Journal ArticleDOI
Effect of peripheral sympathectomy on left ventricular ultrastructure in young spontaneously hypertensive rats
Ernest Page,Suzanne Oparil +1 more
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It is suggested that in this model NGFAS affects mitochondrial concentration either via its effect on arterial blood pressure and/or via some other, unidentified mechanism, and the decreased mitochondrial concentration in myocardial cells of untreated SH rats need not be causally related to the observed cardiac dysfunction.About:
This article is published in Journal of Molecular and Cellular Cardiology.The article was published on 1978-03-01. It has received 14 citations till now. The article focuses on the topics: Ventricular hypertrophy & Left ventricular hypertrophy.read more
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Journal ArticleDOI
Structural and functional consequence of neonatal sympathectomy on the blood vessels of spontaneously hypertensive rats.
TL;DR: One of the primary roles of the overactive sympathetic nervous system in the development of hypertension in SHR is manifested through its trophic effect on the arteries of SHR, which appears to cause a hyperplastic change in the smooth muscle cells in the reactive and resistance vessels.
Journal ArticleDOI
Primary versus secondary structural changes of the blood vessels in hypertension.
Robert M.K.W. Lee,John S. Smeda +1 more
TL;DR: Recent studies involving the mesenteric and renal arteries of Wistar-Kyoto spontaneously hypertensive rats have shown that wall thickening of the vasculature occurs prior to hypertension development and is present even under conditions where the blood pressure has been normalized throughout the animal's life, suggesting that some structural alterations in the blood vessels observed in hypertension are pressure independent and could be of etiological importance in the initiation of hypertension.
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Combined effect of neonatal sympathectomy and adrenal demedullation on blood pressure and vascular changes in spontaneously hypertensive rats.
TL;DR: It is concluded that in sympathectomized SHR, the elevated BP was maintained by the adrenal medulla, and demedullation increased the lumen size of muscular arteries under maximally relaxed conditions, which might explain the further reduction in BP in these animals.
Journal ArticleDOI
The effects of long-term pressure-overload and aging on the myocardium.
TL;DR: Evidence is provided for three conclusions regarding cardiac hypertrophy and hypertension, and aging in SHR: changes which are inevitable with aging are accentuated, certain ultrastructural changes appear to be related to long-term hypertension rather than to the natural aging process.
BookDOI
Functional aspects of the normal, hypertrophied, and failing heart
Francis L. Abel,Walter H. Newman +1 more
TL;DR: The role of mechanical factors in the Regulation of Coronary Blood Flow in Normal and Failing Hearts and the role of Calcium in Heart Function and Metabolism are studied.
References
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Journal ArticleDOI
The nerve-growth factor.
TL;DR: Nerve growth factor is a signaling protein and growth factor implicated in a wide range of development and maintenance functions and has been implicated in immune function, stress response, nerve maintenance, and in neurodegenerative diseases.
Journal ArticleDOI
Development of left ventricular hypertrophy in young spontaneously hypertensive rats after peripheral sympathectomy.
TL;DR: The data suggest that the development of myocardial hypertrophy andMyocardial dysfunction in the SH rat is in part independent of hypertension and plasma renin activity.
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Myofibrillar Mass in Rat and Rabbit Heart Muscle: CORRELATION OF MICROCHEMICAL AND STEREOLOGICAL MEASUREMENTS IN NORMAL AND HYPERTROPHIC HEARTS
TL;DR: After production of left ventricular hypertrophy in rats by constriction of the ascending aorta, both myofibrillar Mg and volume increased proportionately more than tissue dry mass and cell volume, and the ratio of mitochondrial volume to cell volume decreased.
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Ultrastructural changes in hypertrophied myocardium of spontaneously hypertensive rats.
TL;DR: Heterogeneous changes of the contractile material, mitochondria and sarcoplasmic matrix were more prominent, suggesting heterogeneous malfunctions in later stages of cardiac hypertrophy.