Dose-dependent stimulation and inhibition of proximal tubular sodium reabsorption by angiotensin II in the rat kidney

Harris, Peter; Young, J. A.

doi:10.1007/bf00581370

Cited by 350 publications

(200 citation statements)

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“…On the other hand, our observed 36% increase of J V with 10 Ϫ11 M ANG II is about twice as great as that observed by the earlier investigators. Our J V data confirm the earlier observations of others, made in a combination of rat (14,23,38) and rabbit (34) PTs, that increasing levels of basolateral ANG II have a biphasic effect on J V . In addition, we observed that increasing levels of basolateral ANG II have a biphasic effect on J HCO 3 .…”

Section: Effects Of Basolateral Ang II On J Hcosupporting

confidence: 92%

Effects of angiotensin II on the CO₂dependence of HCO₃⁻reabsorption by the rabbit S2 renal proximal tubule

Zhou¹,

Bouyer²,

Boron³

2006

American Journal of Physiology-Renal Physiology

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M tended to reduce stimulation by CO2, and at 10 Ϫ9 M, produced an even greater reduction. In conclusion, the mutual effects of 1) ANG II on the JHCO 3 response to basolateral CO2 and 2) basolateral CO2 on the JHCO 3 responses to ANG II suggest that the signal-transduction pathways for ANG II and basolateral CO2 intersect or merge.kidney; out-of-equilibrium solutions; acid-base; volume reabsorption ONE OF THE MAJOR tasks of the kidneys is to participate, along with the lungs, in the regulation of the acid-base balance of the extracellular fluid. For example, it has long been appreciated that acute respiratory acidosis (i.e., a rise in PCO 2 that causes a fall in pH) rapidly stimulates renal H ϩ secretion (8, 16). The proximal tubule (PT) plays a key role in this acid secretion. In addition to reabsorbing a near-isosmotic fluid that represents about two-thirds of the fluid filtered by the glomerulus, the PT reabsorbs ϳ80% of the filtered HCO 3 Ϫ as follows. The PT cell actively secretes H ϩ into the tubule lumen (1, 6, 35) and uses this H ϩ to titrate filtered HCO 3 Ϫ in the lumen to CO 2 and H 2 O, catalyzed by apical carbonic anhydrase IV (9, 36, 37). The newly formed CO 2 and H 2 O then diffuse into the PT cells, where carbonic anhydrase II (36, 37) catalyzes the regeneration of H ϩ and HCO 3 Ϫ . The cell extrudes the H ϩ across the apical membrane via Na-H exchangers (4, 5, 30) and H ϩ pumps (20), while exporting the HCO 3 Ϫ across the basolateral membrane, mainly via the electrogenic Na/HCO 3 cotransporter (7,15,32,33 (12) on isolated, perfused rabbit PTs. They noted that adding ϳ2 ϫ 10 Ϫ6 M ANG II to the basolateral solution had no detectable effect on the rate of fluid absorption (J V ). In a 1974 rat micropuncture study, Steven (38) reported that ϳ2 ϫ 10 Ϫ5 M basolateral ANG II lowered J V , whereas 1 ϫ 10 Ϫ7 M had no effect. Harris and Young (23) later showed that basolateral ANG II has a biphasic effect on Na ϩ reabsorption in the rat PT, stimulating at low doses (10 Ϫ12 -10 Ϫ10 M) and inhibiting at higher doses (3 ϫ 10 Ϫ7 -3 ϫ 10 Ϫ6 M). Shuster and colleagues (34) in 1984 demonstrated a similar biphasic effect of basolateral ANG II on J V in isolated, perfused rabbit PTs, ruling out a role of sympathetic innervation on the J V response. In 1991, working in isolated, perfused rat proximal straight tubules (PSTs), Garvin (19) found that 10 Ϫ10 M basolateral ANG II increases both J HCO 3 and J V . At about the same time, Chatsudthipong and Chan (14) found that high levels of basolateral ANG II reduce J HCO 3 in rats and that these effects are blocked by saralasin, an antagonist of ANG II receptors.As far as the effects of luminal ANG II are concerned, in a 1988 micropuncture study, Liu and Cogan (26) showed that low-dose luminal ANG II (10 Ϫ12 -10 Ϫ11 M) increases HCO 3 Ϫ reabsorption (J HCO 3 ) even in a denervated rat kidney. The 1990 study on the rat PT by Wang and Chan (39) extended the earlier observations by showing that increasing levels of luminal ANG II have biphasic effects on J HCO 3 as well...

