Bioenergetic remodeling of heart during treatment  of spontaneously hypertensive rats with enalapril

Leary, SC; Michaud, Denise; Lyons, C. N.; Hale, Taben M.; Bushfield, Terri L; Adams, Michael; Moyes, Christopher D.

doi:10.1152/ajpheart.00032.2002

Cited by 23 publications

(18 citation statements)

References 40 publications

(48 reference statements)

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“…ANG II facilitates changes in mitochondrial cytochrome c content (99). These results demonstrate that ANG II can depress mitochondrial energy metabolism and that the augmentation of antioxidants due to upregulation of HO-1 may reverse this depression, resulting in amelioration of mitochondrial function (Fig.…”

Section: Role Of Ho In Blood Pressure Regulationmentioning

confidence: 61%

Heme oxygenase: the key to renal function regulation

Abraham

Cao

Sacerdoti

et al. 2009

American Journal of Physiology-Renal Physiology

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Heme oxygenase (HO) plays a critical role in attenuating the production of reactive oxygen species through its ability to degrade heme in an enzymatic process that leads to the production of equimolar amounts of carbon monoxide and biliverdin/bilirubin and the release of free iron. The present review examines the beneficial role of HO-1 (inducible form of HO) that is achieved by increased expression of this enzyme in renal tissue. The influence of the HO system on renal physiology, obesity, vascular dysfunction, and blood pressure regulation is reviewed, and the clinical potential of increased levels of HO-1 protein, HO activity, and HO-derived end products of heme degradation is discussed relative to renal disease. The use of pharmacological and genetic approaches to investigate the role of the HO system in the kidney is key to the development of therapeutic approaches to prevent the adverse effects that accrue due to an impairment in renal function.

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Section: Role Of Ho In Blood Pressure Regulationmentioning

confidence: 61%

Heme oxygenase: the key to renal function regulation

Abraham

Cao

Sacerdoti

et al. 2009

American Journal of Physiology-Renal Physiology

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“…Since mitochondria, in association with myofibrils, represent a basic index of the potential cardiac work (Kayar et al, 1986;Barth et al, 1992), we suggest that, in the presence of both an accelerated contractile rhythm and a higher pumping capacity, the enlargement of the mitochondrial compartment provides the myofibrillar apparatus with an adequate amount of energetic compounds. A number of signalling mechanisms and transcription factors are known to contribute to the coordinated increase in mitochondrial content that is associated with cardiac growth in response to increased afterload (Leary et al, 2002, and references therein). The increase in the mitochondrial compartment of the compacta myocytes with growth, together with the smaller decrement of the myofibrillar compartment, suggests that the compacta may sustain a higher workload than the spongiosa.…”

Section: Discussionmentioning

confidence: 99%

Cardiac morphodynamic remodelling in the growing eel (Anguilla anguilla L.)

Cerra

Imbrogno

Amelio

et al. 2004

Journal of Experimental Biology

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The morphodynamic changes occurring during growth were evaluated in the eel (Anguilla anguilla L.) heart. Using an in vitro working heart preparation, cardiac performance of small (body mass 96.76±27.49·g; mean ± S.D.) and large (body mass 656±12·g; mean ± S.D.) eels was compared under basal conditions and under loading (i.e. preload and afterload) challenges. A parallel morphometric evaluation of the ventricle was made using light and transmission electron microscope images.The small eel hearts show a basal cardiac output lower than their large counterparts (heart rate fH, 38.93±2.82 and 52.7±1.8·beats·min -1 , respectively; stroke volume VS, 0.27±0.017 and 0.37±0.016·ml·kg -1 , respectively; means ± S.E.M.). The two groups show similar responses at increasing preload, but differ remarkably at increasing afterload. Small eel hearts decreased VS at afterload greater than 3·kPa, in contrast to larger hearts, which maintained constant VS up to 6·kPa. These changes in mechanical performance are related to structural differences.Compared with the small eels, the large eels show an increase in the compacta thickness and in the diameter of the trabeculae in the spongiosa, together with reduction of the lacunary spaces. The increased compacta thickness is attained by enlargements of both the muscular and vascular compartments and reduction of the interstitium; consequently, this layer appears more compacted. Both compacta and spongiosa show higher number of myocytes together with reduced cross-sectional area and myofibrillar compartment. The compacta also shows an increased mitochondrial compartment. Our results document a cardiac morphodynamic remodelling in the growing eel.

