Species‐related differences in inotropic effects of angiotensin II in mammalian ventricular muscle: receptors, subtypes and phosphoinositide hydrolysis

Ishihata, Akira; Endoh, Masao

doi:10.1111/j.1476-5381.1995.tb13247.x

Cited by 68 publications

(42 citation statements)

References 30 publications

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“…Contrasting results have been published about the inotropic effect of Ang II, including data on the rat (33)(34)(35)(36)(37)(38)(39). Ang II induces a positive inotropic response in most species, which is not fully mediated by the ß-adrenergic system (33)(34)(35).…”

Section: Discussionmentioning

confidence: 69%

Angiotensin-(1-7) improves the post-ischemic function in isolated perfused rat hearts

Ferreira

Santos

Almeida

2002

Braz J Med Biol Res

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We evaluated the effects of angiotensin-(1-7) (Ang-(1-7)) on postischemic function in isolated hearts from adult male Wistar rats perfused according to the Langendorff technique. Local ischemia was induced by coronary ligation for 15 min. After ischemia, hearts were reperfused for 30 min. Addition of angiotensin II (Ang II) (0.20 nM, N = 10) or Ang-(1-7) (0.22 nM, N = 10) to the Krebs-Ringer perfusion solution (KRS) before the occlusion did not modify diastolic or systolic tension, heart rate or coronary flow (basal values for Ang-(1-7)-treated hearts: 0.72 ± 0.08 g, 10.50 ± 0.66 g, 216 ± 9 bpm, 5.78 ± 0.60 ml/min, respectively). During the period of occlusion, the coronary flow, heart rate and systolic tension decreased (values for Ang-(1-7)-treated hearts: 2.83 ± 0.24 ml/min, 186 ± 7 bpm, 6.95 ± 0.45 g, respectively). During reperfusion a further decrease in systolic tension was observed in control (4.95 ± 0.60 g) and Ang II-treated hearts (4.35 ± 0.62 g). However, in isolated hearts perfused with KRS containing Ang-(1-7) the further reduction of systolic tension during the reperfusion period was prevented (7.37 ± 0.68 g). The effect of Ang-(1-7) on the systolic tension was blocked by the selective Ang-(1-7) antagonist A-779 (2 nM, N = 9), by the bradykinin B 2 antagonist HOE 140 (100 nM, N = 10), and by indomethacin pretreatment (5 mg/ kg, ip, N = 8). Pretreatment with L-NAME (30 mg/kg, ip, N = 8) did not change the effect of Ang-(1-7) on systolic tension (6.85 ± 0.61 g). These results show that Ang-(1-7) at low concentration (0.22 nM) improves myocardial function (systolic tension) in ischemia/reperfusion through a receptor-mediated mechanism involving release of bradykinin and prostaglandins.

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Section: Discussionmentioning

confidence: 69%

Angiotensin-(1-7) improves the post-ischemic function in isolated perfused rat hearts

Ferreira

Santos

Almeida

2002

Braz J Med Biol Res

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“…Activation of PKC by phorbol 12,13-dibutyrate inhibits the Ang IIinduced stimulation of phosphoinositide hydrolysis and thereby the positive inotropic effect of Ang II in rabbit ventricular myocardium (65). The positive inotropic effect of Ang II shows a wide range of speciesdependent variation, being pronounced in the rabbit ventricular myocardium (66) and is associated with activation of L-type Ca 2+ channels (67, 69), the Na (67,68), and NCX (68). The positive inotropic effect of Ang II is similar to the α-adrenoceptormediated effect, and it is associated with a moderate increase in Ca 2+ transients and an increase in myofilament Ca 2+ sensitivity in rabbit papillary muscle (7) and single ventricular myocytes (68).…”

Section: -3 Ang IImentioning

confidence: 99%

“…Ang II exerts a positive inotropic effect through activation of AT 1 receptors and subsequent acceleration of phosphoinositide hydrolysis (65,66). Activation of PKC by phorbol 12,13-dibutyrate inhibits the Ang IIinduced stimulation of phosphoinositide hydrolysis and thereby the positive inotropic effect of Ang II in rabbit ventricular myocardium (65).…”

