Direct myocardial effects of angiotensin II

Dempsey, PJ; McCallum, ZT; Kent, K M; Cooper, Theodore

doi:10.1152/ajplegacy.1971.220.2.477

Cited by 121 publications

(39 citation statements)

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“…Male albino rabbits weighing 1. allowed to act for 20 min before the administration of All and were present in the organ bath throughout the experiments to avoid any interference with a-and P-adrenoceptor stimulation by catecholamines (Dempsey et al, 1971). In a series of experiments with All antagonists, saralasin, losartan or PD 123319 were allowed to act for 20 min before the administration of All.…”

Section: Isolation Of Rabbit Papillary Muscles and Experimental Procementioning

confidence: 99%

“…In addition to its wellestablished constrictor effect on the vascular smooth muscle, All produces a positive inotropic effect (PIE) in mammalian ventricular myocardium including that of man (Schomisch et al, 1990), dog (Kobayashi et al, 1978) and rabbit (Dempsey et al, 1971) and in the chick heart . In whole animal experiments, All modulates the myocardial contractility via a direct pathway and by an indirect pathway which is mediated by a cardiovascular reflex.…”

Section: Introductionmentioning

confidence: 99%

“…Increased release of catecholamines may contribute to the indirect inotropic effect of All (Ross & White, 1966). The mechanism of the direct PIE caused by All has been postulated to be due to activation of specific All receptors in myocardial cells (Dempsey et al, 1971). Various pathways of intracellular signal transduction have been implicated as possible subcellular mechanisms of the action of All: the activation of the slow Ca2l channel (Freer et al, 1976), acceleration of phosphoinositide hydrolysis and inhibition of adenylate cyclase (Anand-Srivastava, 1989).…”

Section: Introductionmentioning

confidence: 99%

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Pharmacological characteristics of the positive inotropic effect of angiotensin II in the rabbit ventricular myocardium

Ishihata

Endoh

1993

British J Pharmacology

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1 In order to elucidate the mechanism underlying the positive inotropic effect (PIE) of angiotensin II (All), we measured changes in phosphoinositide hydrolysis and contractile force induced by All in the rabbit ventricular myocardium.2 All (1.0 nM-3 jLM) produced a PIE in a concentration-dependent manner in the presence of bupranolol (0.3 pM) and prazosin (O.1 LM), the maximal response being about 40% of that to isoprenaline and the EC50 30 nM.3 The PIE of All was associated with a concentration-dependent increase in the total duration of contraction; the time to peak force and the relaxation time were prolonged.

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Section: Isolation Of Rabbit Papillary Muscles and Experimental Procementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Pharmacological characteristics of the positive inotropic effect of angiotensin II in the rabbit ventricular myocardium

Ishihata

Endoh

1993

British J Pharmacology

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“…To distinguish between direct and indirect effects, which are primarily due to the modulation of the sympathetic nervous system, investigations applying j9-adrenoceptor blockers (152)(153)(154)(155), extrinsic cardiac denervation (147,156), isolated cardiomyocyte preparations (157,158), or isolated perfused hearts (159,160) were performed. On the molecular level the inotropic effects of ANG II are apparently mediated by its influence of calcium homeostasis and transmembranous conductance.…”

Section: Heartmentioning

confidence: 99%

“…On the molecular level the inotropic effects of ANG II are apparently mediated by its influence of calcium homeostasis and transmembranous conductance. Several studies (155,161) showed that ANG II changed the plateau phase of the cardiac action potential increasing its height and duration and leading to a rise in peak developed tension.…”

Section: Heartmentioning

confidence: 99%

The Role of the Renin-Angiotensin System in Cardiovascular Disease.

et al. 1994

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Recent findings have increased our understanding of the role of the renin-angiotensin system in cardiovascular diseases. This was possible by the progress made in molecular biology and the import of this methodology into cardiovascular research by several groups in the past few years. Studies by these groups accumulated evidence especially for the existence and physiological importance of organ-based renin-angiotensin systems and their involvement in the pathogenesis of hypertension and the accompanying disorders of the heart, the kidney, and the vessels. This Review will focus mainly on the relevance of the local renin-angiotensin systems for cardiovascular diseases and the value of transgenic animals as models to analyse these systems (Hypertens Res 1994; 17: 1-16).

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The Effect of Angiotensin on Myocardial Contractility

Ahmed

Levinson

Weisse

et al. 1975

The Journal of Clinical Pharma

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Previous studies of the effect of angiotensin on myocardial contractility have yielded conflicting results. Possible reasons for the observed disparities include differences in techniques for measuring contractility, in species (dog, cat, and man), in myocardial state (normal or diseased), in preparation observed (heart-lung, isolated heart, papillary muscle, atrial myocardium, intact heart), and in dosage schedule. Moreover, there are no reported studies in the intact human heart, normal or diseased, in which contractility measurements are based on velocity-force relations. To resolve the conflict, left ventricular myocardial contractility was measured using the same expressions for the force-velocity relationship in all subjects. Studies were performed in five normal human subjects, six patients with cardiomyopathy, eight normal mongrel dogs, and six dogs with ischemic myocardial scarring, before and during angiotensin infusions in dosages producing 15--20-mm Hg increases of aortic diastolic pressure. Contractile element velocity at peak, dP/dt (Vce) and the Frank-Levinson contractility index (CyIx), which normalizes Vce for diastolic fiber length, decreased during angiotensin infusion in all groups. The mean decreases (11 to 19) per cent in Vce, 15 to 23 per cent in CyIx, SEM's 4-5 per cent) were significant (P values ranging from smaller than 0.05 to smaller 0.005) in the normal hearts of dogs and man and in the scarred canine hearts, in which preangiotensin Vce and CyIx were normal. In the cardiomyopathy group, in which contractility was depressed before angiotensin, the drug elicited a further decrease in Vce (mean fall 17 plus or minus 7 per cent, P smaller than 0.1) and CyIx (26 plus or minus 8 per cent, P smaller than 0.02). We conclude that, in the intact organism, with a normal myocardium or a diffuse or segmental myocardial disease, the administration of angiotensin results in a depression of contractility.

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Direct myocardial effects of angiotensin II

Cited by 121 publications

References 0 publications

Pharmacological characteristics of the positive inotropic effect of angiotensin II in the rabbit ventricular myocardium

Pharmacological characteristics of the positive inotropic effect of angiotensin II in the rabbit ventricular myocardium

The Role of the Renin-Angiotensin System in Cardiovascular Disease.

The Effect of Angiotensin on Myocardial Contractility

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