Comparison of the haemodynamic effects of adenosine monophosphate with sodium nitroprusside in a canine model of acute global left ventricular dysfunction

Finegan, Barry A.; Clanachan, Alexander S.

doi:10.1111/j.1476-5381.1991.tb09848.x

Cited by 3 publications

(1 citation statement)

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“…We have shown previously (Finegan et al, 1990), in normal anaesthetized dogs, that afterload reduction due to Ado receptormediated vasodilatation, increases cardiac output more than equieffective afterload reducing doses of sodium nitroprusside (SNP). A similar result was also observed in a canine model of acute left ventricular dysfunction (Finegan & Clanachan, 1991).…”

Section: Introductionsupporting

confidence: 83%

Cardiovascular selectivity of adenosine receptor agonists in anaesthetized dogs

Gerencer

Finegan

Clanachan

1992

British J Pharmacology

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1 In order to determine the relevance of adenosine (Ado) receptor classification obtained from in vitro methods to the cardiovascular actions of Ado agonists in vivo, the cardiovascular effects of adenosine 5'-monophosphate (AMP), N6-cyclohexyladenosine (CHA, 400 fold A,-selective), 5'-N-ethylcarboxamidoadenosine (NECA, A, kA2) and 2-phenylaminoadenosine (PAA, 5 fold A2-selective) were compared in open-chest, fentanyl-pentobarbitone anaesthetized dogs.2 Graded doses of CHA (10 to 000 tgg kg'-), NECA (0.5 to 100 fig kg'-) or PAA (0.1 to 20 gg kg-') were administered intravenously and changes in haemodynamics and myocardial contractility were assessed 10 min following each dose. The effects of graded infusions of AMP (200 to 1000 ig kg-' min-') were also evaluated. 3 AMP and each of the Ado analogues (NECA> PAA> CHA) increased the systemic vascular conductance index (SVCI) in a dose-dependent manner and reduced mean arterial pressure (MAP). At doses causing similar increases in SVCI, these agonists caused (i) similar reflex increases in heart rate (HR) and cardiac index (CI) and decreases in AV conduction interval (AVj) and (ii) similar increases in coronary vascular conductance (CVC). 4 After cardiac autonomic blockade with atropine (0.2 mg kg-') and propranolol (1 mg kg-'), AMP, CHA and PAA still increased SVCI and CVC and decreased MAP. CHA and PAA had no marked effects on HR, CI or AVi. As in the absence of cardiac autonomic blockade, equieffective vasodilator doses of CHA and PAA had identical effects on CVC, CI and AVj.5 Myocardial contractility, as assessed by E,,,,, measurements, was stimulated by AMP in control animals. Following cardiac autonomic blockade, PAA increased contractility while AMP and CHA had no significant effects. 6 Despite marked.differences in receptor selectivity in vitro, no marked differences between the actions of these Al-and A2-selective Ado receptor agonists on the cardiovascular system in vivo were apparent.Difficulties therefore exist in the application of in vitro Ado receptor selectivity data to the prediction of the cardiovascular effects of Ado agonists in vivo.

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Section: Introductionsupporting

confidence: 83%

Cardiovascular selectivity of adenosine receptor agonists in anaesthetized dogs

Gerencer

Finegan

Clanachan

1992

British J Pharmacology

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Long-term treatment with neutral endopeptidase inhibitor improves cardiac function and reduces natriuretic peptides in rats with chronic heart failure

Maki

Nasa

Yamaguchi

et al. 2001

Cardiovascular Research

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Poster Communications

Kidd¹,

Michel²,

Humphrey³

1993

British J Pharmacology

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Nitric oxide synthase (NOS) is the enzyme responsible for the production of nitric oxide, a putative neurotransmitter. The distribution of this enzyme in rat brain (Vincent & Kamura, 1992) and spinal cord (Valtschanoff et al., 1992) neurones has previously been studied using the NADPH-diaphorase technique. However, this method may not be specific for NOS and therefore a more selective tool would be valuable. Nitroarginine is an inhibitor of NOS which has recently become available in a tritiated form. We have shown that the binding of this radioligand to the soluble enzyme can be prevented by L-arginine (Michel et al., 1993) and have now examined the regional distribution of its binding in the rat cenitral nervous system (CNS) using autoradiography. Frozen sections (20 gin) of unfixed brain and spinal cord, on coated slides, were preincubated in 50 mM Tris.HCI, 3 mM CaCl2 and 0.025% Triton X100 butter, pH 7.4 for 30 min at 25°C, then incubated for 60 min at 4°C with-7 nM [3H]nitroarginine (Michel et al., 1993) with or without 1 jM nitroarginine for non-specific binding, washed for 3 x 10 min and dipped for 10 sec in ice-cold distilled water. The dried slides were apposed to X-ray film for 3 months and the images were quantified using suitable standards. The highest levels of specific binding (grey values, mean ± s. e. mean, n 2 19) were found in the tenia tecta (0.155 ± 0.009), throughout the amygdaloid complex, in particular in the anterior (0.107 ± 0.007) and medial (0.125 ± 0.006) nuclei, the amygdalopiriform transition (0.134 ± 0.005) and in the anterior cerebellum (0.087 ± 0.002). There was also binding in the thalamic bed nucleus of the stria terminalis (0.067 ± 0.005), the dentate gyrus (0.033 ± 0.001), the ventral hippocampal CA3 area (0.051 ± 0.002), layers 1 and 2 of the frontal cortex (0.064 ± 0.003) and the superior gray layer of the superior colliculus (0.053 ± 0.002). The paraventricular nucleus of the hypothalamus and the superficial layers of the dorsal hom of the thoracic and lumbar spinal cord were also labelled but this was not quantifiable at this time point. Binding in the striatum and the rest of the cortex was diffuse and therefore not quantified. There appeared to be few or no specific binding sites in the pons and medulla. The regional distribution of binding sites for [3H]itroargiine in the rat CNS was, in general, similar to that seen with the diaphorase method. There were, however, differences in the cortex and the hindbrain which may be due to the existence of more than one isoform of NOS in the CNS. Thus, [3H]nitroarginine appears to be a very useful ligand for studying the distribution of NOS in the CNS and may also be capable of distinguishing between potential isoforms. More studies are plamned using dual labelling techniques to determine whether [3H]nitroarginine binds to cells, labelled either with the diaphorase method or a specific antibody to the cloned braini isoform of NOS.

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Comparison of the haemodynamic effects of adenosine monophosphate with sodium nitroprusside in a canine model of acute global left ventricular dysfunction

Cited by 3 publications

References 35 publications

Cardiovascular selectivity of adenosine receptor agonists in anaesthetized dogs

Cardiovascular selectivity of adenosine receptor agonists in anaesthetized dogs

Long-term treatment with neutral endopeptidase inhibitor improves cardiac function and reduces natriuretic peptides in rats with chronic heart failure

Poster Communications

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