Differences in regional capillary distribution and myocyte sizes in normal and hypertrophic rat hearts

Gerdes, A. Martin; Callas, Gerald; Kasten, Frederick H.

doi:10.1002/aja.1001560406

Cited by 68 publications

(39 citation statements)

References 22 publications

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“…Hyperthyroidism is associated with an elevated cardiac output, cardiac hypertrophy, and mild hypertension. 37 - 38 The extent of cardiac hypertrophy induced by hyperthyroidism was comparable with that of hypertensive animals, but no change in cardiac cGMP kinase concentration was measured (Table 2).…”

Section: Cgmp Kinase and Cardiac Hypertrophymentioning

confidence: 82%

“…37 -39 - 45 ' 46 Both types of measurements suggest that cardiac hypertrophy caused by thyrotoxicosis is associated with an adequate proliferation of capillaries and that the cross-sectional area of the small arterioles (determined by the minimal coronary resistance) matches the increased ventricular weight. 37 - 38 In contrast, pressure-induced cardiac hypertrophy is reportedly associated with a decreased density of capillaries and a relative decrease in the cross-sectional area of small arterioles. 39 - 45 ' 46 The latter finding does not directly prove that a decreased cross-sectional area is caused by a decreased proliferation of the arterioles since hypertrophy of the walls of the resistance vessels 47 or extravasal compression 48 might as well contribute to a decreased cross-sectional area of the resistance vessels.…”

Section: Discussionmentioning

confidence: 99%

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Decreased cardiac concentration of cGMP kinase in hypertensive animals. An index for cardiac vascularization?

Ecker

Göbel

Hullin

et al. 1989

Circulation Research

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Cyclic GMP (cGMP) kinase is ultimately involved in the regulation of vascular smooth muscle tone. Its tissue concentration was determined in normotensive and hypertensive rats by use of monospecinc antJ-cGMP kinase antibodies. Hearts of spontaneously hypertensive rats and renovascular (Goldblatt II) hypertensive rats contained half the concentration of cGMP kinase than those of the respective normotensive animals. The increase in blood pressure and the resulting left ventricular hypertrophy were correlated inversely with the left ventricular cGMP kinase concentration. This decrease was specific for the left ventricle and was not observed in other tissues. In addition, the cardiac concentration of cGMP kinase was unchanged in hyperthyroid animals that had comparable left ventricular hypertrophy and mild hypertension. This suggested that in severe renovascular hypertension the decrease in cardiac cGMP kinase concentration is caused by a relative lack of cardiac vessel growth during the development of hypertrophy. In agreement with this conclusion, immunohistochemistry of cardiac cross sections showed that cGMP kinase was exclusively located in cardiac vessels. In support of this localization, the maximal arterial blood flow of heart, liver, skeletal muscle, and kidney correlated excellently with the cGMP kinase content of the respective organ. These results suggest that the cGMP kinase concentration of nonsmooth muscle tissues depends on the amount of organ-specific vascular smooth muscle and may be used as an index for the vascularization of these organs. {Circulation Research 1989;65:1361-1369 C yclic GMP (cGMP) is a major relaxing factor in vascular and nonvascular smooth muscle. 1 -4 The cytosolic cGMP level is stimulated by atrial natriuretic peptides, endotheliumderived relaxation factor, and several cardiovascular therapeutics, including sodium nitroprusside and nitroglycerin. The drug-or hormone-induced increase in cGMP is associated with a decrease in the cytosolic calcium concentration in smooth muscle.5 " 7 Recent experiments indicate that activation of cGMP kinase 8 or introduction of active cGMP kinase 7 induces relaxation of smooth muscle strips and/or decreases cytosolic calcium.

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Section: Cgmp Kinase and Cardiac Hypertrophymentioning

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Decreased cardiac concentration of cGMP kinase in hypertensive animals. An index for cardiac vascularization?

Ecker

Göbel

Hullin

et al. 1989

Circulation Research

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“…19,21,22,36 We believe that the spatial context of the mechanical signals that are applied to different areas of the heart may contribute to this regional variation and ultimately shape the architecture of the ventricular wall. For example, in a volume overload, the ventricle is deformed 5 and dilates along the circumferential axis of the heart.…”

Section: Discussionmentioning

confidence: 99%

“…In vivo, myocytes of the endomyocardium undergo a greater increase in cell size than myocytes residing in the midwall or epimyocardium during eccentric hypertrophy. 19,21,41 In concentric hypertrophy, there is a selective increase in cell diameter, very little or no dilation of the ventricular lumen, and a marked increase in the diameter of the ventricular wall. 42 Mapping regional stresses during the contractile cycle indicates that the principal axis of shortening varies considerably less than the local myofiber orientation.…”

Section: Discussionmentioning

confidence: 99%

Regulation of Cardiac Myocyte Protein Turnover and Myofibrillar Structure In Vitro by Specific Directions of Stretch

