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PubMed1985

Regression of hypertrophy in small resistance vessels.

Many studies have documented regression of left ventricular hypertrophy following blood pressure control by some antihypertensive agents but not by others. To determine whether similar differences in regression of wall thickening also occur in resistance vessels during treatment, matched control groups of spontaneously hypertensive rats (SHR) were treated for 12 weeks with either hydralazine or captopril + hydrochlorothiazide and compared with untreated SHR and Wistar-Kyoto rats (WKY). Perfusion pressure was then determined in the hind-limbs of pithed rats under conditions of constant blood flow (4.0 ml/min) and maximal vasodilatation as an index of thickening (hypertrophy) of resistance vessel walls. Treatment with hydralazine or captopril + hydrochlorothiazide controlled blood pressure equally in SHR but had significantly different effects on both left ventricular hypertrophy and resistance vessels. Perfusion pressure was reduced from 37.4 +/- 0.5 mmHg to 33.9 +/- 0.5 mmHg (P < 0.01) with captopril + hydrochlorothiazide but only marginally to 35.9 +/- 0.3 mmHg with hydralazine (P < 0.05 at some levels of flow and P > 0.05 at others). Left ventricular weight was significantly reduced by captopril + hydrochlorothiazide (2.02 +/- 0.02 versus 2.63 +/- 0.05 mg/g, P < 0.01) but only to 2.44 +/- 0.05 by hydralazine. Significant correlations were found both before and following treatment between perfusion pressure and left ventricular weight (r = 0.59, P < 0.01) but not between either of these two parameters and arterial pressure. Thus, despite equal blood pressure control, thickening of resistance vessel walls regressed more with captopril + hydrochlorothiazide than with hydralazine, suggesting that vascular hypertrophy-like left ventricular hypertrophy is not determined by blood pressure levels alone.

Animals↗
PubMed1997

Left ventricular and microvascular hypertrophy in essential hypertension: clinical relevance and prognostic implications.

A considerable number of patients with essential hypertension develop cardiac and vascular structural and functional alterations, indicating an adaptation to the persistently elevated blood pressure. Besides the mechanical stress, neuro-humoral stimuli and possibly the genetic disposition contribute to the process of cardiovascular hypertrophy and remodeling. Left ventricular hypertrophy has been identified as an independent risk factor for cardiovascular events and mortality in these patients and therefore regression of cardiac hypertrophy seems to be a meaningful therapeutic goal. A normalization of myocardial hypertrophy can be achieved with various antihypertensive drugs and combinations, where angiotensin-converting enzyme inhibitors seem to be the most powerful substances. This observation emphasizes the role of the renin-angiotensin-aldosterone system in cardiac diseases. Morphological changes in small resistance arteries do not only represent an adaptation to an elevated peripheral resistance, moreover, they contribute to the persistence of the increase in blood pressure. Investigations on the potential reversibility of small vessel alterations in humans as well as the association with regression of left ventricular hypertrophy will be discussed in this review.

Animals↗
PubMed1996

The histochemistry of reactive masticatory muscle hypertrophy.

There are two types of hypertrophy of the muscles of mastication in man: reactive hypertrophy, the more common form; and nonreactive enlargements-myositic, genetic, myopathic, and idiopathic. Reactive hypertrophy develops when the masticatory muscle workload is increased by local bone and dental disorders; such triggers are not powerful but act over long periods, thus demanding increased endurance. Exercise for endurance has a greater effect on the muscles of mastication than it has on the large muscles of the limbs; these react solely by stimulating the oxidative metabolism of type 1 fibers, whereas masticatory muscle reacts structurally by hypertrophy and progressive type 1 fiber predominance. Eventually enzyme instability of type 1 fibers and end stage atrophy of type 2 fibers may appear. Unexpectedly, lesions have also been found in control masticatory muscle, in particular type 2 fiber specific atrophy like that seen in long-standing acquired autoimmune myasthenia gravis. It is suggested that the adverse lesions in hypertrophied and control masticatory muscle are the consequence of post-activation fatigue.

