The effects of compensated cardiac hypertrophy on dihydropyridine and ryanodine receptors in rat, ferret and guinea-pig hearts

Rannou, F.; Sainte-Beuve, C; Oliviéro, P.; Do, Emmanuelle; Trouvé, Pascal; Charlemagne, D.

doi:10.1016/0022-2828(95)90059-4

Cited by 38 publications

(11 citation statements)

References 38 publications

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“…In rats with left ventricular hypertrophy, the density of L-type calcium channels is not altered (31), whereas the total number of channels is increased. If we assume cardiomyocytes to be cylindrically shaped, the volume of the myocyte will increase more than the membrane area.…”

Section: Discussionmentioning

confidence: 86%

Contractile reserve but not tension is reduced in monocrotaline-induced right ventricular hypertrophy

Versluis¹,

Heslinga²,

Sipkema³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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. Contractile reserve but not tension is reduced in monocrotaline-induced right ventricular hypertrophy. Am J Physiol Heart Circ Physiol 286: H979-H984, 2004. First published October 2, 2003 10.1152/ajpheart.00536.2002The objective of this study was to evaluate the role of right ventricular hypertrophy on developed tension (F dev) and contractile reserve of rat papillary muscle by using a model of monocrotaline (Mct)-induced pulmonary hypertension. Calcium handling and the influence of bicarbonate (HCO 3 Ϫ ) were also addressed with the use of two different buffers (HCO 3 Ϫ and HEPES). Wistar rats were injected with either Mct (40 mg/kg sc) or vehicle control (Con). Isometrically contracting right ventricular papillary muscles were studied at 80% of the length of maximal developed force. Contractile reserve (1 Ϫ F dev/Fmax) was calculated from Fdev and maximal tension (Fmax). Calcium recirculation was determined with postextrasystolic potentiation. Both groups of muscles were superfused with either HCO 3 Ϫ (Con-B and Mct-B, both n ϭ 6) or HEPES (Con-H and Mct-H, both n ϭ 6) buffer. With hypertrophy, contractions were slower but F dev was not changed. However, Fmax was decreased (P Ͻ 0.05). With HCO 3 Ϫ , Fmax decreased from 23.8 Ϯ 6.5 mN⅐mm Ϫ2 in Con-B, to 13.7 Ϯ 3.3 mN⅐mm Ϫ2 in Mct-B. With HEPES, it decreased from 16.3 Ϯ 3.5 mN⅐mm Ϫ2 (n ϭ 6, Con-H) to 8.3 Ϯ 1.6 mN⅐mm Ϫ2 (Mct-H). Contractile reserve during hypertrophy was therefore also decreased (P Ͻ 0. We evaluated the role of hypertrophy on F dev , twitch characteristics, and F max and potentiation in the rat papillary muscle with the use of the Mct model of right ventricular hypertrophy. We also studied the effect of hypertrophy on calcium handling by calculating the fraction of calcium recirculating to the sarcoplasmic reticulum (SR). To study the possible role of pH regulation, we used both the HCO 3 Ϫ and HEPES buffer because it was shown that changing the buffer from HEPES to HCO 3 Ϫ affects cytosolic pH (pH i ) in cardiac muscle (7,21,23). We also mimicked the HEPES buffer by using the Cl Ϫ /HCO 3 Ϫ exchanger blocker 4,4Ј-diisothiocyanostilbene-2,2Ј-disulfonic acid (DIDS), preventing HCO 3 Ϫ from entering the cell, and thus establishing the importance of HCO 3 Ϫ ions. METHODSAnimals. All animals were treated in accordance with the "Guiding Principles in the Care and Use of Laboratory Animals," as approved by the Council of the American Physiological Society and under the regulations of the Institutional Animal Care and Use Committee.Male Wistar rats (Harlan; Zeist, The Netherlands), weighing 170-190 g, were injected subcutaneously with either a single dose (29) of Mct (40 mg/kg in saline) or vehicle (Con).Papillary muscle preparation. Three weeks after Mct injection, the hearts were rapidly removed under ether anesthesia and transferred to ice-cold Tyrode solution. The hearts were transferred to a Langendorff setup and a papillary muscle was dissected as described before (38). The muscle was placed in a muscle bath and suspended between a Perspex pla...

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Section: Discussionmentioning

confidence: 86%

Contractile reserve but not tension is reduced in monocrotaline-induced right ventricular hypertrophy

Versluis¹,

Heslinga²,

Sipkema³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…Further work [16] has indicated that cardiac failure, induced by thoracic aortic banding, in the guinea-pig is associated with depressed relaxation rates and reduced protein expression of phospholamban and the SR Ca 2+ -ATPase. Additionally, the density of ryanodine-sensitive SR Ca 2+ -release channels was shown to be reduced in the mildly hypertrophied guinea-pig heart [27]. It is becoming increasingly apparent that alterations at the level of the cardiac SR have a major role to play in the modified activity of hypertrophied, intact, guinea-pig heart.…”

Section: Discussionmentioning

confidence: 98%

“…The role of intracellular membrane systems in the sensitivity of myocardial relaxation to cardiac load is emphasized by the finding that this ability is not a characteristic of single rat myocytes in which the membranes have been destroyed with detergent treatment [18]. Rannou and colleagues [27] found that the density of ryanodine receptors in guineapig myocardium was reduced during mild hypertrophy, whilst no alteration was demonstrated in the equivalent rat heart [27]. Hence, reduced densities of the SR Ca 2+ -release channel are implicated in mild left ventricular hypertrophy of the guinea-pig, but not in the rat.…”

