The effect of endotoxin on sympathetic responses in the rat isolated perfused mesenteric bed; involvement of nitric oxide and cyclo‐oxygenase products

Fatehi‐Hassanabad, Zahra; Furman, Brian L.; Parratt, J. R.

doi:10.1111/j.1476-5381.1995.tb15141.x

Cited by 25 publications

(9 citation statements)

References 35 publications

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“…Lack of alterations in the mesenteric vascular contractility to NE after LPS administration, at a time when iNOS activity was indeed increased, is in accordance with previous studies with adrenergic agonists (Mitchell et al, 1993;Fatehi-Hassanabad et al, 1995;Eerdmans et al, 1996). Nevertheless, hyporeactivity to NE in perfused mesenteric beds after LPS administration was described previously (MitoloChieppa et al, 1996) and lower responses to methoxamine were observed when this agonist was administered as an infusion instead of as a bolus (Farmer et al, 2001).…”

Section: Discussionsupporting

confidence: 77%

Potentiation of Anandamide Effects in Mesenteric Beds Isolated from Endotoxemic Rats

Orliac

Peroni²,

Celuch³

et al. 2003

J Pharmacol Exp Ther

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The aim of the present experiments was to study the effects of exogenously added anandamide on transient norepinephrine (NE)-induced contractions in mesenteric beds isolated from adult male Sprague-Dawley rats 6 h after the i.p. administration of 5 mg kg Ϫ1 lipopolysaccharide (LPS). LPS treatment induced a 3-fold increase in total nitric-oxide synthase (NOS) activity without modifying either the systolic blood pressure or the vascular reactivity to NE of the isolated mesenteric bed. The endocannabinoid anandamide (0.01-10 M) caused concentration-dependent reductions of the contractile responses to NE in the isolated mesenteric bed. This effect was significantly potentiated after LPS treatment compared with the controls. Anandamide-induced reductions of the contractile responses to NE in mesenteric beds isolated from LPS-treated rats were unmodified by endothelium removal but significantly diminished by either the anandamide amidase inhibitor phenylmethylsulfonyl fluoride (200 M) or the vanilloid receptor antagonist capsazepine (1 M). The vanilloid receptor agonist capsaicin (0.01-100 nM) also caused concentration-dependent relaxations that were potentiated in mesenteric beds from LPStreated rats. Nevertheless, they were unmodified by 1 M capsazepine. It is concluded that the potentiation of anandamide relaxations after LPS treatment, which are evident at early stages of endotoxic shock, could involve the participation of an anandamide metabolite and might be mediated, at least in part, through a vanilloid receptor.

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Section: Discussionsupporting

confidence: 77%

Potentiation of Anandamide Effects in Mesenteric Beds Isolated from Endotoxemic Rats

Orliac

Peroni²,

Celuch³

et al. 2003

J Pharmacol Exp Ther

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“…It has been documented, by using different experimental models, that LPS can induce an increase in the spontaneous release of ACh at the neuromuscular junction (41). In rabbit airways, LPS-induced AHR involved activation of vagal C fibers and the release of neuropeptides (42); moreover, LPS augmented contractile responses and noradrenaline overflow evoked by EFS stimulation in the small mesenteric artery and in the tail (43).…”

Section: Discussionmentioning

confidence: 99%

Protein Prenylation Contributes to the Effects of LPS on EFS–Induced Responses in Human Isolated Bronchi

