The potentiation of cardiodepressant and hypotensive effects of bradykinin by enalapril and captopril both in vitro and in vivo

Prostran, Milica; Samardzić, R; Todorović, Zoran; Jovanović-Mićić, D; Japundžić, Nina; Beleslin, Branko

doi:10.1016/0306-3623(91)90567-p

Cited by 7 publications

(1 citation statement)

References 6 publications

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“…Whereas bradykinin can increase heart rate through sympathoexcitatory reflexes (Veelken et al, 1996) and through local effects on norepinephrine release (Seyedi et al, 1997), bradykinin induces a negative chronotropic effect through intrinsic cardiac cholinergic neurons in the isolated rabbit heart (Izrailtyan and Kresh, 1997) and via a direct effect on the sinus node in ganglion-blocked dogs (Ribuot et al, 1993). Bradykinin also causes bradycardia in anesthetized cats (Prostran et al, 1991) and in hypovolemic rats (Gardiner and Bennett, 1992). Genetic disruption of the B 2 receptor has been reported to increase heart rate in some studies (Emanueli et al, 1999) but not in others (Milia et al, 2001).…”

Section: Tablementioning

confidence: 99%

Bradykinin B₂ Receptor Does Not Contribute to Blood Pressure Lowering during AT₁ Receptor Blockade

Lefèbvre

Shintani²,

Gebretsadik³

et al. 2006

J Pharmacol Exp Ther

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This study tested the hypothesis that endogenous bradykinin contributes to the effects of angiotensin AT 1 receptor blockade in humans. The effect of the bradykinin B 2 receptor antagonist D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Tic-Oic-Arg (HOE-140) (18 g/kg/h i.v. for 6 h) on hemodynamic and endocrine responses to acute and chronic (1-month) treatment with valsartan (160 mg/day) was determined in 13 normotensive and 12 hypertensive salt-deplete subjects. Acute valsartan increased plasma renin activity (PRA) from 5.3 Ϯ 9.9 to 15.6 Ϯ 19.8 ng of angiotensin (Ang) I/ml/h (P Ͻ 0.001) and decreased aldosterone from 18.3 Ϯ 10.5 to 12.0 Ϯ 9.6 ng/dl (P Ͻ 0.001). Chronic valsartan significantly increased baseline PRA (10.5 Ϯ 15.5 ng of Ang I/ml/h; P ϭ 0.004) but did not affect baseline angiotensinconverting enzyme activity or aldosterone. HOE-140 tended to increase the PRA response to valsartan, and it attenuated the decrease in aldosterone following chronic valsartan (P ϭ 0.03). Acute valsartan decreased mean arterial pressure 12.7 Ϯ 6.9% (from 100.2 Ϯ 8.4 to 87.5 Ϯ 9.8 mm Hg in hypertensives and from 82.4 Ϯ 8.6 to 70.3 Ϯ 8.4 mm Hg in normotensives). HOE-140 did not affect the blood pressure response to either acute (effect of valsartan, P Ͻ 0.001; effect of HOE-140, P ϭ 0.98) or chronic (valsartan, P ϭ 0.01; HOE-140, P ϭ 0.84) valsartan. Plasma cGMP was increased significantly during chronic valsartan (P ϭ 0.048) through a bradykinin receptorindependent mechanism (effect of HOE-140, P ϭ 0.13). Both acute (P Ͻ 0.001) and chronic (P Ͻ 0.001) valsartan increased heart rate. HOE-140 augmented the heart rate response to chronic valsartan (P ϭ 0.04). These data suggest that endogenous bradykinin does not contribute significantly to the blood pressure-lowering effect of valsartan through its B 2 receptor.The availability of the specific bradykinin B 2 receptor antagonist D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Tic-Oic-Arg (HOE-140) as well as the combined B 1 and B 2 antagonist D-Arg-Arg-ProHyp-Gly-Thi-Ser-D-Igl-Oic-Arg (B9340) has allowed investigators to determine the contribution of endogenous bradykinin to the effects of angiotensin-converting enzyme (ACE) inhibitors in animals and humans. For example, Gainer et al. (1998) demonstrated that coadministration of HOE-140 attenuated the hemodynamic and endocrine effects of acute ACE inhibition in normotensive subjects and hypertensive subjects of both African-American and Caucasian race. Likewise, HOE-140 attenuated the acute hypotensive response to perindoprilat in normotensive subjects (Squire et al., 2000).In congestive heart failure patients treated chronically with ACE inhibitor, combined B 1 and B 2 inhibition, but not B 2 inhibition alone, caused vasoconstriction (Davie et al., 1999;Witherow et al., 2001).Whether bradykinin contributes to the blood pressure-lowering effect of AT 1 receptor blockade remains to be determined. Unlike ACE inhibition, acute AT 1 receptor blockade does not potentiate the vasodilator effects of exogenous bradykinin in the human forearm vasculature (...

