Angiotensin-(1–7) modulates the ouabain-insensitive Na+-ATPase activity from basolateral membrane of the proximal tubule

Caruso-Neves, Celso; Lara, Lucienne S.; Rangel, L.B.A.; Grossi, A; Lopes, Anibal Gil

doi:10.1016/s0005-2736(00)00219-4

Cited by 44 publications

(39 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This effect was abolished by AT 4 -receptor blockade. In contrast, CarusoNeves et al 37 showed that in pig kidney proximal tubules, Ang-(1-7) did not change Na ϩ ,K ϩ -ATPase activity. In this preparation, Ang-(1-7) selectively modulates Na ϩ -ATPase activity through a losartan-sensitive receptor.…”

Section: Interactions Of Ang-(1-7) With Ang II In the Kidneymentioning

confidence: 88%

“…For instance, the biphasic effect of Ang-(1-7) on straight proximal tubules 36 and the antidiuresis produced in water-loaded rats 35 are completely blocked by losartan. Recently, Caruso-Neves et al 37 found that Ang-(1-7) stimulated Na ϩ -ATPase activity in pig kidney proximal tubules, and this effect was abolished by losartan but not by A-779 or the AT 2 receptor antagonist PD 123,319. This stimulatory action of Ang-(1-7) was similar to the effect of Ang II alone.…”

Section: Interactions Of Ang-(1-7) With Ang II In the Kidneymentioning

confidence: 98%

“…However, when the 2 angiotensin peptides were both present, Na ϩ -ATPase activity was restored to control values, suggesting that Ang-(1-7) modulates Na ϩ -ATPase activity through a losartan-sensitive receptor that is probably different from the receptor involved in the Ang II effect. 37 These findings raised at least 2 possibilities: (1) Ang-(1-7) may act through AT 1 receptors, or more likely, (2) losartan can block a subtype of Ang-(1-7) receptor, an AT 1 -like receptor. 1 The first explanation is unlikely because Ang-(1-7) does not exert most of the actions of Ang II mediated through AT 1 receptors such as vasoconstriction 1 and Ang-(1-7) binds poorly to AT 1 receptors.…”

Section: Interactions Of Ang-(1-7) With Ang II In the Kidneymentioning

confidence: 99%

See 2 more Smart Citations

Interactions Between Angiotensin-(1-7), Kinins, and Angiotensin II in Kidney and Blood Vessels

Santos

Passaglio²,

Pesquero³

et al. 2001

Hypertension

View full text Add to dashboard Cite

Abstract-The heptapeptide angiotensin (Ang)-(1-7) is currently considered one of the biologically active end products of the renin-angiotensin system. The formation of Ang-(1-7) by pathways independent of Ang II generation, the selectivity of its actions, and its peculiar property of exhibiting effects that are partially opposite of those of the parent compound, Ang II, confer a unique biochemical and functional profile to this peptide. In this article, we will review novel aspects of the biological actions of Ang-(1-7), dealing with its interaction with Ang II and kinins, especially in the kidney and blood vessels. Key Words: bradykinin Ⅲ renin-angiotensin system Ⅲ receptors, angiotensin T he heptapeptide angiotensin (Ang)-(1-7) is formed from Ang I and Ang II by tissue peptidases, including neutral endopeptidase (neprilysin), thimet oligopeptidase, prolylcarboxypeptidase, and prolyl-endopeptidase. 1 In addition, the possibility should be considered that at least in the kidney and heart, Ang-(1-7) could be formed from Ang I or Ang II by a pathway involving the ACE-related enzyme ACE2 2,3 ( Figure 1). Once formed, Ang-(1-7) is rapidly hydrolyzed, especially by ACE. 4 Therefore, in the presence of ACE inhibition, the levels of Ang-(1-7), which circulates in blood at concentrations close to those of Ang II, raises several-fold, 5 probably owing to both the increase in Ang I concentration and the decrease in Ang-(1-7) breakdown. The related observation that Ang-(1-7) can increase following long-term administration of angiotensin type 1 (AT 1 ) receptor blockers 1 raises the possibility that Ang-(1-7) contributes to the pharmacological effects of both ACE inhibitors and AT 1 receptor antagonists. Interactions between Ang-(1-7) and Kinins in Blood VesselsMost of the interactions between Ang-(1-7) and bradykinin (BK) have been reported to occur in blood vessels. 1,6 -11 There are 2 major types of interaction: potentiation of BK by Ang-(1-7) and mediation of the vascular actions of Ang-(1-7) by kinins, although the latter does not exclude the former. Potentiation of BK by Ang-(1-7) has been observed in conscious normotensive and hypertensive rats in terms of the BK hypotensive effect in the whole animal 1,6 or the vasodilating action of BK in rat mesenteric microvessels in situ. 1,7 Brosnihan and colleagues 8,9 have shown that preincubation of isolated dog coronary arteries with Ang-(1-7) increased the relaxation produced by BK. Similarly, Almeida et al 10 have shown that Ang-(1-7) at 2 nmol/L concentration increased the vasodilation produced by BK in isolated rat hearts. Interestingly, the venoconstriction produced by BK in rabbit endothelium denuded femoral vein was also potentiated by Ang-(1-7), 11 indicating that the BK potentiating activity of Ang- (1-7) is not an exclusively endothelium-dependent phenomenon. Potentiation of bradykinin by Ang-(1-7) has also been described in other preparations. In Chinese hamster ovary cells co-transfected with the human cDNA for BK-B 2 receptors and ACE, Deddish et al 12 descri...