Adult↗
PubMed1994

Hereditary motor and sensory neuropathy with calf hypertrophy is associated with 17p11.2 duplication.

The demyelinating type of hereditary motor and sensory neuropathy (HMSN I) is characterized by progressive weakness and atrophy of leg muscles. Six patients (age, 25-79 yr) belonging to three generations had calf hypertrophy (6 of 6), foot drop or difficulty with heel walking (4 of 6), pes cavus (3 of 6), absent or depressed tendon jerks in the lower limbs (4 of 6), and mild distal sensory loss (3 of 6). No other family member had leg atrophy. Motor conduction velocities ranged from 20 to 40 m/sec. Sural nerve biopsy showed loss of large myelinated fibers, numerous onion bulbs, and segmental demyelination and remyelination. Computed tomographic scans of leg muscles and histological and morphometric findings in gastrocnemius revealed true muscular hypertrophy. Southern blot and fluorescence in situ hybridization documented the duplication of the entire 17p11.2 segment associated with classical HMSN IA. The pathogenesis of muscle hypertrophy in our cases is unclear. Chronic leg muscle weakness and long-standing partial denervation might cause calf enlargement by a combination of compensatory "work-induced" and "stretch-induced" fiber hypertrophy. Alternatively, that all the affected family members presented calf hypertrophy might suggest the action of a genetic factor associated with the duplication at 17p11.2.

Adult↗
PubMed2005

Role of interleukin-6 in cardiomyocyte/cardiac fibroblast interactions during myocyte hypertrophy and fibroblast proliferation.

The process of cardiac hypertrophy is considered to involve two components: that of cardiac myocyte (CM) enlargement and cardiac fibroblast (CF) proliferation. The interleukin-6 (IL-6) family cytokines have been implicated in a variety of cellular and molecular interactions between myocytes and non-myocytes (NCMs), which in turn have important roles in the development of cardiac hypertrophy. In the study of these interactions, we previously detected very high levels of IL-6 in supernatants of a "dedifferentiated model" of adult ventricular CMs cultured with CFs. In the present study, we have used this in vitro coculture system to examine how IL-6 is involved in the interactions between CMs and CFs during CM hypertrophy and CF proliferation. IL-6 and its signal transducer, 130-kDa glycoprotein (gp130), were detected by immunostaining cultured CMs and CFs with anti-IL-6 or anti-gp130 antibodies. Addition of anti-IL-6 or anti-gp130 antagonist antibodies into CM/CF cocultures induced a significant decrease in expression of atrial natriuretic peptide (ANP) and beta-myosin heavy chain (beta-MHC) in CMs. The presence of IL-6 antagonist also resulted in a decrease in the surface area of 12-day-old CMs cultured with CFs or in the presence of fibroblast conditioned medium (FCM), and decreased fibroblast proliferation in CM/CF cocultures, particularly in the presence of a gp130 antagonist. The results also show that angiotensin II (AngII) is mainly secreted by CFs and induces IL-6 secretion in CMs cultured with CFs or with FCM. In addition, the effects of IL-6 on cardiomyocyte hypertrophy and fibroblast proliferation were inhibited by addition of the AT-1 receptor antagonist, losartan. These results suggest that IL-6 contributes significantly to CM hypertrophy by an autocrine pathway and to fibroblast proliferation by a paracrine pathway and that these effects could be mediated by AngII.

Angiotensin II↗
PubMed2002

Bite performance in clariid fishes with hypertrophied jaw adductors as deduced by bite modeling.

Within clariid fishes several cranial morphologies can be discerned. Especially within anguilliform representatives an increase in the degree of hypertrophy of the jaw adductors occurs. The hypertrophy of the jaw adductors and skeletal modifications in the cranial elements have been linked to increased bite force. The functional significance of this supposed increase in bite force remains obscure. In this study, biomechanical modeling of the cranial apparatus in four clariid representatives showing a gradual increase in the hypertrophy of the jaw adductors (Clarias gariepinus, Clariallabes melas, Channallabes apus, and Gymnallabes typus) is used to investigate whether bite force actually increased. Static bite modeling shows that the apparent hypertrophy results in an increase in bite force. For a given head size, the largest bite forces are predicted for C. apus, the lowest ones for C. gariepinus, and intermediate values are calculated for the other species. In addition, also in absolute measures differences in bite force remain, with C. apus biting distinctly harder than C. gariepinus despite its smaller head size. This indicates that the hypertrophy of the jaw adductors is more than just a correlated response to the decrease in absolute head size. Further studies investigating the ecological relevance of this performance difference are needed.