Section: Introductionmentioning

confidence: 99%

Investigating the relaxation rate, following diazo-2 photolysis, of a skinned trabecular preparation from guinea-pig hypertrophied left ventricle

Johns

Ryder

Hodson

et al. 1999

Pflügers Arch – Eur J Physiol

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Cardiac hypertrophy in the guinea-pig is not accompanied by a large shift in the expression of the predominant isoform of myosin in the left ventricle; however, in this species, thin filament proteins do change. We examined the relaxation, following laser flash photolysis of the photolabile caged Ca2+ chelator diazo-2, of a skinned trabecular preparation from the left ventricle of guinea-pigs that had undergone abdominal aortic banding. Sham-operated animals were used as controls; no guinea-pigs showed any signs of heart failure. We report that mild cardiac hypertrophy does not affect the relaxation rate of Triton-skinned trabeculae from the guinea-pig. However, there was a 35% reduction in the maximum force generated by trabeculae from the left ventricle of the abdominal aortic-banded animals. Additionally, alterations in key troponin subunits occur in the left ventricle of guinea-pigs with mild hypertrophy. We conclude that the thin filament protein changes do not influence trabecular relaxation rates, even though they probably affect maximal force generation. The cellular membrane systems of the intact guinea-pig heart, which were not a factor in this present study, appear to have an important role in the altered cardiac relaxation rates seen in hypertrophy.

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“…[21][22][23][24][25] Changes in RyR expression have also been described during development of cardiac hypertrophy and failure. A decreased number of high-affinity Ryanocline binding sites are observed in compensatory cardiac hypertrophy in the rat, guinea-pig, and ferret, 26 and in canine heart failure. 27,28 In rat cardiac hypertrophy, the decrease in RyR2 mRNA and protein levels and the number of high-affinity binding sites are closely correlated to the length and severity of the pressure overload 29 ; however, no significant changes in RyR2 mRNA level or ryanodine binding were observed in other models.…”

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confidence: 99%

Cellular Distribution of Ca ²⁺ Pumps and Ca ²⁺ Release Channels in Rat Cardiac Hypertrophy Induced by Aortic Stenosis

et al. 1998

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Background-The response of ventricular myocytes to pressure overload is heterogeneous and not spatially coordinated.We investigated whether or not the alterations in SERCA and RyR gene expression are homogeneous within the myocardium. Methods and Results-The cellular distribution of mRNAs and proteins encoding the 2 sarco(endo)plasmic reticulum Ca 2ϩ -ATPase (SERCA) isoforms (SERCA 2a and 2b) and 2 Ca 2ϩ release channels (the ryanodine receptor, RyR, and the IP 3 receptor, IP 3 R) were analyzed by in situ hybridization and immunofluorescence, respectively. Analyses were performed during early (1 and 5 days) and late (1 month) stages of cardiac hypertrophy induced in rat by thoracic aortic stenosis (AS). The results indicated that 1 and 5 days after AS, the cellular distribution of SERCA 2a and RyR2 mRNAs in right ventricle and atrium was similar to controls but the mRNA levels appeared to decrease in some areas of the left ventricle (LV). One month after AS, the distribution of SERCA 2a mRNA and protein became heterogeneous throughout the LV, whereas RyR2 mRNA and protein levels were decreased in a homogeneous manner. SERCA 2b, poorly expressed in both cardiomyocytes and vessels of controls, was increased 4-fold 1 month after AS in coronary arteries only. In both sham (Sh) and AS, SERCA 3 and IP 3 R mRNAs were mainly found in the vessels. Conclusions-In

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The effects of compensated cardiac hypertrophy on dihydropyridine and ryanodine receptors in rat, ferret and guinea-pig hearts

Cited by 38 publications

References 38 publications

Contractile reserve but not tension is reduced in monocrotaline-induced right ventricular hypertrophy

Contractile reserve but not tension is reduced in monocrotaline-induced right ventricular hypertrophy

Investigating the relaxation rate, following diazo-2 photolysis, of a skinned trabecular preparation from guinea-pig hypertrophied left ventricle

Cellular Distribution of Ca ²⁺ Pumps and Ca ²⁺ Release Channels in Rat Cardiac Hypertrophy Induced by Aortic Stenosis

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The effects of compensated cardiac hypertrophy on dihydropyridine and ryanodine receptors in rat, ferret and guinea-pig hearts

Cited by 38 publications

References 38 publications

Contractile reserve but not tension is reduced in monocrotaline-induced right ventricular hypertrophy

Contractile reserve but not tension is reduced in monocrotaline-induced right ventricular hypertrophy

Investigating the relaxation rate, following diazo-2 photolysis, of a skinned trabecular preparation from guinea-pig hypertrophied left ventricle

Cellular Distribution of Ca 2+ Pumps and Ca 2+ Release Channels in Rat Cardiac Hypertrophy Induced by Aortic Stenosis

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Cellular Distribution of Ca ²⁺ Pumps and Ca ²⁺ Release Channels in Rat Cardiac Hypertrophy Induced by Aortic Stenosis