Myosin heavy chain isoforms expression and cyclic AMP concentrations in hypoxia-induced hypertrophied right ventricle in rats

Hashimoto, Takeshi; Sugiyama, Atsushi; Taguchi, Satoshi

doi:10.1016/j.cbpc.2004.04.018

Cited by 2 publications

(5 citation statements)

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“…In the present investigation PDE and AC activities were unchanged by hypoxia compared to normoxia, indicating that cAMP was not reduced by hypoxia. These data confirmed previous works that documented no changes in AC activity in ventricles exposed to long-term hypoxia [14] and pressure overload combined with hypoxia [25]. Another possible induction mechanism involves increases in circulating T 3 concentrations, which have been reported to increase beta-receptor activity [26,27] and to decrease the PDE activity, resulting in high concentrations of cAMP in myocardium [28].…”

Section: Discussionsupporting

confidence: 79%

“…A reduction in sympathetic activity resulted in an increased expression of MHC-β in myocardium because the activation of cyclic AMP (cAMP) preferentially activated the MHC-α mRNA and protein, whereas a reduction of cAMP increased the MHC-β mRNA [12,13]. In the hypoxia-induced hypertrophied right ventricle (RV), we have shown the reduction of the cellular cAMP concentrations, but we failed to find a significant correlation between the cAMP concentrations and the MHC-β isoform expression [14]. It has been reported that hypothyroidism leads to an increased expression of MHC-β isoform [2], but hyperthyroid leads to higher expressions of MHC-α isoform [3].…”

mentioning

confidence: 80%

“…Another possible induction mechanism involves increases in circulating T 3 concentrations, which have been reported to increase beta-receptor activity [26,27] and to decrease the PDE activity, resulting in high concentrations of cAMP in myocardium [28]. We previously found that long-term hypoxia increased PDE activity, but it did not change serum T 3 concentrations [1,14]. In the present short-term hypoxic exposure, we speculate that a transient increase in serum T 3 concentrations resulted in an unchanged PDE activity.…”

Section: Discussionmentioning

confidence: 99%

“…Ventricular membrane preparations for AC and PDE activities were measured, as previously described [14]. Briefly, both ventricles were minced and homogenized in 20 volumes of icecold SET buffer (0.25 M sucrose, 0.1 mM EDTA, 5.0 mM Tris-HCl, pH 7.4).…”

Section: Methodsmentioning

confidence: 99%

“…After diluting a supernatant with 10 volumes of Tris-acetate buffer (100 mM, pH 7.4), a volume of 5 µl of the supernatant was transferred to a 10 × 75 mm disposable tube (Iwaki Lab Ware, Tokyo) in triplicate. The cAMP concentration was measured with the enzymatic fluorometric assay as previously described [14].…”

Section: Methodsmentioning

confidence: 99%

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Hypoxia-Induced Adaptational Shift in MHC-β Isoform Expression in Rat Ventricles