Animals↗
PubMed2002

Skeletal muscle hypertrophy and anti-atrophy effects of clenbuterol are mediated by the beta2-adrenergic receptor.

Analyses were performed to evaluate the roles of the beta1- and beta2-adrenergic receptors in the skeletal muscle hypertrophy and anti-atrophy response to the beta-adrenergic agonist, clenbuterol. Treatment of wild-type mice with clenbuterol resulted in statistically significant hypertrophy of the innervated tibialis anterior and medial gastrocnemius muscles and inhibition of denervation-induced atrophy of these muscles. Treatment of beta1-adrenergic receptor knockout mice with clenbuterol also resulted in statistically significant hypertrophy of the innervated tibialis anterior and medial gastrocnemius muscles and inhibition of denervation-induced atrophy of these muscles. In contrast, in beta2-adrenergic receptor knockout mice and in mice lacking both the beta1- and beta2-adrenergic receptors, clenbuterol treatment did not result in hypertrophy of the innervated tibialis anterior and medial gastrocnemius muscles, nor did it inhibit denervation-induced atrophy in these muscles. Together these data demonstrate that the beta2-adrenergic receptor is responsible for both the skeletal muscle hypertrophy and anti-atrophy effects of the beta-adrenergic agonist clenbuterol.

Adrenergic beta-Agonists↗
PubMed1994

Satellite cell activity is required for hypertrophy of overloaded adult rat muscle.

Hypertrophy of extensor digitorum longus muscle, overloaded by the removal of the synergist tibialis anterior (TA) muscle, in growing rats is inhibited if endogenous satellite cells are sterilized by exposure to irradiation. However, normal muscle growth is not eliminated, only diminished. To test whether irradiated, overloaded muscle can hypertrophy in the absence of normal growth-related stimuli, experiments were conducted on mature rats. TA muscle ablation caused hypertrophy of EDL muscle, characterized by a significant increase in muscle mass and the size of type IIx and type IIb fibers, and a proportional increase in the number of myonuclei. When ablation was preceded by irradiation, hypertrophy did not occur. The results indicate that satellite cell activation, division, and fusion is necessary for compensatory hypertrophy of fully mature muscle, and may be important to the understanding of the limits of recovery of inherited muscle myopathies treated by myogenic cell implantation.

Adaptation, Physiological↗
PubMed2006

Altered expression of thin filament-associated proteins in hypertrophied urinary bladder smooth muscle.

AIMS: Obstruction of the urinary bladder outlet induces detrusor smooth muscle (DSM) hypertrophy. The goal of this study was to determine whether the composition of thin filament-associated proteins, known to play important roles in cytoskeletal structure and/or the regulation of contraction, is altered in DSM during hypertrophy. METHODS: DSM hypertrophy was induced in male rabbits by partial ligation of the urethra. Sham-operated rabbits served as a control. Reverse transcriptase-polymerase chain reaction (RT-PCR) and real-time PCR revealed a significant increase in the expression of mRNAs for basic (h1) calponin (CaP), and alpha-isoform of tropomyosin (Tm) in hypertrophied DSM compared to controls. Western blotting and two-dimensional (2-D) gel electrophoresis showed enhanced expression of these proteins and also a significant increase in the expression of beta-non muscle and gamma-smooth muscle actin in the DSM from obstructed bladders, while alpha-actin remained constant. RESULTS: Enhanced expression of these proteins in the DSM from obstructed bladders was confirmed by immunofluorescence microscopy. Double immunostaining with Cap/Tm and alpha/beta-actin-specific antibodies showed co-localization of these proteins in myocytes. Colocalization of smooth muscle specific myosin and CaP to cytoplasmic filaments in cells dissociated from the hypertrophied DSM indicated that these cells are differentiated smooth muscle cells. CONCLUSIONS: The change in the isoforms of actin, Cap, and Tm may be part of the molecular mechanism for bladder compensation in increased urethral resistance.

