Pressor and renal hemodynamic effects of the novel angiotensin A peptide are angiotensin II type 1A receptor dependent
Recently, a new derivative of angiotensin (Ang) II, called "Ang A," has been discovered to be present in plasma of healthy humans and, in increased concentrations, in end-stage renal failure patients. The objectives of the study were to investigate the blood pressure and renal hemodynamic...
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| Vydáno v: | Hypertension (Dallas, Tex. 1979) Ročník 57; číslo 5; s. 956 |
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| Hlavní autoři: | , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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United States
01.05.2011
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| ISSN: | 1524-4563, 1524-4563 |
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| Abstract | Recently, a new derivative of angiotensin (Ang) II, called "Ang A," has been discovered to be present in plasma of healthy humans and, in increased concentrations, in end-stage renal failure patients. The objectives of the study were to investigate the blood pressure and renal hemodynamic responses to Ang A in normotensive and hypertensive rats and in genetically modified mice and the binding properties of Ang A to Ang II type 1 (AT(1)) or Ang II type 2 (AT(2)) receptors. Intravenous and intrarenal administration of Ang A induced dose-dependent pressor and renal vasoconstrictor responses in normotensive rats, which were blocked by the AT(1) receptor antagonist candesartan but were not altered by the AT(2) receptor ligands PD123319, CGP42112A, or compound 21. Similar responses were observed after intravenous administration in spontaneously hypertensive rats. Deletion of AT(1a) receptors in mice almost completely abolished the pressor and renal vasoconstrictor responses to Ang A, indicating that its effects are mediated via AT(1a) receptors. Ang A was less potent than Ang II in vivo. The in vitro study demonstrated that Ang A is a full agonist for AT(1) receptors, with similar affinity for AT(1) and AT(2) receptors as Ang II. Overall, the responses to Ang A and Ang II were similar. Ang A has no physiological role to modulate the pressor and renal hemodynamic effects of Ang II. |
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| AbstractList | Recently, a new derivative of angiotensin (Ang) II, called "Ang A," has been discovered to be present in plasma of healthy humans and, in increased concentrations, in end-stage renal failure patients. The objectives of the study were to investigate the blood pressure and renal hemodynamic responses to Ang A in normotensive and hypertensive rats and in genetically modified mice and the binding properties of Ang A to Ang II type 1 (AT(1)) or Ang II type 2 (AT(2)) receptors. Intravenous and intrarenal administration of Ang A induced dose-dependent pressor and renal vasoconstrictor responses in normotensive rats, which were blocked by the AT(1) receptor antagonist candesartan but were not altered by the AT(2) receptor ligands PD123319, CGP42112A, or compound 21. Similar responses were observed after intravenous administration in spontaneously hypertensive rats. Deletion of AT(1a) receptors in mice almost completely abolished the pressor and renal vasoconstrictor responses to Ang A, indicating that its effects are mediated via AT(1a) receptors. Ang A was less potent than Ang II in vivo. The in vitro study demonstrated that Ang A is a full agonist for AT(1) receptors, with similar affinity for AT(1) and AT(2) receptors as Ang II. Overall, the responses to Ang A and Ang II were similar. Ang A has no physiological role to modulate the pressor and renal hemodynamic effects of Ang II.Recently, a new derivative of angiotensin (Ang) II, called "Ang A," has been discovered to be present in plasma of healthy humans and, in increased concentrations, in end-stage renal failure patients. The objectives of the study were to investigate the blood pressure and renal hemodynamic responses to Ang A in normotensive and hypertensive rats and in genetically modified mice and the binding properties of Ang A to Ang II type 1 (AT(1)) or Ang II type 2 (AT(2)) receptors. Intravenous and intrarenal administration of Ang A induced dose-dependent pressor and renal vasoconstrictor responses in normotensive rats, which were blocked by the AT(1) receptor