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Section: Tablementioning

confidence: 99%

Bradykinin B₂ Receptor Does Not Contribute to Blood Pressure Lowering during AT₁ Receptor Blockade

Lefèbvre

Shintani²,

Gebretsadik³

et al. 2006

J Pharmacol Exp Ther

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Dopamine efflux by MPTP and hydroxyl radical generation

Obata

2002

Journal of Neural Transmission

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1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) produces a parkinsonian syndrome after its conversion to 1-methyl-4-phenylpyridine (MPP(+)) by B-form monoamine oxidase (MAO) in the brain, which is one of the most potent dopamine (DA)-releasing agents. MPP(+) perfusion into the striatum increases extracellular DA levels and this increase may concomitantly induce the formation of reactive free oxygen radicals, such as hydroxyl radical (.OH). These elevations seem to induce lipid peroxidation of striatum membranes, as detected by increases non-enzymatic formation of 2,3-dihydroxybenzoic acid (DHBA) levels. Sustained increase in striatal DA efflux by MAO inhibition produce.OH generation by products of monoamine. Therefore, reserpine-induced DA depletion clearly decreased MPP(+)-induced.OH formation. Neuromelanine synthesis from DA produce highly reactive free radicals. Nitric oxide (NO) contributes to produce MPP(+)-induced.OH generation via NO synthase (NOS) activation by depolarization. The antioxidation effect of angiotensin converting enzyme (ACE) inhibitor protects against MPP(+)-induced.OH generation due to the suppression of the Ca(2+)-dependent release of DA. These findings may be useful in elucidating the actual mechanism of free radical formation in the pathogenesis of neurodegenerative brain disorders, including Parkinson's disease and traumatic brain injuries. This review describes the free radicals mechanisms involved in MPTP toxicity and their possible involvement in the the pathogenesis of Parkinson's disease.

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Protective effect of imidaprilat, a new angiotensin-converting enzyme inhibitor against 1-methyl-4-phenylpyridinium ion-induced ⋅OH generation in rat striatum

Obata

1999

European Journal of Pharmacology

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The potentiation of cardiodepressant and hypotensive effects of bradykinin by enalapril and captopril both in vitro and in vivo

Cited by 7 publications

References 6 publications

Bradykinin B₂ Receptor Does Not Contribute to Blood Pressure Lowering during AT₁ Receptor Blockade

Bradykinin B₂ Receptor Does Not Contribute to Blood Pressure Lowering during AT₁ Receptor Blockade

Dopamine efflux by MPTP and hydroxyl radical generation

Protective effect of imidaprilat, a new angiotensin-converting enzyme inhibitor against 1-methyl-4-phenylpyridinium ion-induced ⋅OH generation in rat striatum

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The potentiation of cardiodepressant and hypotensive effects of bradykinin by enalapril and captopril both in vitro and in vivo

Cited by 7 publications

References 6 publications

Bradykinin B2 Receptor Does Not Contribute to Blood Pressure Lowering during AT1 Receptor Blockade

Bradykinin B2 Receptor Does Not Contribute to Blood Pressure Lowering during AT1 Receptor Blockade

Dopamine efflux by MPTP and hydroxyl radical generation

Protective effect of imidaprilat, a new angiotensin-converting enzyme inhibitor against 1-methyl-4-phenylpyridinium ion-induced ⋅OH generation in rat striatum

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Bradykinin B₂ Receptor Does Not Contribute to Blood Pressure Lowering during AT₁ Receptor Blockade

Bradykinin B₂ Receptor Does Not Contribute to Blood Pressure Lowering during AT₁ Receptor Blockade