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PubMed1999

Cell cycle inhibitors (p27Kip1 and p21CIP1) cause hypertrophy in LLC-PK1 cells.

BACKGROUND: Angiotensin II has been reported to induce renal tubular hypertrophy, but the mechanisms of this hypertrophy are not well known. We evaluated the roles of cyclin-dependent kinase (CDK) inhibitors in renal tubular hypertrophy. METHODS: To elucidate whether CDK inhibitors cause renal tubular hypertrophy, we produced adenovirus vectors containing coding sequences of the CDK inhibitors p27Kip1 (AxCAp27), p21CIP1 (AxCAp21), and p16INK4 (AxCAp16), and we investigated the effect of these gene transfers on epidermal growth factor (EGF)-induced proliferation in LLC-PK1 cells. We evaluated the cell cycle and hypertrophy by measurements of the [3H]-leucine and [3H]-thymidine incorporation, the protein:DNA ratio, flow cytometry, and CDK4 and CDK2 kinase assays. RESULTS: AxCAp27 and AxCAp21 caused significant increases in [3H]-leucine incorporation and the protein:DNA ratio but did not change the [3H]-thymidine incorporation. Conversely, AxCAp16 inhibited EGF-stimulated [3H]-thymidine incorporation but did not change the [3H]-leucine incorporation. AxCAp27, AxCAp21, and AxCAp16 all inhibited EGF-stimulated CDK4 kinase activity (to 15.6, 14.1, and 21.9% of control, respectively). Forward light-scatter analysis demonstrated that AxCAp27 and AxCAp21 increased the cell size but that AxCAp16 effected no change in cell size. CONCLUSION: These findings suggest that p27Kip1 and p21CIP1 may play an important role in hypertrophy of renal tubule cells by reducing pRb phosphorylation. On the other hand, p16INK4 was not found to cause hypertrophic changes in EGF-treated LLC-PK1 cells.

Adenoviridae↗
PubMed1999

Molecular mechanisms of diabetic renal hypertrophy.

Altered growth of renal cells is one of the early abnormalities detected after the onset of diabetes. Cell culture studies whereby renal cells are exposed to high glucose concentrations have provided a considerable amount of insight into mechanisms of growth. In the glomerular compartment, there is a very early and self-limited proliferation of mesangial cells with subsequent hypertrophy, whereas proximal tubular cells primarily undergo hypertrophy. There is overwhelming evidence from in vivo and cell culture studies that induction of the transforming growth factor-beta (TGF-beta) system mediates the actions of high ambient glucose and that this system is pivotal for the hypertrophy of mesangial and tubular cells. Other factors such as hemodynamic forces, protein glycation products, and several mediators (for example, angiotensin II, endothelin-1, thromboxane, and platelet-derived growth factor) may further amplify the synthesis of TGF-beta and/or the expression of its receptors in the diabetic state. Cellular hypertrophy can be characterized by cell cycle arrest in the G1 phase. The molecular mechanism arresting mesangial cells in the G1 phase of the cell cycle is the induction of cyclin-dependent kinase (CdK) inhibitors such as p27Kip1 and p21, which bind to and inactivate cyclin-CdK complexes responsible for G1-phase exit. High-glucose-induced activation of protein kinase C and stimulated TGF-beta expression appear to be essential for stimulated expression of p27Kip1. In addition, a decreased turnover of protein caused by the inhibition of proteases contributes to hypertrophy. The development of irreversible renal changes in diabetes mellitus such as glomerulosclerosis and tubulointerstitial fibrosis is always preceded by the early hypertrophic processes in the glomerular and the tubular compartments. It may still be debated whether diabetic renal hypertrophy will inevitably lead to irreversible fibrotic changes in the absence of other factors such as altered intraglomerular hemodynamics and genetic predisposition. Nevertheless, understanding cellular growth on a molecular level may help design a novel therapeutic approach to prevent or treat diabetic nephropathy effectively.

Animals↗
PubMed1999

Nifedipine does not impede clenbuterol-stimulated muscle hypertrophy.