Simpson

Majeski

Borg

et al. 1999

Circulation Research

103

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Abstract-We have examined how different degrees (0.5%, 1.0%, 2.5%, 5.0%, and 10.0%) and directions of stretch regulate the turnover and accumulation of contractile proteins in cultured neonatal cardiac myocytes (NCMs). In pulse-chase experiments, stellate-shaped NCMs with random arrays of myofibrils (MFs) exhibited a threshold response to stretch. With respect to unstretched controls, the turnover of the contractile protein pool was suppressed 50% to 100% in stellate NCMs stretched 1.0% to 5.0% and was unaltered in stellate NCMs stretched 0.5% or 10.0%. The posttranslational metabolism of myosin heavy chain (MHC) and actin was regulated in parallel with the total contractile protein pool. The turnover of the cytoplasmic protein pool remained unchanged in response to stretch. NCMs plated onto an aligned matrix of type I collagen expressed an elongated, rod-like cell shape. The MFs of these cells were distributed in parallel with one another along a single unique axis. The tissue-like pattern of organization of these cultures made it possible to assay how specific directions of stretch affected cardiac protein turnover and MF organization. In pulse-chase experiments, stretch in parallel with the MFs did not alter the turnover of the total contractile protein pool, the cytoplasmic protein pool, MHC, or actin. The total cellular concentration of MHC and actin remained constant, and MF alignment was not overtly affected. In contrast, even modest degrees of stretch across the short axis of the MFs suppressed total contractile protein turnover, the turnover of MHC and actin, and promoted the accumulation of these MF subunits. The parallel alignment of MFs deteriorated in myocytes stretched greater than 5%. The characteristic response of aligned myocytes to stretch was not affected by the contractile state of the cells. Key Words: stretch Ⅲ myofibril Ⅲ hypertrophy T he intact myocardium is composed of a complex array of muscle cells that are distributed in a series of discrete, overlapping cellular layers. Within each cell layer, the rodlike myocytes of the heart are distributed in parallel with one another along a common axis. In the subendocardium and subepicardium of the left ventricle, the myocytes are arranged in a longitudinal orientation that is in parallel with the long axis of the heart. 1 The muscle cells of the midwall radiate in a circumferential pattern around the ventricular lumen and are oriented Ϸ90°off-axis with respect to the more superficial and deep cell layers. 2 Adjacent cell layers are interconnected and tethered to one another by an elaborate network of collagen fibrils. 3 As a result of the intricate organization of the intact heart, cardiac myocytes are subjected to a very complex set of mechanical forces during the contractile cycle. For example, in working hearts, the axis of shortening during contraction varies considerably less than the local myofiber direction. 2,4,5 The data from these experiments indicate that any given local population of myocytes may be exposed to a unique combination ...

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“…Although TH and analogues are pro-angiogenic in various models, as reported earlier, their effects at the microvascular level remain controversial, with reports of unchanged (Wachtlova et al 1985, Breisch et al 1989, Heron & Rakusan 1994 or even reduced (Gerdes et al 1979, Weiss & Grover 1987, Tomanek et al 1995, Anjos-Ramos et al 2006 cardiac capillary density in hyperthyroid rats. Cardiac capillary density was found to be increased in hypothyroid rats (Heron & Rakusan 1994) and rabbits (Tomanek et al 1993).…”

Section: Introductionmentioning

confidence: 99%

Influence of thyroid state on cardiac and renal capillary density and glomerular morphology in rats

Rodríguez-Gómez

Banegas

Wangensteen

et al. 2012

Journal of Endocrinology

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The purpose was to analyse the cardiac and renal capillary density and glomerular morphology resulting from a chronic excess or deficiency of thyroid hormones (THs) in rats. We performed histopathological, morphometrical and immunohistochemical analyses in hypothyroid and hyperthyroid rats to evaluate the density of mesenteric, renal and cardiac vessels at 4 weeks after induction of thyroid disorders. The main angiogenic factors in plasma, heart and kidney were measured as possible mediators of vascular changes. Mesenteric vessel branching was augmented and decreased in hyper-and hypothyroid rats respectively. The numerical density of CD31-positive capillaries was higher in left and right ventricles and in cortical and medullary kidney from both hyper-and hypothyroid rats vs controls. Numbers of podocytes and glomeruli per square millimetre were similar among groups. Glomerular area and percentage mesangium were greater in the hyperthyroid vs control or hypothyroid groups. No morphological renal lesions were observed in any group. Vascularisation of the mesenteric bed is related to TH levels, but an increased capillarity was observed in heart and kidney in both thyroid disorders. This increase may be produced by higher tissue levels of angiogenic factors in hypothyroid rats, whereas haemodynamic factors would predominate in hyperthyroid rats. Our results also indicate that the renal dysfunctions of thyroid disorders are not related to cortical or medullary microvascular rarefaction and that the proteinuria of hyperthyroidism is not secondary to a podocyte deficit. Finally, TH or its analogues may be useful to increase capillarity in renal diseases associated with microvascular rarefaction.

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Differences in regional capillary distribution and myocyte sizes in normal and hypertrophic rat hearts

Cited by 68 publications

References 22 publications

Decreased cardiac concentration of cGMP kinase in hypertensive animals. An index for cardiac vascularization?

Decreased cardiac concentration of cGMP kinase in hypertensive animals. An index for cardiac vascularization?

Regulation of Cardiac Myocyte Protein Turnover and Myofibrillar Structure In Vitro by Specific Directions of Stretch

Influence of thyroid state on cardiac and renal capillary density and glomerular morphology in rats

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