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Section: Effects Of Basolateral Ang II On J Hcosupporting

confidence: 92%

Effects of angiotensin II on the CO₂dependence of HCO₃⁻reabsorption by the rabbit S2 renal proximal tubule

Zhou¹,

Bouyer²,

Boron³

2006

American Journal of Physiology-Renal Physiology

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“…We have previously observed that the administration of competitive antagonists to All normalizes the glomerular and tubular responses to glycine during treatment with L-NMMA (12), suggesting that NO normally functions within the proximal nephron to antagonize the anti-reabsorptive effects of All (40). Armed with the new knowledge that glycine increases intrarenal All concentration, we now propose that infusion ofthis substance induces parallel increases in NO and All activity with the glomerular hemodynamic outcome contingent upon the net balance between the two systems.…”

Section: Discussionmentioning

confidence: 99%

Arginine feeding modifies cyclosporine nephrotoxicity in rats.

Nicola

Thomson²,

Wead³

et al. 1993

J. Clin. Invest.

121

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“…Investigations of the luminal actions of angiotensin in vivo (Harris & Young, 1977;Wang & Chan, 1990) and in vitro (Li et al, 1994) have indicated that picomolar to nanomolar concentrations of angiotensin II stimulate sodium and bicarbonate transport whereas micromolar concentrations cause inhibition. We have used nonpeptide angiotensin receptor blockers to examine whether endogenously produced angiotensin II in the proximal tubular lumen exerts a modulatory influence upon fluid absorption in the anaesthetized rat.…”

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confidence: 99%

Modulation by locally produced luminal angiotensin II of proximal tubular sodium reabsorption via an AT₁ receptor

Hiranyachattada

Harris

1996

British J Pharmacology

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The concentration of angiotensin II reported in proximal tubular fluid in anaesthetized rats is considerably higher than in plasma, indicating secretion of this peptide into the tubular lumen. Shrinking split-drop micropuncture was used to examine the effect of endogenous angiotensin on sodium and water absorption in the proximal convoluted tubule. Addition of losartan, a nonpeptide AT, receptor blocker, to intratubular fluid increased fluid uptake by 15.7+3.9% (10-' M) and 24.7+9.4% (10-4 M) whereas the AT2 inhibitor, PD123319 had no effect. We conclude that angiotensin II is secreted into proximal tubular fluid and, in the anaesthetized rat, is maintained at a concentration that inhibits sodium and water transport via AT, receptors.

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Dose-dependent stimulation and inhibition of proximal tubular sodium reabsorption by angiotensin II in the rat kidney

Cited by 350 publications

References 9 publications

Effects of angiotensin II on the CO₂dependence of HCO₃⁻reabsorption by the rabbit S2 renal proximal tubule

Effects of angiotensin II on the CO₂dependence of HCO₃⁻reabsorption by the rabbit S2 renal proximal tubule

Arginine feeding modifies cyclosporine nephrotoxicity in rats.

Modulation by locally produced luminal angiotensin II of proximal tubular sodium reabsorption via an AT₁ receptor

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Dose-dependent stimulation and inhibition of proximal tubular sodium reabsorption by angiotensin II in the rat kidney

Cited by 350 publications

References 9 publications

Effects of angiotensin II on the CO2dependence of HCO3−reabsorption by the rabbit S2 renal proximal tubule

Effects of angiotensin II on the CO2dependence of HCO3−reabsorption by the rabbit S2 renal proximal tubule

Arginine feeding modifies cyclosporine nephrotoxicity in rats.

Modulation by locally produced luminal angiotensin II of proximal tubular sodium reabsorption via an AT1 receptor

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Effects of angiotensin II on the CO₂dependence of HCO₃⁻reabsorption by the rabbit S2 renal proximal tubule

Effects of angiotensin II on the CO₂dependence of HCO₃⁻reabsorption by the rabbit S2 renal proximal tubule

Modulation by locally produced luminal angiotensin II of proximal tubular sodium reabsorption via an AT₁ receptor