Actins↗
PubMed1998

Selective increase in cardiac IGF-1 in a rat model of ventricular hypertrophy.

There is evidence that insulin-like growth factor-1 (IGF-1) plays a role in the development of left ventricular hypertrophy, but it is uncertain whether cardiac IGF-1 changes before or after hypertension is established, and whether circulating IGF-1 are involved in cardiac hypertrophy. We have investigated changes in circulating and left ventricular IGF-1 and in the expression of the IGF-1 gene in the left ventricles of rats during the development of hypertensive left ventricular hypertrophy (Goldblatt model; 2 kidney-1 clamped). Our results show that the left ventricular contents of IGF-1 and its mRNA were increased at one and four weeks of hypertension and hypertrophy, and that both returned to control values after nine weeks. These changes were unrelated to the seric concentration of IGF-1 in the blood. These results show that local rather than circulating IGF-1 levels contributed to the development of renovascular hypertensive left ventricular hypertrophy.

Animals↗
PubMed2000

Loss of the normal epicardial to endocardial gradient of cftr mRNA expression in the hypertrophied rabbit left ventricle.

The electrical instability of hypertrophied and failing hearts is caused by delayed repolarisation, which is thought to be due in part to altered levels and/or patterns of expression of ion channel genes. The aim of this study was to investigate changes in the levels and pattern of cystic fibrosis transmembrane conductance regulator (cftr) mRNA expression in a combined pressure and volume overload model of heart failure in the rabbit, using in situ mRNA hybridisation. There was a decrease in cftr mRNA expression, primarily due to a decrease in epicardial expression and, hence, loss of the normal epicardial to endocardial gradient of cftr mRNA expression in the rabbit left ventricle. In contrast there was an increase in atrial natriuretic factor (anf) mRNA expression in the hypertrophied hearts with preferential reexpression in subendocardial regions. The patterns of both cftr and anf mRNA expression in the hypertrophied hearts were similar to those seen in embryonic hearts. This suggests that the reversion to an embryonic pattern of gene expression in cardiac hypertrophy applies to ion channel genes. The loss of the normal transmural gradient of repolarising ion channels is likely to contribute to instability of repolarisation in the hypertrophied heart and hence increased risk of cardiac arrhythmias in patients with heart failure.

Animals↗
PubMed1994

Cardiac hypertrophy alters expression of Na+,K(+)-ATPase subunit isoforms at mRNA and protein levels in rat myocardium.

In myocardium from different rat models of cardiac hypertrophy, expression of Na+,K(+)-ATPase isoforms has been shown to be altered at the mRNA level. However, it has not been determined whether these alterations translate into changes at the protein level. This distinction is important because post-transcriptional events have been shown to regulate isoform expression. In the present study, relative abundances of the Na+,K(+)-ATPase isoforms were examined in hypertrophied left ventricles of renovascular hypertensive rats at both the protein and mRNA levels, using immunoblotting and dot blot hybridization, respectively. Stenosis of the left renal artery elicited an increase in systolic blood pressure, cardiac hypertrophy, and a shift in expression of the myosin heavy chain isoforms. In hypertrophied left ventricles, expression of the alpha 1 isoform remained unchanged at both mRNA and protein levels, whereas the relative abundances of both alpha 2-mRNA and -protein decreased, to 0.63 and 0.54, respectively, of controls. In addition, the abundance of beta 1-mRNA remained unchanged, whereas beta 1-protein decreased to 0.67 of controls. These results suggest that in hypertrophied myocardium of renovascular hypertensive rats Na+,K(+)-ATPase isoform expression is altered at both the protein and mRNA levels, and that pretranslational as well as translational/post-translational mechanisms may be involved.