The mechanism(s) responsible for beta2-adrenergic receptor-mediated skeletal muscle and cardiac hypertrophy remains undefined. This study examined whether calcium influx through L-type calcium channels contributed to the development of cardiac and skeletal muscle (plantaris; gastrocnemius; soleus) hypertrophy during an 8-day treatment with the beta2-adrenergic receptor agonist clenbuterol. Concurrent blockade of L-type calcium channels with nifedipine did not reverse the hypertrophic action of clenbuterol. Moreover, nifedipine treatment alone resulted in both cardiac and soleus muscle hypertrophy (6% and 7%, respectively), and this effect was additive to the clenbuterol-mediated hypertrophy in the heart and soleus muscles. The hypertrophic effects of nifedipine were not associated with increases in total beta-adrenergic receptor density, nor did nifedipine reverse clenbuterol-mediated beta-adrenergic receptor downregulation in either the left ventricle or soleus muscle. Both nifedipine and clenbuterol-induced hypertrophy increased total protein content of the soleus and left ventricle, with no change in protein concentration. In conclusion, our results support the hypothesis that beta2-adrenergic receptor agonist-induced muscle hypertrophy is mediated by mechanisms other than calcium influx through L-type calcium channels.

Adrenergic beta-Agonists↗
PubMed2002

Prevalence and prognosis of electrocardiographic left ventricular hypertrophy, ST segment depression and negative T-wave; the Copenhagen City Heart Study.

AIMS: To evaluate the prevalence and the independent prognosis of electrocardiographic left ventricular hypertrophy by voltage only, ST depression and negative T wave, isolated negative T wave and left ventricular hypertrophy plus ST depression and negative T wave for cardiac morbidity and mortality, without known ischaemic heart disease at baseline. METHODS AND RESULTS: Follow-up data from the Copenhagen City Heart Study were used. Subjects were 5243 men and 6391 women, age range 25-74 years. End-points were (1) myocardial infarction, (2) ischaemic heart disease and (3) cardiovascular disease mortality. Relative risk was age- and sex-adjusted, and multivariately adjusted for known cardiovascular risk factors. During 7 years follow-up, left ventricular hypertrophy plus ST depression and negative T wave had an age-adjusted relative risk of 3.78 (95% confidence interval 2.29-6.25) for myocardial infarction, 4.27 (2.95-6.16) for ischaemic heart disease and 3.75 (2.41-5.85) for cardiovascular disease. A negative T wave, ST depression and negative T wave changes, and left ventricular hypertrophy with negative T wave also carry independent prognostic information for myocardial infarction, ischaemic heart disease and cardiovascular disease. CONCLUSIONS: Electrocardiographic left ventricular hypertrophy with ST depression and negative T wave changes are the electrocardiographic abnormalities with the greatest prognostic information for future cardiac events. Electrocardiographic negative T waves, ST depression and negative T wave abnormalities and left ventricular hypertrophy with negative T waves, also have prognostic information.

Adult↗
PubMed2000

Dietary creatine monohydrate supplementation increases satellite cell mitotic activity during compensatory hypertrophy.

Nutritional status influences muscle growth and athletic performance, but little is known about the effect of nutritional supplements, such as creatine, on satellite cell mitotic activity. The purpose of this study was to examine the effect of oral creatine supplementation on muscle growth, compensatory hypertrophy, and satellite cell mitotic activity. Compensatory hypertrophy was induced in the rat plantaris muscle by removing the soleus and gastrocnemius muscles. Immediately following surgery, a group of six rats was provided with elevated levels of creatine monohydrate in their diet. Another group of six rats was maintained as a non-supplemented control group. Twelve days following surgery, all rats were implanted with mini-osmotic pumps containing the thymidine analog 5-bromo-2'-deoxyuridine (BrdU) to label mitotically active satellite cells. Four weeks after the initial surgery the rats were killed, plantaris muscles were removed and weighed. Subsequently, BrdU-labeled and non-BrdU-labeled nuclei were identified on enzymatically isolated myofiber segments. Muscle mass and myofiber diameters were larger (P < 0.05) in the muscles that underwent compensatory hypertrophy compared to the control muscles, but there were no differences between muscles from creatine-supplemented and non-creatine-supplemented rats. Similarly, compensatory hypertrophy resulted in an increased (P < 0.05) number of BrdU-labeled myofiber nuclei, but creatine supplementation in combination with compensatory hypertrophy resulted in a higher (P < 0.05) number of BrdU-labeled myofiber nuclei compared to compensatory hypertrophy without creatine supplementation. Thus, creatine supplementation in combination with an increased functional load results in increased satellite cell mitotic activity.

