Angiotensin-(1-7) increases osmotic water permeability in isolated toad skin

Santos, J C; Jerez, Susana; Bruno, María Peral de; Coviello, Alfredo

doi:10.1590/s0100-879x2000000900018

Cited by 10 publications

(6 citation statements)

References 25 publications

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“…Previous investigations have shown that Ang (1-7) serves a protective role by counteracting the effects of locally-generated Ang II in cardiovascular research [26] . In some cardiovascular diseases, the increased Ang (1-7) levels may serve some role in treatments with ACE inhibitors or AT1 receptor antagonists [19,20] . However, no studies have focused on the effects of Ang (1-7) treatment on diabetes.…”

Section: Discussionmentioning

confidence: 99%

Chronic angiotensin (17) injection accelerates STZ-induced diabetic renal injury¹

Shao

Zhou

et al. 2008

Acta Pharmacologica Sinica

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Aim: The renin-angiotensin system (RAS) plays a critical role in blood pressure control and body fluid and electrolyte homeostasis. In the past few years, angiotensin (Ang) (1-7) has been reported to counteract the effects of Ang II and was even considered as a new therapeutical target in RAS. The present study aimed to investigate the effect of Ang (1-7) administration on a diabetic animal model and the modulation on local RAS. Methods: Streptozotocin (STZ) injection-induced diabetic rats were used in the experiment. The animals were divided into 3 groups: (1) control; (2) STZ-induced diabetes; and (3) STZ-induced diabetes with chronic Ang (1-7) treatment [D+Ang (1-7)]. In the D+Ang(1-7) group, a dose of 25 µg·kg of Ang (1-7) was continually injected through the jugular vein by embedding miniosmotic pump for 6 weeks. Plasma glucose, ratio of kidney to body weight, and 24 h urine protein and serum creatinine were monitored by conventional measurement. Plasma and renal Ang II levels were measured by radioimmunoassay. Ang-converting enzyme (ACE), ACE2, Ang II type 1 (AT1) receptor, Ang II type 2 (AT2) receptor, Ang (1-7) Mas receptor, and TGF-β1 mRNA levels were measured by real time PCR; ACE, ACE2, and TGF-β1 protein levels were analyzed by Western blotting. Results:The renal function of diabetic rats was significantly retrogressed when compared with that of control rats. After the treatment by constant Ang (1-7) vein injection for 6 weeks, renal function was found to be even worse than diabetic rats, and both TGF-β1 mRNA and protein levels were elevated in the D+Ang(1-7) group compared with the diabetic rats. The real-time PCR result also showed an increase in ACE mRNA expression and decrease in ACE2 mRNA level in the D+Ang(1-7) group when compared with diabetic rats. The number of AT1 receptors increased in the Ang (1-7)-injected group, while the number of AT2 and Mas receptors decreased. Conclusion: Exogenous Ang (1-7) injection did not ameliorate STZinduced diabetic rat renal injury; on the contrary, it accelerated the progressive diabetic nephropathies.

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Section: Discussionmentioning

confidence: 99%

Chronic angiotensin (17) injection accelerates STZ-induced diabetic renal injury¹

Shao

Zhou

et al. 2008

Acta Pharmacologica Sinica

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“…Studies have shown that Ang-(1-7) participates in water and electrolyte homeostasis, specially by demonstrating that the kidney is an organ in which it is both formed [9,13,14,31,32] and acts [2,4,9,11,15,16,17,19,23,29,31,33,36,37,42]. The kidney is an important site for the synthesis of Ang-(1-7) since many renal enzymes can cleave Ang I and Ang II, including prolylendopeptidase, neutral endopeptidase 24:11 and metalloendopeptidase 24:15 [9,13,14,32,33,41].…”