Animals↗
PubMed1997

Regression of cardiac hypertrophy normalizes glucose metabolism and left ventricular function during reperfusion.

It is not yet known if the alterations in myocardial glucose metabolism and the exaggerated left ventricular dysfunction that occur during reperfusion in hypertrophied hearts are reversible. Thus, we studied isolated working hearts from aortic-banded (n = 29) and sham-operated control (n = 32) male Sprague-Dawley rats with or without enalapril maleate treatment (25.6 +/- 0.8 mg/kg per day, p.o.) to determine the effect of regression of cardiac hypertrophy on myocardial glucose metabolism and post-ischemic heart function. Hearts were perfused with buffer containing 1.2 mM palmitate, 11 mM [5-3H]/[U-14C]-glucose, 0.5 mM lactate and 100 microU/ml insulin. Glucose metabolism [rates of glycolysis (3H2O production) and rates of oxidation (14CO2 production) of exogenous glucose] and heart function (heart rate x peak systolic pressure) were measured during 30 min pre-ischemic perfusion and 60 min of reperfusion following 20 min of global, no-flow ischemia. Hearts from untreated aortic-banded rats were hypertrophied, being 27.6 +/- 1.8% larger than hearts from untreated control rats. Enalapril treatment caused regression of cardiac hypertrophy that normalized heart weight in aortic-banded rats. Rates of glycolysis of exogenous glucose in hearts from untreated aortic-banded rats were accelerated compared to rates in hearts from untreated control rats during pre-ischemic perfusion (4391 +/- 97 v 2652 +/- 69 nmol glucose/min per g dry wt, respectively, P < 0.05) and reperfusion (2402 +/- 58 v 1597 +/- 88 nmol glucose/min per g dry wt. respectively, P < 0.05). In contrast, rates of glycolysis of exogenous glucose in hearts from enalapril-treated aortic-banded rats were normalized before and after ischemia. Rates of glycolysis of exogenous glucose in hearts of control rats were not affected by enalapril treatment. Oxidation of exogenous glucose was not different among groups either before or after ischemia. Function of hearts from untreated aortic-banded rats at the end of reperfusion was significantly less than that of hearts from untreated control rats (23.9 +/- 2.6 v 32.2 +/- 0.7 mmHg x beats per min/1000, respectively, P < 0.05). As with myocardial glucose metabolism function of hearts from aortic-banded rats treated with enalapril was normalized during reperfusion. Thus, pharmacologically induced regression of pressure-overload cardiac hypertrophy normalizes glucose metabolism as well as left ventricular function during reperfusion.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Protein kinase C activity and expression in rabbit left ventricular hypertrophy.

Protein Kinase C (PKC) is implicated in the induction of myocardial hypertrophy. Recent studies showed an increased activity and expression of PKC in rat left ventricular hypertrophy, but we demonstrated a decreased PKC activity and content in rabbit heart failure. The present study was designed to evaluate whether these differences were due to species or model differences. PKC activity and expression were measured in a model of mild ventricular overload, induced by a 40-50% constriction of the abdominal aorta in rabbits. Left ventricular (LV) weight/body weight ratio was increased by 14, 21 and 36% after 4, 18 and 42 days of stenosis, respectively. PKC activity was significantly decreased after 18 and 42 days of stenosis in the particulate fraction of LV, but it was not modified in the cytosolic fraction leading to a significantly decreased translocation index (particulate/total activity ratio): 18.6 +/- 2.2% and 19.4 +/- 1.6% at 18 days and 42 days of aortic stenosis, respectively, compared with 25.7 +/- 2.0% and 25.8 +/- 1.2% in corresponding sham-operated rabbits (both Ps < 0.05). Similarly, PKC content, measured by immunoblotting, was not modified in the cytosolic fractions, but decreased significantly in the particulate fractions after 18 and 42 days of stenosis. These data are, thus, different from those obtained in rat LV hypertrophy showing species differences in PKC expression in hypertrophy. They also show that hypertrophy may take place without induction of PKC.