Administration, Oral↗
PubMed2003

QT dispersion in elderly athletes with left ventricular hypertrophy.

The purpose of this study was to examine the QT dispersion in elderly endurance athletes with left ventricular (LV) hypertrophy. Sixteen athletes (males, mean age 67.6 +/- 4.5 years) with mild to moderate LV hypertrophy, were compared with 16 age-matched hypertensive patients with similar degree of LV hypertrophy and 16 age-matched healthy sedentary controls. All the participants underwent echocardiogram and 12-lead electrocardiogram. QT dispersion was defined as the difference between maximum and minimum QT intervals in the different leads. QT dispersion was corrected (QTc) for heart rate according to Bazett's formula. The results showed in athletes and hypertensive patients comparable LV mass (258.2 +/- 14.2 vs. 262.4 +/- 16.8 g, ns), which was significantly higher than that of controls (p < 0.001). Trained subjects had QT dispersion (38.6 +/- 10.2 ms) and QTc dispersion (39.4 +/- 11.3 ms) significantly lower than hypertensive patients (QT dispersion: 68.4 +/- 11.4 ms; QTc dispersion: 72.2 +/- 8.4, p < 0.001) and comparable with controls (QT dispersion: 44.3 +/- 8.4 ms; QTc dispersion: 46.2 +/- 6.2 ms, ns). In conclusion, in elderly athletes training-induced myocardial hypertrophy was characterized by a QT dispersion significantly lower than hypertensive myocardial hypertrophy. This could provide a simple and inexpensive screening method for differentiating physiologic from pathologic myocardial hypertrophy in elderly subjects.

Aged↗
PubMed1995

Aldosterone levels and cardiac hypertrophy in professional cyclists.

Aldosterone has been associated with the development of cardiac hypertrophy and a correlation has been found between levels of aldosterone and the degree of cardiac hypertrophy in hypertensive patients. Our study aimed to test the relation between physiologic cardiac hypertrophy and serum aldosterone in a group of highly trained cyclists. Determination of the left ventricular mass index (LVMI) was performed in a group of 40 professional cyclists by using Devereux's formula with correction for body surface area. After an overnight fast, blood samples were collected and serum aldosterone levels were measured using RIA. LVMI and serum aldosterone were intercorrelated using linear regression analysis. Twenty-three of the 40 cyclists (58%) presented an LVMI > 130 g.m-1 and the other 17 subjects (42%) presented an LVMI < 130 g.m-1. Serum aldosterone levels did not correlate with LVMI in either of the groups (LVMI > 130 g.m-1, r = -0.089; LVMI < 130 g.m-1, r = 0.146). The lack of correlation of this hypertrophy with serum aldosterone levels suggests that physiologic hypertrophy of the athlete's heart could be caused by a different stimulus to that seen in pathologic hypertrophy of hypertensives.

Adult↗
PubMed1995

An atypical variant of Fabry's disease in men with left ventricular hypertrophy.

BACKGROUND: Fabry's disease is considered very rare. Left ventricular hypertrophy is one of the common manifestations in adults with classic hemizygous disease. Recently, several cases of an atypical variant of hemizygous Fabry's disease, with manifestations limited to the heart, have been reported. Therefore, we assessed the incidence of hemizygosity for Fabry's disease among male patients with left ventricular hypertrophy. METHODS: We measured plasma alpha-galactosidase activity in 230 consecutive male patients with left ventricular hypertrophy. Clinical manifestations were assessed, endomyocardial biopsies were performed, and the patients were screened for mutations in the alpha-galactosidase gene. RESULTS: Seven of the 230 patients with left ventricular hypertrophy (3 percent) had low plasma alpha-galactosidase activity (0.4 to 1.2 nmol per hour per milliliter; 4 to 14 percent of the mean value in normal controls). These seven unrelated patients, ranging in age from 55 to 72 years, did not have angiokeratoma, acroparesthesias, hypohidrosis, or corneal opacities, which are typical manifestations of Fabry's disease. Endomyocardial biopsy was performed in five patients and revealed marked sarcoplasmic vacuolization in all five. Samples from four patients were examined by electron microscopy and revealed typical lysosomal inclusions with a concentric lamellar configuration in all four. Two patients had novel missense mutations in exon 1 (Ala20Pro) and exon 6 (Met296lle). The remaining five had no mutations in the coding region of the alpha-galactosidase gene, but the amounts of the alpha-galactosidase messenger RNA were markedly lower than normal. CONCLUSIONS: Seven unrelated patients with atypical variants of hemizygous Fabry's disease were found among 230 men with left ventricular hypertrophy (3 percent). Fabry's disease should be considered as a cause of unexplained left ventricular hypertrophy.

