Angiotensin-(1-7) potentiates the coronary vasodilatatory effect of bradykinin in the isolated rat heart
Rev. bras. pesqui. méd. biol
; Braz. j. med. biol. res;33(6): 709-13, Jun. 2000. graf
Article
de En
| LILACS
| ID: lil-262039
Bibliothèque responsable:
BR1.1
ABSTRACT
It has been shown that angiotensin-(1-7) (Ang-(1-7)) infusion potentiates the bradykinin (BK)-induced hypotensive response in conscious rats. The present study was conducted to identify Ang-(1-7)-BK interactions in the isolated rat heart perfused according to the Langendorff technique. Hearts were excised and perfused through the aortic stump under a constant flow with Krebs-Ringer solution and the changes in perfusion pressure and heart contractile force were recorded. Bolus injections of BK (2.5, 5, 10 and 20 ng) produced a dose-dependent hypotensive effect. Ang-(1-7) added to the perfusion solution (2 ng/ml) did not change the perfusion pressure or the contractile force but doubled the hypotensive effect of the lower doses of BK. The BK-potentiating Ang-(1-7) activity was blocked by pretreatment with indomethacin (5 mg/kg, ip) or L-NAME (30 mg/kg, ip). The Ang-(1-7) antagonist A-779 (50 ng/ml in Krebs-Ringer) completely blocked the effect of Ang-(1-7) on BK-induced vasodilation. These data suggest that the potentiation of the BK-induced vasodilation by Ang-(1-7) can be attributed to the release of nitric oxide and vasodilator prostaglandins through an Ang-(1-7) receptor-mediated mechanism.
Texte intégral:
1
Indice:
LILACS
Sujet Principal:
Vasodilatateurs
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Angiotensine-I
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Bradykinine
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Vaisseaux coronaires
Limites du sujet:
Animals
langue:
En
Texte intégral:
Braz. j. med. biol. res
/
Rev. bras. pesqui. méd. biol
Thème du journal:
BIOLOGIA
/
MEDICINA
Année:
2000
Type:
Article
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Congress and conference