Local cardiac effects of substance P: roles of acetylcholine and noradrenaline

Chiao, Hsi; Caldwell, Robert W.

doi:10.1111/j.1476-5381.1995.tb13224.x

Cited by 21 publications

(10 citation statements)

References 33 publications

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“…We have also considered the possibility that endogenously released NO might affect cardiac function. This was studied by the application of substance P, based on the fact that local cardiac effects of substance P have been described (Chiao & Caldwell, 1995) and the effects of substance P in other tissues are mediated, at least partially, by NO (Jin et al, 1993;Ziche et al, 1993). Fc in isolated left atria remained, however, virtually unaffected after the application of substance P 100 pmol I`(in the presence of atropine 1 pmol I`and atenolol 10 pmol 1`97.3% of control values; n = 3).…”

Section: Evaluation Of Resultsmentioning

confidence: 99%

The ineffectiveness of the NO‐cyclic GMP signaling pathway in the atrial myocardium

Nawrath

Bäumner

Rupp

et al. 1995

British J Pharmacology

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1 This study was performed to determine whether nitric oxide (NO) has direct effects on force of contraction (Fc) in atrial myocardium from rats, rabbits, guinea-pigs, frogs, and man. 2 Glyceryl trinitrate, isosorbide dinitrate, 3-morpholino-sydnonimine hydrochloride (SIN-1), and Snitroso-N-acetylpenicillamine (SNAP) did not signficantly reduce Fc in the various preparations investigated, either given alone or after stimulation of a-or fi-adrenoceptors.3 SNAP did not change the time course of contractions in rat, guinea-pig and human preparations. 4 8-Bromo-guanosine-3':5'-cyclic monophosphate (8-Br-cyclic GMP) produced a negative inotropic effect in rat, guinea-pig and human atrial preparations and shortened time to peak tension and relaxation time in human preparations. 5 High K+ (85 mmol 1I`)-induced contracture in rat heart muscle was reduced by 8-Br-cyclic GMP but not by SIN-1. 6 N-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthase, failed to influence muscarinic effects on Fc or frequency from rat and guinea-pig hearts. 7 We conclude that NO, under the experimental conditions described here, has no direct effects on the heart, although cyclic GMP may be involved in the regulation of myocardial contraction.

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Section: Evaluation Of Resultsmentioning

confidence: 99%

The ineffectiveness of the NO‐cyclic GMP signaling pathway in the atrial myocardium

Nawrath

Bäumner

Rupp

et al. 1995

British J Pharmacology

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“…More recently, the nodose ganglia's afferent neurons were also shown to project directly to different chambers of the rat heart and exhibit a variety of neurochemical phenotypes Kosta et al 2010). On the other hand, substance P, as a co-neurotransmitter, has a modulatory effect on the synthesis and release of other neurotransmitters, such as acetylcholine, neuropeptide Y and norepinephrine, which results in altered local autonomic neuron-regulated organ function (Chiao & Caldwell 1995;Mukda et al 2009). Therefore, it is possible that the increase in substance P synthesis in the nodose ganglia in response to pulmonary exposure to UFTiO 2 alters cardiac autonomic neuron activity either through the medullar cardiovascular regulatory centre or through the nodose ganglia's afferent neurons, which directly project to the cardiac chambers and modulate the synthesis and release of other co-existing neurotransmitters.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary exposure of rats to ultrafine titanium dioxide enhances cardiac protein phosphorylation and substance P synthesis in nodose ganglia

Kan

Young

et al. 2011

Nanotoxicology

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The inhalation of engineered nanoparticles stimulates the development of atherosclerosis and impairs vascular function. However, the cardiac effects of inhaled engineered nanoparticles are unknown. Here, we investigate the effects of ultrafine titanium dioxide (UFTiO(2)) on the heart, and we define the possible mechanisms underlying the measured effects. Pulmonary exposure of rats to UFTiO(2) increased the phosphorylation levels of p38 mitogen-activated protein kinase and cardiac troponin I, but not Akt, in the heart and substance P synthesis in nodose ganglia. Circulatory levels of pro-inflammatory cytokines, and blood cell counts and differentials were not significantly changed after pulmonary exposure. Separately, the incubation of cardiac myocytes isolated from naïve adult rat hearts in vitro with UFTiO(2) did not alter the phosphorylation status of the same cardiac proteins. In conclusion, the inhalation of UFTiO(2) enhanced the phosphorylation levels of cardiac proteins. Such responses are likely independent of systemic inflammation, but may involve a lung-neuron-regulated pathway.

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“…The primary pharmacological action of SP in the isolated spontaneously beating heart is to decrease heart rate and relax coronary resistance vessels [22-24]. The effects of SP on the cardiac system can be blocked by atropine, a competitive antagonist of the muscarinic acetylcholine receptor, showing that it is mediated by the cholinergic nerves [23,25].…”

Section: Introductionmentioning

confidence: 99%

Increased susceptibility to cardiovascular effects of dihydrocapcaicin in resuscitated rats. Cardiovascular effects of dihydrocapsaicin

Fosgerau

Ristagno

Jayatissa

et al. 2010

BMC Cardiovasc Disord

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BackgroundSurvivors of a cardiac arrest often have persistent cardiovascular derangements following cardiopulmonary resuscitation including decreased cardiac output, arrhythmias and morphological myocardial damage. These cardiovascular derangements may lead to an increased susceptibility towards the external and internal environment of the cardiovascular system as compared to the healthy situation.MethodsHere we tested the hypothesis that the cardiovascular system in healthy rats and rats resuscitated from a cardiac arrest may be differentially affected by a transient receptor potential vanilloid type 1 agonist, by continuous intravenous infusion of dihydrocapsaicin (DHC).ResultsCompared to baseline, infusion of DHC caused an initial increase in mean arterial blood pressure in both healthy and resuscitated rats of 25% and 10%, respectively. Also, we observed an initial response of tachycardia in both healthy and resuscitated rats of 30% and 20%, respectively. Then, at high levels of DHC infusion (> 2.0 mg/kg/hr) we observed two single episodes of transient bradycardia and hypotension in 33% of the healthy rats, which was consistent with a TRPV1 agonist induced Bezold-Jarisch reflex. In contrast, in resuscitated rats we observed multiple episodes of bradycardia/hypotension in 100% of the rats and at a dose of DHC of 0.65 mg/kg/hr. Notably, this DHC effect could be completely blocked in the resuscitated rats by pre-treatment with atropine, a muscarinic acetylcholine antagonist.ConclusionsOur results indicate that the susceptibility of the rats towards TRPV1 agonist induced Bezold-Jarisch reflex is increased in those resuscitated from cardiac arrest compared to the healthy situation.

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Local cardiac effects of substance P: roles of acetylcholine and noradrenaline

Cited by 21 publications

References 33 publications

The ineffectiveness of the NO‐cyclic GMP signaling pathway in the atrial myocardium

The ineffectiveness of the NO‐cyclic GMP signaling pathway in the atrial myocardium

Pulmonary exposure of rats to ultrafine titanium dioxide enhances cardiac protein phosphorylation and substance P synthesis in nodose ganglia

Increased susceptibility to cardiovascular effects of dihydrocapcaicin in resuscitated rats. Cardiovascular effects of dihydrocapsaicin

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