Adolescent↗
PubMed2003

Distinct transglutaminase 2-independent and transglutaminase 2-dependent pathways mediate articular chondrocyte hypertrophy.

Altered chondrocyte differentiation, including development of chondrocyte hypertrophy, mediates osteoarthritis and pathologic articular cartilage matrix calcification. Similar changes in endochondral chondrocyte differentiation are essential for physiologic growth plate mineralization. In both articular and growth plate cartilages, chondrocyte hypertrophy is associated with up-regulated expression of certain protein-crosslinking enzymes (transglutaminases (TGs)) including the unique dual-functioning TG and GTPase TG2. Here, we tested if TG2 directly mediates the development of chondrocyte hypertrophic differentiation. To do so, we employed normal bovine chondrocytes and mouse knee chondrocytes from recently described TG2 knockout mice, which are phenotypically normal. We treated chondrocytes with the osteoarthritis mediator IL-1 beta, with the all-trans form of retinoic acid (ATRA), which promotes endochondral chondrocyte hypertrophy and pathologic calcification, and with C-type natriuretic peptide, an essential factor in endochondral development. IL-1 beta and ATRA induced TG transamidation activity and calcification in wild-type but not in TG2 (-/-) mouse knee chondrocytes. In addition, ATRA induced multiple features of hypertrophic differentiation (including type X collagen, alkaline phosphatase, and MMP-13), and these effects required TG2. Significantly, TG2 (-/-) chondrocytes lost the capacity for ATRA-induced expression of Cbfa1, a transcription factor necessary for ATRA-induced chondrocyte hypertrophy. Finally, C-type natriuretic peptide, which did not modulate TG activity, comparably promoted Cbfa1 expression and hypertrophy (without associated calcification) in TG2 (+/+) and TG2 (-/-) chondrocytes. Thus, distinct TG2-independent and TG2-dependent mechanisms promote Cbfa1 expression, articular chondrocyte hypertrophy, and calcification. TG2 is a potential site for intervention in pathologic calcification promoted by IL-1 beta and ATRA.

Alkaline Phosphatase↗
PubMed2004

E2F-1 regulates the expression of a subset of target genes during skeletal myoblast hypertrophy.

Cellular hypertrophy, or growth without division, is an adaptive response to various physiological and pathological stimuli in postmitotic muscle. We demonstrated previously that angiotensin II stimulates hypertrophy in C2C12 myoblasts by transient activation of the cyclin-dependent kinase 4 complex, subsequent phosphorylation of retinoblastoma protein, release of histone deacetylase 1 from the retinoblastoma protein inhibitory complex, and partial activation of the transcription factor E2F-1. These observations led us to propose a model in which partial inactivation of the retinoblastoma protein complex leads to the derepression of a subset of E2F-1 targets necessary for cell growth without division during hypertrophy. We now present data that support this model and suggest the mechanism by which E2F-1 regulates hypertrophy. We examined expression profiles of angiotensin II-stimulated myoblasts and identified a subset of E2F-1 target genes that are specifically regulated during the hypertrophic response. We showed that the expression of E2F-1 targets involved in G1/S transit, DNA replication, and mitosis is not altered during the hypertrophic response, while the expression of E2F-1-regulated genes controlling early G1 progression, cytoskeletal organization, protein synthesis, mitochondrial function, and programmed cell death is up-regulated. Furthermore, we demonstrated that activation of cytochrome c oxidase genes occurs during the development of hypertrophy and that cytochrome c oxidase IV is a direct transcriptional target of E2F-1. These studies demonstrated that E2F-1 activity at specific promoters is dependent on physiological circumstances and that E2F-1 should be considered a potential target in the treatment of pathologic hypertrophy.

Animals↗
PubMed2005

Nuclear factor-kappaB activation leads to down-regulation of fatty acid oxidation during cardiac hypertrophy.