Section: -3 Ang IImentioning

confidence: 99%

Signal Transduction and Ca2+ Signaling in Intact Myocardium

Endoh

2006

J Pharmacol Sci

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Abstract. The experimental procedures to simultaneously detect contractile activity and Ca 2+transients by means of the Ca 2+ sensitive bioluminescent protein aequorin in multicellular preparations, and the fluorescent dye indo-1 in single myocytes, provide powerful tools to differentiate the regulatory mechanisms of intrinsic and external inotropic interventions in intact cardiac muscle. The regulatory process of cardiac excitation-contraction coupling is classified into three categories; upstream (Ca 2+ mobilization), central (Ca 2+ binding to troponin C), and / or downstream (thin filament regulation of troponin C property or crossbridge cycling and crossbridge cycling activity itself) mechanisms. While a marked increase in contractile activity by the Frank-Starling mechanism is associated with only a small alteration in Ca 2+ transients (downstream mechanism), the force-frequency relationship is primarily due to a frequencydependent increase of Ca 2+ transients (upstream mechanism) in mammalian ventricular myocardium. The characteristics of regulation induced by β-and α-adrenoceptor stimulation are very different between the two mechanisms: the former is associated with a pronounced facilitation of an upstream mechanism, whereas the latter is primarily due to modulation of central and / or downstream mechanisms. α-Adrenoceptor-mediated contractile regulation is mimicked by endothelin ET A -and angiotensin II AT 1 -receptor stimulation. Acidosis markedly suppresses the regulation induced by Ca 2+ mobilizers, but certain Ca 2+ sensitizers are able to induce the positive inotropic effect with central and / or downstream mechanisms even under pathophysiological conditions.

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“…In addition, the present results provide an insight into the reason for the wide range of controversial findings on the inotropic effects of G q PCR agonists in experimental animals in previous studies, that is, no inotropic effect (5,6,10,25), a PIE (5,6,10,26), or a NIE (27 -30). While diverse factors, including different cardiac location (atrial or ventricular), species of animals, and experimental conditions (including stimulation frequency and experimental temperature) may contribute to the variable findings, the present observations imply that the extent of concomitant receptor activation induced by neurotransmitters, endogenous peptides, or hormones may contribute significantly to the difference in functional expression.…”

Section: Physiological and Pathophysiological Relevance Of Current Obmentioning

confidence: 97%

Differential Inotropic Effects of Endothelin-1, Angiotensin II, and Phenylephrine Induced by Crosstalk With cAMP-Mediated Signaling Process in Dog Ventricular Myocardium

et al. 2004

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Abstract. Endothelin-1 (ET-1), angiotensin II (Ang II), and phenylephrine, an a 1 -adrenoceptor agonist, share the common signaling process, resulting in activation of G q protein-coupled receptor (G q PCR) to activate the hydrolysis of phosphoinositide (PI). They do not elicit any inotropic effect in isolated dog ventricular muscle. In the presence of forskolin or IBMX (3-isobutyl-1-methylxanthine), ET-1 produced a dual effect, that is, a positive inotropic effect (PIE) and / or a negative inotropic effect (NIE) depending on concentrations of forskolin or IBMX present simultaneously with ET-1. Phenylephrine produced a definite PIE and Ang II induced a small and transient PIE in the presence of forskolin or IBMX, but they did not elicit a NIE. Facilitation of Ca2+ influx via L-type Ca 2+ channel may play a crucial role in the crosstalk because G q PCR agonists produced, likewise a PIE in the presence of Bay k 8644. G q PCR agonists failed to induce a PIE in the presence of dihydroouabain or elevated [Ca 2+ ] o . These findings indicate that the accumulation of cAMP or activation of L-type Ca 2+ channels markedly modulates the inotropic response to G q PCR agonists in a manner that leads to a PIE in dog ventricular myocardium. In addition, ET-1, but not Ang II or phenylephrine, activates the signal transduction process that results in a NIE.

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Species‐related differences in inotropic effects of angiotensin II in mammalian ventricular muscle: receptors, subtypes and phosphoinositide hydrolysis

Cited by 68 publications

References 30 publications

Angiotensin-(1-7) improves the post-ischemic function in isolated perfused rat hearts

Angiotensin-(1-7) improves the post-ischemic function in isolated perfused rat hearts

Signal Transduction and Ca2+ Signaling in Intact Myocardium

Differential Inotropic Effects of Endothelin-1, Angiotensin II, and Phenylephrine Induced by Crosstalk With cAMP-Mediated Signaling Process in Dog Ventricular Myocardium

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