antagonist candesartan but were not altered by the AT(2) receptor ligands PD123319, CGP42112A, or compound 21. Similar responses were observed after intravenous administration in spontaneously hypertensive rats. Deletion of AT(1a) receptors in mice almost completely abolished the pressor and renal vasoconstrictor responses to Ang A, indicating that its effects are mediated via AT(1a) receptors. Ang A was less potent than Ang II in vivo. The in vitro study demonstrated that Ang A is a full agonist for AT(1) receptors, with similar affinity for AT(1) and AT(2) receptors as Ang II. Overall, the responses to Ang A and Ang II were similar. Ang A has no physiological role to modulate the pressor and renal hemodynamic effects of Ang II. Recently, a new derivative of angiotensin (Ang) II, called "Ang A," has been discovered to be present in plasma of healthy humans and, in increased concentrations, in end-stage renal failure patients. The objectives of the study were to investigate the blood pressure and renal hemodynamic responses to Ang A in normotensive and hypertensive rats and in genetically modified mice and the binding properties of Ang A to Ang II type 1 (AT(1)) or Ang II type 2 (AT(2)) receptors. Intravenous and intrarenal administration of Ang A induced dose-dependent pressor and renal vasoconstrictor responses in normotensive rats, which were blocked by the AT(1) receptor antagonist candesartan but were not altered by the AT(2) receptor ligands PD123319, CGP42112A, or compound 21. Similar responses were observed after intravenous administration in spontaneously hypertensive rats. Deletion of AT(1a) receptors in mice almost completely abolished the pressor and renal vasoconstrictor responses to Ang A, indicating that its effects are mediated via AT(1a) receptors. Ang A was less potent than Ang II in vivo. The in vitro study demonstrated that Ang A is a full agonist for AT(1) receptors, with similar affinity for AT(1) and AT(2) receptors as Ang II. Overall, the responses to Ang A and Ang II were similar. Ang A has no physiological role to modulate the pressor and renal hemodynamic effects of Ang II. |
| Author | Walther, Thomas Dupont, Alain G Chai, Siew Yeen Albiston, Anthony L Vauquelin, Georges Tourwé, Dirk Smolders, Ilse Vanderheyden, Patrick Demaegdt, Heidi Van Eeckhaut, Ann Yang, Rui Nahmias, Clara Lukaszuk, Aneta |
| Author_xml | – sequence: 1 givenname: Rui surname: Yang fullname: Yang, Rui organization: Department of Pharmacology, Vrije Universiteit Brussel, Laarbeeklaan 103, B-1090 Brussels, Belgium – sequence: 2 givenname: Ilse surname: Smolders fullname: Smolders, Ilse – sequence: 3 givenname: Patrick surname: Vanderheyden fullname: Vanderheyden, Patrick – sequence: 4 givenname: Heidi surname: Demaegdt fullname: Demaegdt, Heidi – sequence: 5 givenname: Ann surname: Van Eeckhaut fullname: Van Eeckhaut, Ann – sequence: 6 givenname: Georges surname: Vauquelin fullname: Vauquelin, Georges – sequence: 7 givenname: Aneta surname: Lukaszuk fullname: Lukaszuk, Aneta – sequence: 8 givenname: Dirk surname: Tourwé fullname: Tourwé, Dirk – sequence: 9 givenname: Siew Yeen surname: Chai fullname: Chai, Siew Yeen – sequence: 10 givenname: Anthony L surname: Albiston fullname: Albiston, Anthony L – sequence: 11 givenname: Clara surname: Nahmias fullname: Nahmias, Clara – sequence: 12 givenname: Thomas surname: Walther fullname: Walther, Thomas – sequence: 13 givenname: Alain G surname: Dupont fullname: Dupont, Alain G |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21464395$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Angiotensin II Type 1 Receptor Blockers - pharmacology Angiotensins - metabolism Angiotensins - pharmacology Animals Benzimidazoles - pharmacology Blood Pressure - drug effects Blood Pressure - physiology Dose-Response Relationship, Drug Hypertension - metabolism Kidney - drug effects Kidney - metabolism Male Mice Mice, Knockout Rats Rats, Inbred SHR Rats, Inbred WKY Receptor, Angiotensin, Type 1 - genetics Receptor, Angiotensin, Type 1 - metabolism Renal Circulation - drug effects Renal Circulation - physiology Statistics, Nonparametric Tetrazoles - pharmacology Vasoconstriction - drug effects Vasoconstriction - physiology |
| Title | Pressor and renal hemodynamic effects of the novel angiotensin A peptide are angiotensin II type 1A receptor dependent |
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