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“…Because AP-1 regulates cytochrome c expression (437), it was suggested that JNK may facilitate changes in the mitochondrial content of cytochrome c in response to ANG II (241).…”

Section: The Renin-angiotensin Systemmentioning

confidence: 99%

Angiotensin II blockade: how its molecular targets may signal to mitochondria and slow aging. Coincidences with calorie restriction and mTOR inhibition

Cavanagh

Inserra

Ferder

2015

American Journal of Physiology-Heart and Circulatory Physiology

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de Cavanagh EM, Inserra F, Ferder L. Angiotensin II blockade: how its molecular targets may signal to mitochondria and slow aging. Coincidences with calorie restriction and mTOR inhibition. Am J Physiol Heart Circ Physiol 309: H15-H44, 2015. First published May 1, 2015; doi:10.1152/ajpheart.00459.2014, renin angiotensin system blockade (RAS-bl), and rapamycin-mediated mechanistic target of rapamycin (mTOR) inhibition increase survival and retard aging across species. Previously, we have summarized CR and RAS-bl's converging effects, and the mitochondrial function changes associated with their physiological benefits. mTOR inhibition and enhanced sirtuin and KLOTHO signaling contribute to the benefits of CR in aging. mTORC1/mTORC2 complexes contribute to cell growth and metabolic regulation. Prolonged mTORC1 activation may lead to age-related disease progression; thus, rapamycin-mediated mTOR inhibition and CR may extend lifespan and retard aging through mTORC1 interference. Sirtuins by deacetylating histone and transcription-related proteins modulate signaling and survival pathways and mitochondrial functioning. CR regulates several mammalian sirtuins favoring their role in aging regulation. KLOTHO/fibroblast growth factor 23 (FGF23) contribute to control Ca 2ϩ , phosphate, and vitamin D metabolism, and their dysregulation may participate in age-related disease. Here we review how mTOR inhibition extends lifespan, how KLOTHO functions as an aging suppressor, how sirtuins mediate longevity, how vitamin D loss may contribute to age-related disease, and how they relate to mitochondrial function. Also, we discuss how RAS-bl downregulates mTOR and upregulates KLOTHO, sirtuin, and vitamin D receptor expression, suggesting that at least some of RAS-bl benefits in aging are mediated through the modulation of mTOR, KLOTHO, and sirtuin expression and vitamin D signaling, paralleling CR actions in age retardation. Concluding, the available evidence endorses the idea that RAS-bl is among the interventions that may turn out to provide relief to the spreading issue of age-associated chronic disease. mechanistic target of rapamycin; vitamin D; caloric restriction; renin-angiotensin system EFFORTS AIMED AT DECIPHERING the mechanisms that underlie the aging process have unveiled three interventions that can increase survival and retard age-related diseases from lower organisms to mammals, i.e., caloric restriction (CR) (84,85,140,160,334), mechanistic target of rapamycin (mTOR; originally mammalian TOR) inhibition by rapamycin (173,196,281), and renin-angiotensin system blockade (RAS-bl) (20, 21, 26,63,253,284,354), although the latter has been less studied. In light of these findings, some intriguing questions come to mind: Do these interventions attenuate aging by interfering with common mechanisms? Do the mechanisms that are interfered with by CR, rapamycin, and RAS-bl mutually affect each other? Are there any pathways involved exclusively with a certain intervention?Previously (101), we have discussed the converging effects d...

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Bioenergetic remodeling of heart during treatment of spontaneously hypertensive rats with enalapril

Cited by 23 publications

References 40 publications

Heme oxygenase: the key to renal function regulation

Heme oxygenase: the key to renal function regulation

Cardiac morphodynamic remodelling in the growing eel (Anguilla anguilla L.)

Angiotensin II blockade: how its molecular targets may signal to mitochondria and slow aging. Coincidences with calorie restriction and mTOR inhibition

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