Little is known about the mechanisms responsible for the fall in fatty acid oxidation during the development of cardiac hypertrophy. We focused on the effects of nuclear factor (NF)-kappaB activation during cardiac hypertrophy on the activity of peroxisome proliferator-activated receptor (PPAR) beta/delta, which is the predominant PPAR subtype in cardiac cells and plays a prominent role in the regulation of cardiac lipid metabolism. Phenylephrine-induced cardiac hypertrophy in neonatal rat cardiomyocytes caused a reduction in the expression of pyruvate dehydrogenase kinase 4 (Pdk4), a target gene of PPARbeta/delta involved in fatty acid utilization, and a fall in palmitate oxidation that was reversed by NF-kappaB inhibitors. Lipopolysaccharide stimulation of NF-kappaB in embryonic rat heart-derived H9c2 myotubes, which only express PPARbeta/delta, caused both a reduction in Pdk4 expression and DNA binding activity of PPARbeta/delta to its response element, effects that were reversed by NF-kappaB inhibitors. Coimmunoprecipitation studies demonstrated that lipopolysaccharide strongly stimulated the physical interaction between the p65 subunit of NF-kappaB and PPARbeta/delta, providing an explanation for the reduced activity of PPARbeta/delta. Finally, we assessed whether this mechanism was present in vivo in pressure overload-induced cardiac hypertrophy. In hypertrophied hearts of banded rats the reduction in the expression of Pdk4 was accompanied by activation of NF-kappaB and enhanced interaction between p65 and PPARbeta/delta. These results indicate that NF-kappaB activation during cardiac hypertrophy down-regulates PPARbeta/delta activity, leading to a fall in fatty acid oxidation, through a mechanism that involves enhanced protein-protein interaction between the p65 subunit of NF-kappaB and PPARbeta/delta.

Animals↗
PubMed2001

Analyses of muscular activity, energy metabolism, and muscle fiber type composition in a patient with bilateral masseteric hypertrophy.

Hyperwork of the masseter muscles due to habitual parafunction is thought to induce masseteric hypertrophy (so called work hypertrophy). However, the causes underlying this disease are not yet fully understood. Recently, we had a patient with bilateral masseteric hypertrophy, and we performed a partial excision of the masseter muscles. In this patient's case, we examined muscular activity, energy metabolism, and fiber type composition of the masseter muscles using electromyograms (EMG), 31P-magnetic resonance spectroscopy (MRS), and enzyme-histochemistry. The EMG showed no hyperactivity, and the 31P-MRS showed normal energy spectral patterns and PCr contents of the masseter muscles. The fiber type composition, however, in the muscles in this case was very different from that in muscles with "work hypertrophy" and also that in normal masseter muscles: 1. Loss of type IIB fibers; 2. Increases in type IIA and in type IM & IIC fibers; and 3. Decrease in type I fibers. The findings suggest that this is not a case of work hypertrophy but a case of compensatory hypertrophy possibly due to a lack of high-tetanus-tension type IIB fibers.

Adenosine Triphosphate↗
PubMed2003

Effects of calcium channel antagonists on left ventricular hypertrophy and diastolic function in patients with essential hypertension.

Hypertensive patients characteristically exhibit left ventricular (LV) hypertrophy and diastolic dysfunction. The effects of antihypertensive agents on LV hypertrophy and diastolic dysfunction do not always correlate with the degree of blood pressure reduction, but their effects on the sympathetic nervous system and renin-angiotensin system (RA system) are thought to be important. We investigated the effects of amlodipine and cilnidipine, N- and L-type calcium channel antagonists that suppress both blood pressure elevation and sympathetic activities, on LV hypertrophy and diastolic function. Patients with essential hypertension were randomly assigned to receive either amlodipine, cilnidipine or nifedipine CR (which does not block N-type calcium channels) for 6 months. The LV mass index was determined using M-mode echocardiography. The E/A ratio, i.e., the ratio of maximum amplitude between the early diastolic wave (E wave) and the atrial systolic wave (A wave) in the LV inflow pattern, and the deceleration time for the E wave were determined using pulse Doppler echocardiography. Systolic and diastolic blood pressures significantly decreased from the baseline values in all three groups, with no significant differences among the groups. The LV mass index had significantly decreased when it was evaluated 3 months after the initiation of treatment in the cilnidipine group and when it was evaluated 6 months after the initiation of treatment in the amlodipine group; only a slight decrease was observed in the nifedipine CR group. A significant decrease in the deceleration time and a significant increase in the E/A ratio were observed after 3 months of treatment in the cilnidipine and amlodipine groups but not in the nifedipine CR group. Thus, the effects of long-acting calcium channel antagonists on hypertensive LV hypertrophy and LV diastolic function varied from one antagonist to the other. Left ventricular hypertrophy and diastolic function improved in the cilnidipine and amlodipine groups, but not in the nifedipine CR group. These results indicate that the suppression of sympathetic nerve activity by the blockade of N-type calcium channels contributes to the improvement of LV hypertrophy and diastolic function.

