Endogenous production of angiotensin II modulates rat proximal tubule transport.

Quan, Albert; Baum, Michel

doi:10.1172/jci118745

Cited by 105 publications

(110 citation statements)

References 27 publications

(43 reference statements)

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“…The mechanism for this increase in fractional fluid reabsorption in proximal tubules of ACE 2/2 mice was not explored in this study, but it is likely that it is related in some way to the reduced SNGFR. Our observations are unexpected in view of previous demonstrations that the intratubular administration of converting enzyme inhibitors caused a marked reduction in proximal fluid reabsorption (30) and that the same effect was seen with angiotensin II receptor blockers (31). These findings clearly show that an acute reduction in local angiotensin II formation and action can exert a profound inhibitory effect on fluid reabsorption.…”

Section: Discussioncontrasting

confidence: 76%

Micropuncture determination of nephron function in mice without tissue angiotensin-converting enzyme

Hashimoto¹,

Adams²,

Bernstein³

et al. 2005

American Journal of Physiology-Renal Physiology

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Section: Discussioncontrasting

confidence: 76%

Micropuncture determination of nephron function in mice without tissue angiotensin-converting enzyme

Hashimoto¹,

Adams²,

Bernstein³

et al. 2005

American Journal of Physiology-Renal Physiology

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“…Furthermore, immunolocalisation of the AT1 receptor also strongly suggests that Ang II has a widespread role in maintenance of epithelial structure and function (Vinson et al, 1995. Such functions may include the regulation of water and electrolyte transport (Vinson et al, 1995;Quan and Baum, 1996) as well as mitosis and tissue differentiation (Bedecs et al, 1997;Li et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Localisation of renin-angiotensin system (RAS) components in breast

et al. 2006

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Angiotensin II has mitogenic and angiogenic effects and its receptors are widespread, particularly in epithelial tissue. Tissue renin angiotensin systems (tRASs) may be a local source of angiotensin II that has specific paracrine functions. To investigate the presence of a tRAS in normal human breast and tumours. Immunocytochemistry, and quantitative RT -PCR was used to establish: (i) the presence and localisation of RAS components, (ii) the possibility of their involvement in cancer. (1) mRNA coding for angiotensinogen, prorenin, angiotensin converting enzyme (ACE), and both AT1 and AT2 receptors was demonstrated in normal and diseased breast tissues. (2) (pro)renin was identified in epithelial cells in both normal and diseased tissue, but in invasive carcinoma, its distribution was mostly confined to fibroblasts or could not be detected at all. (3) Angiotensin converting enzyme was shown in epithelial cells in both normal and malignant tissue. The results are consistent with the hypothesis that a tRAS is present in the breast, and is disrupted in invasive cancer.

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“…Indeed, picomolar concentrations of systemic angiotensin II stimulate proximal tubule transport (24); in addition, endogenously produced angiotensin II also stimulates proximal fluid reabsorption in vivo, an effect that is blunted when losartan is added to the luminal fluid (33). Furthermore, in this segment, basolateral and apical angiotensin II receptors are not coupled to the same transduction pathways because, in the proximal tubule brush-border membrane, angiotensin II does not activate PLC activity but activates PLA 2 independently of the presence of calcium.…”

Section: Discussionmentioning

confidence: 99%

“…intratubular angiotensin II concentration that stimulates proximal sodium reabsorption (33). In the more distal part of the nephron, angiotensin II also directly stimulates sodium reabsorption by activating Na ϩ /H ϩ exchange and the amiloridesensitive Na ϩ channel (2,23,37).…”

mentioning

confidence: 99%

Angiotensin II inhibits NaCl absorption in the rat medullary thick ascending limb

Lerolle¹,

Leviel²,

Lebrun³

et al. 2004

American Journal of Physiology-Renal Physiology

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in the medullary thick ascending limb of Henle (MTALH) contributes to NaCl balance and is also responsible for the creation of medullary interstitial hypertonicity. Despite the presence of angiotensin II subtype 1 (AT1) receptors in both the luminal and the basolateral plasma membranes of MTALH cells, no information is available on the effect of angiotensin II on NaCl reabsorption in MTALH and, furthermore, on angiotensin II-dependent medullary interstitial osmolality. MTALHs from male Sprague-Dawley rats were isolated and microperfused in vitro; transepithelial net chloride absorption (JCl) as well as transepithelial voltage (V te) were measured. Luminal or peritubular 10 Ϫ11 and 10 Ϫ10 M angiotensin II had no effect on JCl or V te. However, 10 Ϫ8 M luminal or peritubular angiotensin II reversibly decreased both J Cl and Vte. The effect of both luminal and peritubular angiotensin II was prevented by the presence of losartan (10 Ϫ6 M). By contrast, PD-23319, an AT 2-receptor antagonist, did not alter the inhibitory effect of 10 Ϫ8 M angiotensin II. Finally, no additive effect of luminal and peritubular angiotensin II was observed. We conclude that both luminal and peritubular angiotensin II inhibit NaCl absorption in the MTALH via AT1 receptors. Because of intrarenal angiotensin II synthesis, angiotensin II concentration in medullary tubular and interstitial fluids may be similar in vivo to the concentration that displays an inhibitory effect on NaCl reabsorption under the present experimental conditions. in vitro microperfusion; renal tubule; NaCl transport; angiotensin II subtype 1; losartan ANGIOTENSIN II IS A POTENT regulator of extracellular fluid volume, mainly through its direct effects on renal tubular sodium reabsorption, as well as on aldosterone synthesis. Acute systemic infusion of low-dose angiotensin II stimulates overall tubular sodium reabsorption and decreases urine sodium excretion, independently of changes in renal or systemic hemodynamics (5, 15). In rat experiments using in vivo superficial tubule microperfusion, systemic angiotensin II infusion at 20 ng⅐kg Ϫ1 ⅐min Ϫ1 , which achieves a subpressor, physiological plasma concentration (picomolar range), stimulates proximal water and NaCl reabsorption (24). Conversely, saralazin infusion, which suppresses endogenous angiotensin II activity, inhibits proximal tubule absorption (24). In addition, endogenously produced angiotensin II is responsible for a nanomolar intratubular angiotensin II concentration that stimulates proximal sodium reabsorption (33). In the more distal part of the nephron, angiotensin II also directly stimulates sodium reabsorption by activating Na ϩ /H ϩ exchange and the amiloridesensitive Na ϩ channel (2, 23, 37). Finally, angiotensin II stimulates aldosterone synthesis and thereby indirectly enhances sodium reabsorption via the epithelial sodium channel in the cortical collecting duct (26) and likely via the thiazidesensitive sodium-chloride cotransporter in the distal convoluted tubule (21).In the loop of Henle, available...

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Endogenous production of angiotensin II modulates rat proximal tubule transport.

Cited by 105 publications

References 27 publications

Micropuncture determination of nephron function in mice without tissue angiotensin-converting enzyme

Micropuncture determination of nephron function in mice without tissue angiotensin-converting enzyme

Localisation of renin-angiotensin system (RAS) components in breast

Angiotensin II inhibits NaCl absorption in the rat medullary thick ascending limb

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