decrease chloride transport. The fact that propranolol inhibits chloride transport by norepinephrine yet blocks the effect of ANG II is also consistent with an α effect of norepinephrine to block the inhibition of chloride transport by ANG II. Both α- and β-adrenergic signaling pathways must act to disrupt ANG II signaling at some point in their intracellular signaling. These studies show that hormonal interactions are important in the net regulation of transport in this nephron segment.

Perspectives and Significance

The present study shows that there is an interaction between norepinephrine and ANG II in their actions on chloride transport in the mTAL. This is another example of how different hormones and physiological conditions interact to affect transport. While there are advantages to studying the regulation of transport in vivo, some segments are not accessible, and examination of one factor in isolation of other hormones and renal nerves is often quite difficult. Whole animal clearance studies examine multiple nephron segments at one time and often do not provide mechanistic answers at the cellular level. Direct evaluation of an epithelium using in vitro approaches allows one to study the effect of a single perturbation on transport or signal transduction in a homogeneous cellular preparation. However, there are often interactions in vivo that are not directly obvious in vitro. Thus, it is not better to examine an issue using one approach or another but in vitro studies and in vivo studies should be complementary to examine mechanisms and significance of physiological perturbations.

GRANTS

This work was supported by National Institutes of Health Grants DK41612, DK078596, T32 DK07257, and the O'Brien Center Grant P30DK079328.

DISCLOSURES

No conflicts of interest are declared by the authors.