Hashimoto

Sugiyama

Taguchi

2005

JJP

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Abstract:We investigated whether the shift of cardiac myosin heavy chain (MHC) isoform observed during exposure to hypoxia is secondary to hypertrophy, or whether it is directly related to the hypoxic stress. Twelve male Wistar-Kyoto rats, 14 weeks old, were randomly assigned to two groups: sea-level control group (CO) and hypoxia group (HX). The CO group was housed 4 weeks at 1,011 hPa, and the HX group was housed for 4 weeks at 701 hPa. The expression of MHC- was significantly increased (600%) in the HX group as compared to the CO group in the right ventricle (p < 0.01). An increased ventricular mass induced by hypoxic exposure was associated with an increased expression of MHC- in the right ventricle (p < 0.05). In the left ventricle, the MHC- exChronic exercise training induces physiological cardiac hypertrophy. In contrast, hypertension induces pathological cardiac hypertrophy caused by pressure overload. Previous studies have been demonstrated that pathologically hypertrophied ventricles produced an increase in the expression of myosin heavy chain MHC-β [1-4]. MHC-β exhibits a greater economy of force production than MHC-α; thus the increase in the expression of MHC-β would be a compensation to augment the efficiency of muscle contraction in hypertrophied ventricles in which ATP synthesis cannot meet the demand [1,5,6]. Several investigations have suggested that hemodynamic overload was a primary factor for cardiac hypertrophy and that it altered MHC-β gene expression [1,[7][8][9].Ichikawa et al. [10] demonstrated that blocking the action of endothelin-1 with a receptor antagonist reduced ventricular hypertrophy and inhibited the change in the pression was significantly increased (295%) in the HX group as compared to the CO group without ventricular hypertrophy (p < 0.01). No differences were observed in the adenylyl cyclase activity or in the phosphodiesterase activities in both ventricles between the CO and HX groups (p > 0.05). Oxidative enzymatic activities (citrate synthase and three-hydroxyacyl-CoA dehydrogenase) were unchanged in both ventricles following 4 weeks of hypoxia (p > 0.05). These findings suggest that, besides cardiac hypertrophy, the hypoxia-induced adaptational change to the MHC- isoform may be mediated through a specific mechanism related to the stress of hypoxia. [The Japanese Journal of Physiology, 55: 109-115, 2005]

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Section: Discussionsupporting

confidence: 79%

mentioning

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Hypoxia-Induced Adaptational Shift in MHC-β Isoform Expression in Rat Ventricles

Hashimoto

Sugiyama

Taguchi

2005

JJP

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Acute hypoxia modifies cAMP levels induced by inhibitors of phosphodiesterase‐4 in rat carotid bodies, carotid arteries and superior cervical ganglia

Nunes

Batuca

Monteiro

2010

British J Pharmacology

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Background and purpose: Phosphodiesterase (PDE) inhibitors are useful to treat hypoxia-related diseases and are used in experiments studying the effects of oxygen on 3′-5′-cyclic adenosine monophosphate (cAMP) production. We studied the effects of acute hypoxia on cAMP accumulation induced by PDE inhibitors in oxygen-specific chemosensors, the carotid bodies (CBs) and in non-chemosensitive CB-related structures: carotid arteries (CAs) and superior cervical ganglia (SCG). Experimental approach: Concentration-response curves for the effects of a non-specific PDE inhibitor [isobutylmethylxanthine (IBMX) ], PDE4 selective inhibitors (rolipram, Ro 20-1724) and a PDE2 selective inhibitor (erythro-9-(2-hydroxy-3-nonyl)adenine) on cAMP levels were obtained in normoxic (20% O2/5% CO2) or hypoxic (5% O2/5% CO2) conditions. Key results: Responses to the PDE inhibitors were compatible with the presence of PDE4 in rat CBs, CAs and SCG but in the absence of PDE2 in CAs and CBs. Acute hypoxia enhanced the effects of IBMX and PDE4 inhibitors on cAMP accumulation in CAs and CBs. In SCG, acute hypoxia reduced cAMP accumulation induced by all the four PDE inhibitors tested. Differences between the effects of Ro 20-1724 and rolipram on cAMP were found in CAs and CBs during hypoxia. Conclusions and implications:The effects of PDE4 inhibitors could be potentiated or inhibited by acute hypoxia depending on the PDE isoforms of the tissue. The similarities between the characterization of PDE4 inhibitors at the CBs and CAs, under normoxia and hypoxia, did not support a specific role for cAMP in the oxygen-sensing machinery at the CB and suggested that no direct CB-mediated, hyperventilatory, adverse effects would be expected with administration of PDE4 inhibitors.

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Myosin heavy chain isoforms expression and cyclic AMP concentrations in hypoxia-induced hypertrophied right ventricle in rats

Cited by 2 publications

References 16 publications

Hypoxia-Induced Adaptational Shift in MHC-β Isoform Expression in Rat Ventricles

Hypoxia-Induced Adaptational Shift in MHC-β Isoform Expression in Rat Ventricles

Acute hypoxia modifies cAMP levels induced by inhibitors of phosphodiesterase‐4 in rat carotid bodies, carotid arteries and superior cervical ganglia

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