Effect of angiotensin-(1–7) on ATPase activities in several tissues

Ordieres, Marı́a Graciela López; Gironacci, Mariela M.; Arnaiz, Georgina Rodrı́guez de Lores; Peña, Clara

doi:10.1016/s0167-0115(98)00113-x

Cited by 30 publications

(15 citation statements)

References 21 publications

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“…Low concentrations of Ang-(1-7) (10 -12 M) stimulate, while higher concentrations (10 -8 M) inhibit fluid absorption [27]. It has been also demonstrated that Ang-(1-7) has similar biphasic effects on ATPase activity in rat kidney [28]. Moreover, it has been recently reported that Ang-(1-7) selectively modulates the Na + -ATPase activity present in basolateral membranes of renal proximal tubules through a different AT 1 receptor than that which in 'physiological' concentration is activated by ANG II [29].…”

Section: Discussionmentioning

confidence: 94%

Intrarenal Infusion of Angiotensin-(1–7) Modulates Renal Functional Responses to Exogenous Angiotensin II in the Rat

Bürgelová

Kramer

Teplan

et al. 2002

Kidney Blood Press Res

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In the present study we investigated the possible role of angiotensin-(1–7) [Ang-(1–7)] in modulating renal functional responses to intrarenal (i.e.) infusion of angiotensin II (ANG II) in normotensive anesthetized rats. ANG II (6 ng/min, n = 14) decreased glomerular filtration rate (GFR), renal plasma flow (RPF), absolute and fractional sodium excretion by –24 ± 5, –25 ± 6, –44 ± 6 and –28 ± 7%, respectively (p < 0.05). i.r. infusion of Ang-(1–7) (50 ng/min, n = 13) did not significantly alter GFR (+6 ± 4%) but reduced RPF by –19 ± 7% (p < 0.05). Ang-(1–7) increased absolute and fractional sodium excretion by +36 ± 6 and +37 ± 8%, respectively (p < 0.05). Infusion of Ang-(1–7) did not prevent the decreases in GFR and RPF but completely blunted the decreases in absolute (–2 ± 2%) and fractional sodium excretion (–4 ± 4%) induced by ANG II (n = 11). Blockade of the Ang-(1–7) receptor by [7-D-Ala]-Ang-(1–7) (5 µg/min, n = 11) significantly decreased GFR, RPF, absolute and fractional sodium excretion by –28 ± 7, –20 ± 5, –32 ± 7 and –24 ± 4%, respectively (p < 0.05), suggesting that the action of endogenous ANG II is unopposed by compensatory effect of endogenous Ang-(1–7). i.r. infusion of Ang-(1–7) (n = 10) did not alter the effect of Ang-(1–7) receptor blockade on RPF (–21 ± 6%) but blunted its effects on GFR (+4 ± 3%) and absolute (+7 ± 5%) and fractional (+6 ± 4%) urinary sodium excretion probably by displacing the receptor blocker. While exogenous ANG II during blockade of the Ang-(1–7) receptor and the AT₂ receptor (by PD 123319; 1 µg/min i.r., n = 9) resulted in the same decreases in absolute and fractional sodium excretion (–39 ± 8 and –38 ± 6%, respectively, p < 0.05) as did ANG II in the absence of Ang-(1–7) receptor blockade. These results suggest that in normotensive rats high i.r. Ang-(1–7) concentration attenuates the tubular, i.e. sodium reabsorptive effect, but not the vascular effect of exogenous i.r. ANG II. Results obtained during blockade of Ang-(1–7) and of AT₂ receptors imply that AT₂ receptors play a role in tubular sodium reabsorption in the presence of high ANG II concentration

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Section: Discussionmentioning

confidence: 94%

Intrarenal Infusion of Angiotensin-(1–7) Modulates Renal Functional Responses to Exogenous Angiotensin II in the Rat

Bürgelová

Kramer

Teplan

et al. 2002

Kidney Blood Press Res

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“…These effects were abolished by ouabain (De Mello 2004). Additionally, Ang-(1-7) decreased total (Na C , K C , Mg 2C )-ATPase activity in sheep atrium (Lopez Ordieres et al 1998). Also, the antiarrhythmogenic effect of Ang-(1-7) was blocked by the Ang-(1-7) antagonist A-779 and by the cyclooxygenase (COX) inhibitor indomethacin (Ferreira et al 2001).…”

Section: Figurementioning

confidence: 98%

“…In this context, Ang-(1-7) seems to limit transcellular sodium flux by modulating the activity of transporters via phospholipase A2 activation in tubular epithelial cells (Andreatta-van Leyen et al 1993). Moreover, this heptapeptide appears to be a potent inhibitor of Na C -K C -ATPase activity in the renal cortex and in isolated convoluted proximal tubules (Handa et al 1996, Lopez Ordieres et al 1998, Burgelova et al 2002, De Souza et al 2004, Dilauro & Burns 2009, Pinheiro & Simoes 2012. This inhibitory effect is reversed by the AT 2 receptor antagonist PD 123319 in a dose-dependent manner in the inner cortex basolateral membrane from pig kidney.…”

Section: Vascular Actions Of the Ace2/ang-(1-7)/mas Axismentioning

confidence: 99%

Angiotensin-converting enzyme 2, angiotensin-(1–7) and Mas: new players of the renin–angiotensin system