REFERENCES

  • 1.Bailly C, Imbert-Teboul M, Roinel N, Amiel C. Isoproterenol increases Ca, Mg, and NaCl reabsorption in mouse thick ascending limb. Am J Physiol Renal Fluid Electrolyte Physiol 258: F1224–F1231, 1990 [DOI] [PubMed] [Google Scholar]
  • 2.Baum M, Quigley R. Inhibition of proximal convoluted tubule transport by dopamine. Kidney Int 54: 1593–1600, 1998 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Baum M, Quigley R, Quan A. Effect of luminal angiotensin II on rabbit proximal convoluted tubule bicarbonate absorption. Am J Physiol Renal Physiol 273: F595–F600, 1997 [DOI] [PubMed] [Google Scholar]
  • 4.Baum M, Toto RD. Lack of a direct effect of atrial natriuretic factor in the rabbit proximal tubule. Am J Physiol Renal Fluid Electrolyte Physiol 250: F66–F69, 1986 [DOI] [PubMed] [Google Scholar]
  • 5.Bell PD, Peti-Peterdi J. Angiotensin II stimulates macula densa basolateral sodium/hydrogen exchange via type 1 angiotensin II receptors. J Am Soc Nephrol 10Suppl 11: S225–S229, 1999 [PubMed] [Google Scholar]
  • 6.Braam B, Mitchell KD, Fox J, Navar LG. Proximal tubular secretion of angiotensin II in rats. Am J Physiol Renal Fluid Electrolyte Physiol 264: F891–F898, 1993 [DOI] [PubMed] [Google Scholar]
  • 7.Cogan MG. Atrial natriuretic factor can increase renal solute excretion primarily by raising glomerular filtration. Am J Physiol Renal Fluid Electrolyte Physiol 250: F710–F714, 1986 [DOI] [PubMed] [Google Scholar]
  • 8.Cogan MG. Angiotensin II: a powerful controller of sodium transport in the early proximal tubule. Hypertension 15: 451–458, 1990 [DOI] [PubMed] [Google Scholar]
  • 9.Dagan A, Habbib S, Gattineni J, Dwarakanath V, Baum M. Prenatal programming of rat thick ascending limb chloride transport by low protein diet and dexamethasone. Am J Physiol Regul Integr Comp Physiol 297: R93–R99, 2009 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10.DiBona GF. Nervous kidney. Interaction between renal sympathetic nerves and the renin-angiotensin system in the control of renal function. Hypertension 36: 1083–1088, 2000 [DOI] [PubMed] [Google Scholar]
  • 11.DiBona GF. Peripheral and central interactions between the renin-angiotensin system and the renal sympathetic nerves in control of renal function. Ann NY Acad Sci 940: 395–406, 2001 [DOI] [PubMed] [Google Scholar]
  • 12.Fransen R, Boer WH, De Roos R, Boer P, Koomans HA. Effects of low-dose angiotensin II infusion on loop segment reabsorption: a free-flow micropuncture study in rats. Clin Sci (Lond) 88: 351–358, 1995 [DOI] [PubMed] [Google Scholar]
  • 13.Garvin JL. Inhibition of Jv by ANF in rat proximal straight tubules requires angiotensin. Am J Physiol Renal Fluid Electrolyte Physiol 257: F907–F911, 1989 [DOI] [PubMed] [Google Scholar]
  • 14.Garvin JL. ANF inhibits norepinephrine-stimulated fluid absorption in rat proximal straight tubules. Am J Physiol Renal Fluid Electrolyte Physiol 263: F581–F585, 1992 [DOI] [PubMed] [Google Scholar]
  • 15.Good DW. Effects of potassium on ammonia transport by medullary thick ascending limb of the rat. J Clin Invest 80: 1358–1365, 1987 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16.Good DW, George T, Wang DH. Angiotensin II inhibits HCO-3 absorption via a cytochromeP -450-dependent pathway in MTAL. Am J Physiol Renal Physiol 276: F726–F736, 1999 [DOI] [PubMed] [Google Scholar]
  • 17.Good DW, Knepper MA, Burg MB. Ammonia and bicarbonate transport by thick ascending limb of rat kidney. Am J Physiol Renal Fluid Electrolyte Physiol 247: F35–F44, 1984 [DOI] [PubMed] [Google Scholar]
  • 18.Handa RK, Johns EJ. Interaction of the renin-angiotensin system and the renal nerves in the regulation of rat kidney function. J Physiol 369: 311–321, 1985 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 19.Harris PJ, Thomas D, Morgan TO. Atrial natriuretic peptide inhibits angiotensin-stimulated proximal tubular sodium and water reabsorption. Nature 326: 697–698, 1987 [DOI] [PubMed] [Google Scholar]
  • 20.Harris PJ, Young JA. Dose-dependent stimulation and inhibition of proximal tubular sodium reabsorption by angiotensin II in the rat kidney. Pflügers Arch 367: 295–297, 1977 [DOI] [PubMed] [Google Scholar]
  • 21.Johns EJ. The role of angiotensin II in the antidiuresis and antinatriuresis induced by stimulation of the sympathetic nerves to the rat kidney. J Auton Pharmacol 7: 205–214, 1987 [DOI] [PubMed] [Google Scholar]
  • 22.Johns EJ. Role of angiotensin II and the sympathetic nervous system in the control of renal function. J Hypertens 7: 695–701, 1989 [PubMed] [Google Scholar]
  • 23.Knepper MA. Urea transport in isolated thick ascending limbs and collecting ducts from rats. Am J Physiol Renal Fluid Electrolyte Physiol 245: F634–F639, 1983 [DOI] [PubMed] [Google Scholar]