show abstract

Section: Interactions Of Ang-(1-7) With Ang II In the Kidneymentioning

confidence: 88%

Section: Interactions Of Ang-(1-7) With Ang II In the Kidneymentioning

confidence: 98%

Section: Interactions Of Ang-(1-7) With Ang II In the Kidneymentioning

confidence: 99%

See 1 more Smart Citation

Interactions Between Angiotensin-(1-7), Kinins, and Angiotensin II in Kidney and Blood Vessels

Santos

Passaglio²,

Pesquero³

et al. 2001

Hypertension

View full text Add to dashboard Cite

show abstract

“…When Ang 1-7 and A779 were used at equimolar doses, Ang 1-7 antagonist failed to block Ang 1-7-induced depressor response against AT1R blockade; suggesting that Ang 1-7 may act via the AT2R (43). Therefore, there is a complex interaction between RAS receptors (4, 6), and some actions of Ang 1-7 may also be blocked by AT1R (1,5) or AT2R antagonists (9); suggesting a crosstalk between the MasR and Ang II receptors (20). Other data indicated that the antidiuretic effect of AVE0991 that mimics the effects of Ang 1-7 was completely blocked by PD123319 and partially blocked by losartan (43).…”

Section: Discussionmentioning

confidence: 99%

Role of Mas receptor antagonist (A779) in renal hemodynamics in condition of blocked angiotensin II receptors in rats

Mansoori

Oryan

Nematbakhsh

2016

Acta Physiologica Hungarica

View full text Add to dashboard Cite

The vasodilatory effect of angiotensin 1–7 (Ang 1-7) is exerted in the vascular bed via Mas receptor (MasR) gender dependently. However, the crosstalk between MasR and angiotensin II (Ang II) types 1 and 2 receptors (AT1R and AT2R) may change some actions of Ang 1-7 in renal circulation. In this study by blocking AT1R and AT2R, the role of MasR in kidney hemodynamics was described. In anaesthetized male and female Wistar rats, the effects of saline as vehicle and MasR blockade (A779) were tested on mean arterial pressure (MAP), renal perfusion pressure (RPP), renal blood flow (RBF), and renal vascular resistance (RVR) when both AT1R and AT2R were blocked by losartan and PD123319, respectively. In male rats, when AT1R and AT2R were blocked, there was a tendency for the increase in RBF/wet kidney tissue weight (RBF/KW) to be elevated by A779 as compared with the vehicle (P=0.08), and this was not the case in female rats. The impact of MasR on renal hemodynamics appears not to be sexual dimorphism either when Ang II receptors were blocked. It seems that co-blockade of all AT1R, AT2R, and MasR may alter RBF/ KW in male more than in female rats. These findings support a crosstalk between MasR and Ang II receptors in renal circulation.

show abstract

“…In rabbit proximal tubular cells, ANG-(1-7) inhibits sodium reabsorption by activating phospholipase A2 [184]. In addition, in isolated basolateral membranes of kidney proximal tubules [175,185], ANG-(1-7) modulated the activity of Na + /K + -ATPase, and in isolated pig kidney inner cortical membranes [186], it inhibited Na + -ATPase activity via an effect that was reversed by an AT2 receptor antagonist. Furthermore, in isolated proximal tubules, i) ANG-(1-7) stimulated the release of arachidonic acid [184], and ii) the inhibition of prostaglandin release that resulted from COX inhibition attenuated the ANG-(1-7)-induced increase in urine flow and sodium excretion [187].…”

Section: Actions Of Ang-(1-7) In the Kidneymentioning

confidence: 99%

ANG II, ANG-(1-7), ALDO and AVP biphasic effects on Na+/H+ transport: the role of cellular calcium

Mello-Aires¹,

Dellova²,

Castelo‐Branco³

et al. 2017

Nephrol Renal Dis

View full text Add to dashboard Cite

This article reviews the main body of knowledge regarding NHE1 and NHE3 exchangers and their interaction with Angiotensin II, Angiotensin-(1-7), Aldosterone and Arginine Vasopressin, particularly their renal actions. This work addresses the biphasic effects of different hormonal doses on NHE1 or NHE3 in proximal tubule in Wistar, SHR (hypertensives) and their control WKY (normotensives) rats or MDCK cells (which share similarities with the collecting duct). The hormones were applied alone, with their inhibitors or plus agents that change the [Ca 2+ ]i. The data are compatible with hormonal stimulation of these exchangers by increases of [Ca 2+ ]i in lower range, and inhibition at high [Ca 2+ ]i. In MDCK cells and Wistar rats, low doses of ANG II, ALDO or AVP stimulated the exchangers, while high doses inhibited them. ANG-(1-7), in Wistar or WKY rats has inverse, dose-dependent effects. In SHR rats, the biphasic effects of ANG-(1-7) were similar to the effects of ANG II, ALDO or AVP in Wistar rats. The interactions between these effects may represent a mechanism that regulates extracellular volume. In hypertensives animals, a high plasma level of ANG-(1-7) inhibited NHE3 in the proximal tubule, which mitigated hypertension. Figure 6 shows a schematic model to describe these biphasic hormonal effects.

show abstract

Angiotensin-(1–7) modulates the ouabain-insensitive Na+-ATPase activity from basolateral membrane of the proximal tubule

Cited by 44 publications

References 26 publications

Interactions Between Angiotensin-(1-7), Kinins, and Angiotensin II in Kidney and Blood Vessels

Interactions Between Angiotensin-(1-7), Kinins, and Angiotensin II in Kidney and Blood Vessels

Role of Mas receptor antagonist (A779) in renal hemodynamics in condition of blocked angiotensin II receptors in rats

ANG II, ANG-(1-7), ALDO and AVP biphasic effects on Na+/H+ transport: the role of cellular calcium

Contact Info

Product

Resources

About