Amlodipine↗
PubMed1988

Transforming growth factor-beta-induced growth inhibition and cellular hypertrophy in cultured vascular smooth muscle cells.

We have explored the hypothesis that hypertrophy of vascular smooth muscle cells may be regulated, in part, by growth inhibitory factors that alter the pattern of the growth response to serum mitogens by characterizing the effects of the potent growth inhibitor, transforming growth factor-beta (TGF-beta), on both hyperplastic and hypertrophic growth of cultured rat aortic smooth muscle cells. TGF-beta inhibited serum-induced proliferation of rat aortic smooth muscle cells (ED50 = 2 pM); this is consistent with previously reported observations in bovine aortic smooth muscle cells (Assoian et al. 1982. J. Biol. Chem. 258:7155-7160). Growth inhibition was due in part to a greater than twofold increase in the cell cycle transit time in cells that continued to proliferate in the presence of TGF-beta. TGF-beta concurrently induced cellular hypertrophy as assessed by flow cytometric analysis of cellular protein content (47% increase) and forward angle light scatter (32-50% increase), an index of cell size. In addition to being time and concentration dependent, this hypertrophy was reversible. Simultaneous flow cytometric evaluation of forward angle light scatter and cellular DNA content demonstrated that TGF-beta-induced hypertrophy was not dependent on withdrawal of cells from the cell cycle nor was it dependent on growth arrest of cells at a particular point in the cell cycle in that both cycling cells in the G2 phase of the cell cycle and those in G1 were hypertrophied with respect to the corresponding cells in vehicle-treated controls. Chronic treatment with TGF-beta (100 pM, 9 d) was associated with accumulation of cells in the G2 phase of the cell cycle in the virtual absence of cells in S phase, whereas subsequent removal of TGF-beta from these cultures was associated with the appearance of a significant fraction of cycling cells with greater than 4c DNA content, consistent with development of tetraploidy. Results of these studies support a role for TGF-beta in the control of smooth muscle cell growth and suggest that at least one mechanism whereby hypertrophy and hyperploidy may occur in this, as well as other cell types, is by alterations in the response to serum mitogens by potent growth inhibitors such as TGF-beta.

Animals↗
PubMed1996

Prevalence of left ventricular hypertrophy in a hypertensive population.

AIMS: This investigation was set up to study the prevalence of left ventricular hypertrophy in a hypertensive population with reference to a normotensive control group. From the general population 3498 men and women aged 35, 45, 55 and 65 years old were invited to a health examination. Participants with blood pressure above 160 mmHg systolic or 95 mmHg diastolic or those taking antihypertensive medication or having done so during the previous 6 months were asked to undergo an echocardiographic examination. Normotensive controls were randomly selected from the same population. Of 552 participants in the final study population, 194 were normotensive controls and 358 were in the hypertensive group. Echocardiographic measurements were made according to the Penn conventions and indexed for body surface. Cut-off values for left ventricular hypertrophy were 134 g.m-2 for males and 102 g.m-2 for women. RESULTS: Overall, the prevalence of left ventricular hypertrophy was 14%/20% (men/women) in normotensives and 25%/26% in hypertensives (P < 0.01). After subdivision by age and sex, there was a significant difference in the prevalence of left ventricular hypertrophy between normotensives and hypertensives only in the 65-year-old group (P < 0.02 for males and P < 0.05 for females). CONCLUSIONS: The association between blood pressure and left ventricular hypertrophy in the general population is weak. Left ventricular hypertrophy is only significantly more frequent among hypertensives as compared to normotensives in older people.

Adult↗
PubMed2002

Cardiac-specific overexpression of a high Ca2+ affinity mutant of SERCA2a attenuates in vivo pressure overload cardiac hypertrophy.