Santos

Ferreira

Verano‐Braga

et al. 2012

Journal of Endocrinology

439

369

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Angiotensin (Ang)-(1-7) is now recognized as a biologically active component of the reninangiotensin system (RAS). Ang-(1-7) appears to play a central role in the RAS because it exerts a vast array of actions, many of them opposite to those attributed to the main effector peptide of the RAS, Ang II. The discovery of the Ang-converting enzyme (ACE) homolog ACE2 brought to light an important metabolic pathway responsible for Ang-(1-7) synthesis. This enzyme can form Ang-(1-7) from Ang II or less efficiently through hydrolysis of Ang I to Ang-(1-9) with subsequent Ang-(1-7) formation by ACE. In addition, it is now well established that the G protein-coupled receptor Mas is a functional binding site for Ang-(1-7). Thus, the axis formed by ACE2/Ang-(1-7)/Mas appears to represent an endogenous counterregulatory pathway within the RAS, the actions of which are in opposition to the vasoconstrictor/ proliferative arm of the RAS consisting of ACE, Ang II, and AT 1 receptor. In this brief review, we will discuss recent findings related to the biological role of the ACE2/Ang-(1-7)/Mas arm in the cardiovascular and renal systems, as well as in metabolism. In addition, we will highlight the potential interactions of Ang-(1-7) and Mas with AT 1 and AT 2 receptors.

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“…7,18 Several studies indicated that Ang-(1-7) effects are tissuespecific, that is, the heptapeptide activates Na ϩ , K ϩ -ATPase in rat brain synaptosomal membranes, whereas a biphasic effect on this enzymatic system is observed in rat renal membranes. 19 Furthermore, Gironacci et al 8 have reported a facilitatory effect of the heptapeptide on the sympathetic neurotransmission in rat atria. Conversely, this stimulatory action was not detected in the rabbit vas deferens.…”

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confidence: 99%

Angiotensin-(1-7) Reduces Norepinephrine Release Through a Nitric Oxide Mechanism in Rat Hypothalamus

et al. 2000

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Abstract-Angiotensin (Ang)-(1-7) elicits a facilitatory presynaptic effect on peripheral noradrenergic neurotransmission, and because biological responses to the heptapeptide on occasion are tissue specific, the present investigation was undertaken to study its action on noradrenergic neurotransmission at the central level. In rat hypothalamus labeled with [ 3 H]-norepinephrine, 100 to 600 nmol/L Ang-(1-7) diminished norepinephrine released by 25 mmol/L KCl. This effect was blocked by the selective angiotensin type 2 receptor antagonist PD 123319 (1 mol/L) and by the specific Ang-(1-7) receptor antagonist ]Ang-(1-7) (1 mol/L) but not by losartan (10 nmol/L to 1 mol/L), a selective angiotensin type 1 receptor antagonist. The inhibitory effect on noradrenergic neurotransmission caused by Ang-(1-7) was prevented by 10 mol/L N -nitro-L-arginine methylester, an inhibitor of nitric oxide synthase activity, and was restored by 100 mol/L L-arginine, precursor of nitric oxide synthesis. Methylene blue (10 mol/L), an inhibitor of guanylate cyclase considered as the target of nitric oxide action, as well as Hoe 140 (10 mol/L), a bradykinin B 2 -receptor antagonist, prevented the inhibitory effect of the heptapeptide on neuronal norepinephrine release, whereas no modification was observed in the presence of 0.1 to 10 mol/L indomethacin, a cyclooxygenase inhibitor. Our results indicate that Ang-(1-7) has a tissue-specific neuromodulatory effect on noradrenergic neurotransmission, being inhibitory at the central nervous system by a nitric oxide-dependent mechanism that involves angiotensin type 2 receptors and local bradykinin production. Key Words: angiotensin Ⅲ norepinephrine Ⅲ nitric oxide Ⅲ angiotensin antagonist Ⅲ bradykinin Ⅲ prostaglandins A ngiotensin (Ang)-(1-7) is considered a bioactive end product of the renin-angiotensin system formed from Ang I metabolism through an enzymatic pathway independent of the angiotensin-converting enzyme. 1 It can be formed either from Ang I or Ang II by a prolyl-endopeptidase that cleaves the Pro-Phe bond. 1,2 Ferrario and coworkers 2 demonstrated the presence of Ang-(1-7) in several regions of the rat brain such as the hypothalamus, amygdala, and medulla oblongata but not in the cerebral cortex and cerebellum. In addition, type 1 (AT 1 ) and type 2 (AT 2 ) Ang receptors were described in several regions and nucleus of the central nervous system, including the hypothalamus. 3,4 Although Ang-(1-7) is not an agonist in terms of activating vasoconstriction, 5 stimulating thirst, 6 or promoting aldosterone secretion, 5 the heptapeptide causes neuronal excitation in the paraventricular nucleus of hypothalamus and dorsal vagal complex of the medulla oblongata, 7 facilitates the noradrenergic neurotransmission, 8 and stimulates prostaglandin 9 -11 and vasopressin release 12 with potency comparable to that of Ang II. Conversely, some of the effects of Ang-(1-7) are opposite to those elicited by Ang II, that is, it displays an antiproliferative action on vascular smooth muscle cells, 13 produ...

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Effect of angiotensin-(1–7) on ATPase activities in several tissues

Cited by 30 publications

References 21 publications

Intrarenal Infusion of Angiotensin-(1–7) Modulates Renal Functional Responses to Exogenous Angiotensin II in the Rat

Intrarenal Infusion of Angiotensin-(1–7) Modulates Renal Functional Responses to Exogenous Angiotensin II in the Rat

Angiotensin-converting enzyme 2, angiotensin-(1–7) and Mas: new players of the renin–angiotensin system

Angiotensin-(1-7) Reduces Norepinephrine Release Through a Nitric Oxide Mechanism in Rat Hypothalamus

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