Effect of sodium deprivation on cardiac hypertrophy in spontaneously hypertensive rats: Influence of aging

Sen, Subha; Young, D. R.

doi:10.1016/0022-2828(91)90979-v

Cited by 8 publications

(8 citation statements)

References 22 publications

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“…Myosin was extracted from approximately 300 mg of the ventricle, as described previously. 9 The tissue was homogenized in a saline buffer and centrifuged at 3,000 rpm. The supernatant was discarded and the pellet washed again in phosphate‐buffered saline.…”

Section: Methodsmentioning

confidence: 99%

Myocardial Response to Stress in Cardiac Hypertrophy and Heart Failure: Effect of Antihypertensive Drugs^a

Sen

1999

Annals of the New York Academy of Sciences

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The myocardium's response to increased stress or load is not stereotyped. Differences have been observed in the heart's molecular composition and performance characteristics when exposed to stress. Myosin isoforms gradually change during development of hypertrophy, whereas collagen levels change only during the chronic phase of hypertrophy. Cardiac hypertrophy can regress if treated with antihypertensive drugs, but the myocardium of the post-hypertrophic heart no longer has the same composition as it did before hypertrophy. In rat studies of the effects of antihypertensive drugs on cardiac functional reserve, captopril showed a regression of hypertrophy associated with a lower baseline stroke volume and, after dobutamine stress, a dose-dependent rise in stroke volume. In untreated rates captopril showed no change in stroke volume. In hydralazine-treated rats, there was no change in reserve after dobutamine stress, whereas propranolol treatment resulted in partial regression and a slight change in stroke volume. Overall, our data suggests that development of hypertension and hypertrophy plays a role in changes in the molecular structure of the myocardium, especially during the chronic phase of hypertrophy and heart failure. This complex process cannot be explained by one factor but involves a combination of factors. Identification of each factor would be of importance for the development of appropriate therapeutic agents.

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Section: Methodsmentioning

confidence: 99%

Myocardial Response to Stress in Cardiac Hypertrophy and Heart Failure: Effect of Antihypertensive Drugs^a

Sen

1999

Annals of the New York Academy of Sciences

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“…Alterations in the composition and distribution of isoforms of contractile proteins in hypertension have been demonstrated [62, 63]. However, little has been reported on either the modification or the changes in the composition of these proteins in hyperhomocysteinemia.…”

Section: Contractile Proteins and Hypertension: H2s Is A Key Playermentioning

confidence: 99%

Homocysteine to Hydrogen Sulfide or Hypertension

Sen

Mishra

Tyagi

et al. 2010

Cell Biochem Biophys

146

127

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Hyperhomocysteinemia, an increased level of plasma homocysteine, is an independent risk factor for the development of premature arterial fibrosis with peripheral and cerebro-vascular, neurogenic and hypertensive heart disease, coronary occlusion and myocardial infarction, as well as venous thromboembolism. It is reported that hyperhomocysteinemia causes vascular dysfunction by two major routes: (1) increasing blood pressure and, (2) impairing the vasorelaxation activity of endothelial-derived nitric oxide. The homocysteine activates metalloproteinases and induces collagen synthesis and causes imbalances of elastin/collagen ratio which compromise vascular elastance. The metabolites from hyperhomocysteinemic endothelium could modify components of the underlying muscle cells, leading to vascular dysfunction and hypertension. Homocysteine metabolizes in the body to produce H 2 S, which is a strong antioxidant and vasorelaxation factor. At an elevated level, homocysteine inactivates proteins by homocysteinylation including its endogenous metabolizing enzyme, cystathionine γ-lyase. Thus, reduced production of H 2 S during hyperhomocysteinemia exemplifies hypertension and vascular diseases. In light of the present information, this review focuses on the mechanism of hyperhomocysteinemia-associated hypertension and highlights the novel modulatory role of H 2 S to ameliorate hypertension.

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“…However, independent of sympathetically-mediated changes in peripheral vascular function, chronically elevated SNA can have direct effects on myocardial structure and function. Administration of sub-pressor doses of noradrenaline have been reported to have a direct trophic effect on cardiac myocytes and increase left ventricular mass and wall thickness in animals (Sen and Young, 1991; Simpson, 1983). Similarly, it has recently been demonstrated in essential hypertensive patients that left ventricular hypertrophy, as determined using cardiac magnetic resonance imaging, is related to elevations in muscle SNA (Burns et al, 2007).…”

Section: Consequences Of Central Sympathetic Overactivitymentioning

confidence: 99%

Central sympathetic overactivity: Maladies and mechanisms

Fisher¹,

Young²,

Fadel³

2009

Autonomic Neuroscience

163

136

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There is growing evidence to suggest that many disease states are accompanied by chronic elevations in sympathetic nerve activity. The present review will specifically focus on central sympathetic overactivity and highlight three main areas of interest: 1) the pathological consequences of excessive sympathetic nerve activity; 2) the potential role of centrally derived nitric oxide in the genesis of neural dysregulation in disease; and 3) the promise of several novel therapeutic strategies targeting central sympathetic overactivity. The findings from both animal and human studies will be discussed and integrated in an attempt to provide a concise update on current work and ideas in these important areas.

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Effect of sodium deprivation on cardiac hypertrophy in spontaneously hypertensive rats: Influence of aging

Cited by 8 publications

References 22 publications

Myocardial Response to Stress in Cardiac Hypertrophy and Heart Failure: Effect of Antihypertensive Drugs^a

Myocardial Response to Stress in Cardiac Hypertrophy and Heart Failure: Effect of Antihypertensive Drugs^a

Homocysteine to Hydrogen Sulfide or Hypertension

Central sympathetic overactivity: Maladies and mechanisms

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Effect of sodium deprivation on cardiac hypertrophy in spontaneously hypertensive rats: Influence of aging

Cited by 8 publications

References 22 publications

Myocardial Response to Stress in Cardiac Hypertrophy and Heart Failure: Effect of Antihypertensive Drugsa

Myocardial Response to Stress in Cardiac Hypertrophy and Heart Failure: Effect of Antihypertensive Drugsa

Homocysteine to Hydrogen Sulfide or Hypertension

Central sympathetic overactivity: Maladies and mechanisms

Contact Info

Product

Resources

About

Myocardial Response to Stress in Cardiac Hypertrophy and Heart Failure: Effect of Antihypertensive Drugs^a

Myocardial Response to Stress in Cardiac Hypertrophy and Heart Failure: Effect of Antihypertensive Drugs^a