In cardiomyocytes, calcium plays important roles as a signal in cardiac hypertrophy and contraction-relaxation cycling. Elevation of Ca2+ concentration in myoplasm is associated with the onset and progression of hypertrophy as well as the enhancement of contractility. The cardiac Ca2+ ATPase (SERCA2a) of the sarcoplasmic reticulum plays a dominant role in lowering cytoplasmic calcium levels during relaxation and is regulated by phospholamban (PLN). To examine whether the modulation of SERCA2a activity results in the attenuation of cardiac hypertrophy and enhancement of contractility, we generated transgenic mice (TG) overexpressing a high calcium affinity SERCA2a mutant (K397/400E), lacking a functional association with PLN. In the TG hearts, the apparent affinity of SERCA2a for Ca2+ significantly increased compared with their nontransgenic littermate controls. The TG showed increased contraction and relaxation, with increases in the amplitude of Ca2+ transient and rapid Ca2+ decay. Upon induction of pressure overload by transverse aortic constriction, the TG developed less cardiac hypertrophy than littermate controls did. The activation of Ca2+-sensitive protein kinase C by pressure overload was significantly attenuated in the TG hearts. Our findings indicate an association of SERCA2a activity with cardiac hypertrophy and thus a new therapeutic target for the prevention and treatment of cardiac hypertrophy.

Animals↗
PubMed2001

Myocardial and coronary effects of propofol in rabbits with compensated cardiac hypertrophy.

BACKGROUND: Myocardial effects of propofol have been previously investigated but most studies have been performed in healthy hearts. This study compared the cardiac effects of propofol on isolated normal and hypertrophic rabbits hearts. METHODS: The effects of propofol (10-1,000 microM) on myocardial contractility, relaxation, coronary flow and oxygen consumption were investigated in hearts from rabbits with pressure overload-induced left ventricular hypertrophy (LVH group, n = 20) after aortic abdominal banding and from sham-operated control rabbits (SHAM group, n = 10), using an isolated and erythrocyte-perfused heart model. In addition, to assess the myocardial and coronary effects of propofol in more severe LVH, hearts with a degree of hypertrophy greater than 140% were selected (severe LVH group, n = 7). RESULTS: The cardiac hypertrophy model induced significant left ventricular hypertrophy (136+/-21%, P < 0.05). The pressure-volume relation showed normal systolic function but an altered diastolic compliance in hypertrophic hearts. Propofol only decreased myocardial contractility and relaxation at supratherapeutic concentrations (> or = 300 microM) in SHAM and LVH groups. The decrease in myocardial performances was not significantly different in SHAM and LVH groups. Propofol induced a significant increase in coronary blood flow which was not significantly different between groups. In severe LVH group, the degree of hypertrophy reached to 157+/-23%. Similarly, the effects of concentrations of propofol were not significantly different from the SHAM group. CONCLUSIONS: Propofol only decreased myocardial function at supratherapeutic concentrations. The myocardial and coronary effects of propofol were not significantly modified in cardiac hypertrophy.

Anesthetics, Intravenous↗
PubMed1994

New developments in the epidemiology of left ventricular hypertrophy.

Left ventricular hypertrophy is associated with an increased risk of coronary heart disease and all-cause mortality. Electrocardiographic criteria for left ventricular hypertrophy have high specificity but low sensitivity. Recent advances in methodology have improved the sensitivity of the electrocardiogram for detecting left ventricular hypertrophy. Criteria for left ventricular hypertrophy have been developed from epidemiologic studies using M-mode echocardiography. The prevalence of left ventricular hypertrophy is influenced by blood pressure, age, sex, and obesity. Recent studies have shown that waist-to-hip ratio, hyperinsulinemia, a dominant late systolic peak in the arterial pressure waveform, and a decrease in nocturnal blood pressure decline are also determinants of left ventricular mass. Left ventricular hypertrophy is associated with an increased incidence of ventricular arrhythmias and with an impairment in coronary flow reserve. Newer imaging techniques, such as two- and three-dimensional echocardiography, magnetic resonance imaging, and ultra-fast computed tomography are more accurate and reproducible than M-mode echocardiography, but these methodologies are expensive and not readily available for assessment of left ventricular mass.

Cardiac Volume↗