Cazzola

Calzetta

Page³

et al. 2011

Am J Respir Cell Mol Biol

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Rho/Ras signaling pathways may play an important role in the mechanism of LPS-induced inflammation and bronchoconstriction. In this study, we investigated the effect of LPS on the transmural contractile tension induced by electrical field stimulation (EFS) of human isolated bronchi. The possible contribution of Rho/Ras signaling pathways was examined by using geranylgeranyl-pyrophosphate (GGPP) and farnesyl-pyrophosphate (FPP), the selective geranylgeranyl-pyrophosphate-transferase inhibitor GGTI2133, and the selective farnesyl-pyrophosphate transferase inhibitor FTI276, the hydroxy-3-methylglutaryl coenzyme A reductase inhibitor simvastatin and the Rho-associated coiled-coil-forming protein serine/threonine kinase inhibitor Y27632. LPS (300 ng/ml) significantly enhanced the EFS-induced contractile force of human bronchi (P < 0.05). The plateau was reached at 105.0 (±4.1) minutes; the maximal effect (Emax) value was 267.47 (±8.88) %, with a time to evoke a half-maximal contraction (t(1/2)) of 40.5 (±2.0) minutes. Pretreatment with GGPP (5 μM) enhanced the EFS-mediated contractile tension (Emax, 164.56 ± 9.80% and the t(1/2) 23.0 ± 2.5 min). Pretreatment with FPP (5 μM) was effective, as was GGPP, in enhancing the EFS response (Emax, of 189.23 ± 12.98% and a t(1/2) of 17.0 ± 4.5 min). Furthermore, GGTI2133 (500 nM) and FTI276 (10 nM) significantly inhibited the effects of GGPP and FPP on EFS-induced response. Pretreatment with GGPP (5 μM) significantly enhanced the EFS response compared with the control and LPS-treated tissues; GGTI2133 (500 nM) significantly inhibited the EFS-induced contractile tension in LPS (300 ng/ml)-treated tissues, and it was not possible to calculate the t(1/2). In addition, simvastatin and Y27632 (both 1 μM) were effective in abolishing the contracturant effect of LPS. Our results provide mechanistic evidence for the enhanced bronchoconstriction induced by LPS in human isolated airways, the contribution of Rho/Ras pathways in this LPS response, and the protective role of statins.

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“…We suggest that this is due to modulation of cardiac autonomic transmission. First, NO can attenuate the cardiac responses to sympathetic stimulation both by inhibiting neuronal noradrenaline release [37] at the prejunctional level [38] and by inhibiting its effects on cardiac β-adrenoceptors [39]. This would be one explanation of why NO, released for example during preconditioning [40] and exercise or following the administration of NO donors [41], is able to reduce the severity of ischaemia-induced ventricular arrhythmias.…”

Section: Discussionmentioning

confidence: 99%

Delayed cardioprotective effects of exercise in dogs are aminoguanidine sensitive: possible involvement of nitric oxide

Babai¹,

SZIGETI²,

Parratt³

et al. 2002

Clinical Science

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Dogs were subjected to exercise on a treadmill, using a protocol in which the speed and slope were increased every 3 min, and which elevated both heart rate (to a mean of 198+/-14 beats.min(-1)) and mean arterial blood pressure (to 150+/-4 mmHg). Then, 24 or 48 h later, the dogs were anaesthetized with a mixture of alpha-chloralose and urethane and subjected to a 25 min occlusion of the left anterior descending coronary artery. The control dogs (instrumented but not exercised) were subjected to the same procedure. In some dogs the nitric oxide synthase inhibitor aminoguanidine (50 mg.kg(-1); intravenous) was administered 30 min before occlusion. Baroreflex sensitivity (BRS) was determined by the rapid bolus injection of phenylephrine 60 min before, and again 3 min after, the onset of occlusion. Exercise markedly reduced the consequences of coronary artery occlusion 24 h (but not 48 h) later, without modifying myocardial tissue blood flow. In the exercised dogs there were reductions in arrhythmia severity [ventricular fibrillation (VF) during occlusion, 0%; survival from the combined ischaemia/reperfusion insult, 70%] compared with controls (VF during occlusion, 36%; survival, 9%). BRS was preserved during occlusion in the exercised dogs (before occlusion, 1.60+/-0.54 ms.mmHg(-1); 3 min after occlusion, 1.37+/-0.4 ms.mmHg(-1)), but not in controls (before occlusion, 1.28+/-0.29 ms.mmHg(-1); 3 min after occlusion, 0.45+/-0.12 ms.mmHg(-1); P<0.05), and other ischaemic changes (inhomogeneity of electrical activation and changes in the ST-segment, recorded over the ischaemic region) were also less marked in the exercised dogs. Exercise-induced cardioprotection was abolished by aminoguanidine (VF during occlusion, 25%; survival, 0%). The results show that even a single period of exercise affords delayed protection against ischaemia/reperfusion-induced VF and other ischaemic changes. Since this protection is abolished by aminoguanidine, and since (inducible) NO synthase activity was elevated 3-fold in left ventricular samples 24 h after exercise, we suggest that this protection is mediated by nitric oxide.

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The effect of endotoxin on sympathetic responses in the rat isolated perfused mesenteric bed; involvement of nitric oxide and cyclo‐oxygenase products

Cited by 25 publications

References 35 publications

Potentiation of Anandamide Effects in Mesenteric Beds Isolated from Endotoxemic Rats

Potentiation of Anandamide Effects in Mesenteric Beds Isolated from Endotoxemic Rats

Protein Prenylation Contributes to the Effects of LPS on EFS–Induced Responses in Human Isolated Bronchi

Delayed cardioprotective effects of exercise in dogs are aminoguanidine sensitive: possible involvement of nitric oxide

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