Section: Introductionmentioning

confidence: 99%

“…Dense immunostaining for Ang-(1- 7) immunoreactivity has been demonstrated in areas related to osmoregulation, such as the supraoptic and paraventricular nuclei of the hypothalamus and neurohypophysis [5,8,22] and there is substantial evidence that Ang-(1-7) acts in various nephron segments [2,9,11,15,16,17,19,23,29,31,33,36,37,42] with variable effects on Na + and water excretion [2,9,11,15,17,23,29,31,33,37,42]. Handa et al have reported an increase in Na + and water excretion after intrarenal injection of Ang- (1)(2)(3)(4)(5)(6)(7) in Na + -replete, anaesthetized male Wistar rats with denervated kidneys [16,17].…”

Section: Introductionmentioning

confidence: 99%

Angiotensin-(1–7) stimulates water transport in rat inner medullary collecting duct: evidence for involvement of vasopressin V2 receptors

Magaldi

Cesar

Araújo

et al. 2003

Pflugers Arch - Eur J Physiol

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The peptide angiotensin-(1-7) [Ang-(1-7)] is known to enhance water transport in rat inner medullary collecting duct (IMCD). The aim of this study was to determine the mechanism of the Ang-(1-7) effect on osmotic water permeability (Pf). Pf was measured in the normal rat IMCD perfused in vitro in presence of agonists [Ang-(1-7), arginine vasopressin (AVP) and Ang-(3-8)], and antagonists of the angiotensin and the vasopressin cascade. Ang-(1-7), but not Ang-(3-8), increased Pf significantly. The effect of Ang-(1-7) on Pf was abolished by its selective antagonist, A-779, added before or after Ang-(1-7). Prostaglandin E2 and the protein kinase A inhibitor H8 also blocked the Ang-(1-7) effect. Blockade of vasopressin V1 receptors by antagonists did not change the Ang-(1-7) effect, but pre-treatment with a V2 antagonist abolished the effect of Ang-(1-7) on Pf. Similarly, pre-treatment with A-779 inhibited AVP's effect on Pf. Forskolin-stimulated Pf was blocked both by A-779 and by the V2 antagonist. Finally, Ang-(1-7) increased cAMP levels in fresh IMCD cell suspensions whilst the forskolin-stimulated cAMP synthesis was decreased by A-779 and the V2 antagonist. These data provide evidence that Ang-(1-7) interacts via its receptor with the AVP V2 system through a mechanism involving adenylate-cyclase activation.

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“…Contrasting with the data obtained for mammals, Santos et al 32 reported that the stimulatory effect of Ang-(1-7) on water transport in the frog skin was not blocked by A-779 or losartan but was completely abolished by PD 123,319. On the other hand, the effect of Ang II was blocked by losartan.…”

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

confidence: 75%

“…On the other hand, other reports also pointed out for a major role of this angiotensin in water transport. [32][33][34][35] Despite the existence of considerable evidence for a specific renal receptor for Ang-(1-7), some of the actions of this heptapeptide are completely blocked by AT 1 receptor antagonists. 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.…”

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

confidence: 99%

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

Santos

Passaglio²,

Pesquero³

et al. 2001

Hypertension

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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...

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Angiotensin-(1-7) increases osmotic water permeability in isolated toad skin

Cited by 10 publications

References 25 publications

Chronic angiotensin (17) injection accelerates STZ-induced diabetic renal injury¹

Chronic angiotensin (17) injection accelerates STZ-induced diabetic renal injury¹

Angiotensin-(1–7) stimulates water transport in rat inner medullary collecting duct: evidence for involvement of vasopressin V2 receptors

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

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Angiotensin-(1-7) increases osmotic water permeability in isolated toad skin

Cited by 10 publications

References 25 publications

Chronic angiotensin (17) injection accelerates STZ-induced diabetic renal injury1

Chronic angiotensin (17) injection accelerates STZ-induced diabetic renal injury1

Angiotensin-(1–7) stimulates water transport in rat inner medullary collecting duct: evidence for involvement of vasopressin V2 receptors

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

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Chronic angiotensin (17) injection accelerates STZ-induced diabetic renal injury¹

Chronic angiotensin (17) injection accelerates STZ-induced diabetic renal injury¹