  • 24.Kovacs G, Peti-Peterdi J, Rosivall L, Bell PD. Angiotensin II directly stimulates macula densa Na-2Cl-K cotransport via apical AT(1) receptors. Am J Physiol Renal Physiol 282: F301–F306, 2002 [DOI] [PubMed] [Google Scholar]
  • 25.Lerolle N, Bourgeois S, Leviel F, Lebrun G, Paillard M, Houillier P. Angiotensin II inhibits NaCl absorption in the rat medullary thick ascending limb. Am J Physiol Renal Physiol 287: F404–F410, 2004 [DOI] [PubMed] [Google Scholar]
  • 26.Liu FY, Cogan MG. Angiotensin II: a potent regulator of acidification in the rat early proximal convoluted tubule. J Clin Invest 80: 272–275, 1987 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 27.Liu FY, Cogan MG. Angiotensin II stimulation of hydrogen ion secretion in the rat early proximal tubule. Modes of action, mechanism, and kinetics. J Clin Invest 82: 601–607, 1988 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 28.Liu FY, Cogan MG. Angiotensin II stimulates early proximal bicarbonate absorption in the rat by decreasing cyclic adenosine monophosphate. J Clin Invest 84: 83–91, 1989 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 29.Morgunov NS, You YD, Hirsch DJ. Response of mouse proximal straight tubule and medullary thick ascending limb to B-agonist1, 2. J Am Soc Nephrol 4: 1151–1158, 1993 [DOI] [PubMed] [Google Scholar]
  • 30.Navar LG, Imig JD, Zou L, Wang CT. Intrarenal production of angiotensin II. Semin Nephrol 17: 412–422, 1997 [PubMed] [Google Scholar]
  • 31.Navar LG, Lewis L, Hymel A, Braam B, Mitchell KD. Tubular fluid concentrations and kidney contents of angiotensins I and II in anesthetized rats. J Am Soc Nephrol 5: 1153–1158, 1994 [DOI] [PubMed] [Google Scholar]
  • 32.Nishiyama A, Seth DM, Navar LG. Renal interstitial fluid angiotensin I and angiotensin II concentrations during local angiotensin-converting enzyme inhibition. J Am Soc Nephrol 13: 2207–2212, 2002 [DOI] [PubMed] [Google Scholar]
  • 33.Nishiyama A, Seth DM, Navar LG. Renal interstitial fluid concentrations of angiotensins I and II in anesthetized rats. Hypertension 39: 129–134, 2002 [DOI] [PubMed] [Google Scholar]
  • 34.Nishiyama A, Seth DM, Navar LG. Angiotensin II type 1 receptor-mediated augmentation of renal interstitial fluid angiotensin II in angiotensin II-induced hypertension. J Hypertens 21: 1897–1903, 2003 [DOI] [PubMed] [Google Scholar]
  • 35.Pech V, Kim YH, Weinstein AM, Everett LA, Pham TD, Wall SM. Angiotensin II increases chloride absorption in the cortical collecting duct in mice through a pendrin-dependent mechanism. Am J Physiol Renal Physiol 292: F914–F920, 2007 [DOI] [PubMed] [Google Scholar]
  • 36.Peti-Peterdi J, Bell PD. Regulation of macula densa Na:H exchange by angiotensin II. Kidney Int 54: 2021–2028, 1998 [DOI] [PubMed] [Google Scholar]
  • 37.Peti-Peterdi J, Warnock DG, Bell PD. Angiotensin II directly stimulates ENaC activity in the cortical collecting duct via AT(1) receptors. J Am Soc Nephrol 13: 1131–1135, 2002 [DOI] [PubMed] [Google Scholar]
  • 38.Plato CF. Alpha-2 and beta-adrenergic receptors mediate NE's biphasic effects on rat thick ascending limb chloride flux. Am J Physiol Regul Integr Comp Physiol 281: R979–R986, 2001 [DOI] [PubMed] [Google Scholar]
  • 39.Quan A, Baum M. Endogenous production of angiotensin II modulates rat proximal tubule transport. J Clin Invest 97: 2878–2882, 1996 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 40.Quan A, Baum M. The renal nerve is required for regulation of proximal tubule transport by intraluminally produced ANG II. Am J Physiol Renal Physiol 280: F524–F529, 2001 [DOI] [PubMed] [Google Scholar]
  • 41.Quan A, Baum M. Renal nerve stimulation augments effect of intraluminal angiotensin II on proximal tubule transport. Am J Physiol Renal Physiol 282: F1043–F1048, 2002 [DOI] [PubMed] [Google Scholar]
  • 42.Schuster VL, Kokko JP, Jacobson HR. Angiotensin II directly stimulates sodium transport in rabbit proximal convoluted tubules. J Clin Invest 73: 507–515, 1984 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 43.Seikaly MG, Arant BS, Jr., Seney FD., Jr Endogenous angiotensin concentrations in specific intrarenal fluid compartments of the rat. J Clin Invest 86: 1352–1357, 1990 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 44.Wang T, Giebisch G. Effects of angiotensin II on electrolyte transport in the early and late distal tubule in rat kidney. Am J Physiol Renal Fluid Electrolyte Physiol 271: F143–F149, 1996 [DOI] [PubMed] [Google Scholar]
  • 45.Wong KR, Berry CA, Cogan MG. Chloride transport in the rat S1 proximal tubule. Am J Physiol Renal Fluid Electrolyte Physiol 268: F723–F729, 1995. [DOI] [PubMed] [Google Scholar]

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