Animals↗
PubMed1997

The effects of hypertrophy and diabetes on cardiac pyruvate dehydrogenase activity.

Alterations in substrate selection and utilisation are characteristics of heart failure of different etiologies and these changes may be involved in the development of contractile dysfunction. Regulation of pyruvate dehydrogenase (PDH) is crucial in determining the relative contribution of glucose oxidation to energy production; however, the role of PDH in the development of heart failure has not been clarified. In this study, we present a reliable and simple method for assaying both the active and total forms of PDH (PDHa and PDHt respectively) in cardiac tissue, and have compared the effects of pressure overload hypertrophy and diabetes on PDH activity. PDHa and PDHt were measured in extracts of hypertrophied hearts after 5 weeks of pressure overload or in hearts after 7 weeks following induction of diabetes. There was no significant change in PDHt in the hypertrophied group, but the fraction of PDH in the active form significantly decreased from 61+/-1% in controls to 36+/-1% (P<0.05). Following diabetes, there was a decrease in the ratio of PDHa:PDHt from 60+/-3% to 11+/-1% (P<0.0001) and PDHt activity -6.2+/-0.9 to 2.7+/-0.4 micromol/min/g wet weight (P<0.02)]. This study reports for the first time that (i) concomitant with the development of compensated hypertrophy, there is a decrease in the fraction of PDH in the active form; and (ii) in the diabetic heart, there is marked decrease in total PDH activity in addition to a decrease in the fraction of PDH in the active form. These results indicate that myocardial substrate delivery to the mitochondria may be impaired in both hypertrophy and diabetes, which may lead to the energy depleted state observed in heart failure.

Animals↗
PubMed1999

Chronic pressure overload cardiac hypertrophy and failure in guinea pigs: I. Regional hemodynamics and myocyte remodeling.

A chronic pressure overload animal model was created in young guinea pigs by surgical constriction of the descending thoracic aorta. Hemodynamics, echocardiography and myocyte size characterization demonstrated compensated pressure overloaded left ventricular (LV) hypertrophy at 4 weeks (4 wk), and congestive left heart failure 6 months (6 mo) after aortic constriction. Compared to age-matched sham-surgery control groups, the cell length and length/width ratio of isolated LV myocytes were significantly increased at 6 mo but not at 4 wk. LV myocyte lengthening was statistically correlated to an increase in LV chamber dimension and diastolic wall stress at 6 mo. These data demonstrate that myocyte lengthening occurs in mechanical overload-induced congestive heart failure, contributes to LV chamber dilatation, and is associated with increased end-diastolic wall stress. Myocytes of the other three chambers remained morphometrically normal at 4 wk. Hypertrophy of left atrial (LA) and right ventricular and atrial myocytes was evident at 6 mo. Increases in both cell length and cross-sectional area contributed significantly to the hypertrophy in the three chambers. More than 85% of LV myocytes were binucleate and the binucleation remained unchanged in the sham-surgery group from the tested 4 wk to 6 mo time point. LV hypertrophy and failure showed no significant effects on the binucleation of LV myocytes. By contrast, over 96% of LA myocytes were mononucleate. The mononucleate percent of LA myocytes was not appreciably altered during either normal growth or hypertrophy induced by secondary hemodynamic overload due to LV failure.

Animals↗
PubMed2000

Calcium handling and role of endothelin-1 in monocrotaline right ventricular hypertrophy of the rat.

We investigated the role of endothelin-1 (ET-1) in right ventricular function and intracellular Ca(2+)(Ca(2+)(i)) handling of isolated perfused rat hearts with right ventricular hypertrophy induced by monocrotaline (50 mg/kg). Nine weeks after monocrotaline (n=9) or saline (control n=9) treatment, hearts were perfused isovolumically at 37 degrees C and right ventricular function (fluid-filled balloon), right ventricular intracellular Ca(2+) transients (aequorin bioluminescence method) and the effects of ET-1 were determined. Monocrotaline-treated rats developed considerable right ventricular hypertrophy (right ventricular weight:body weight ratio: 1.07+/-0.13 v. 0.60+/-0.03 in controls P<0.05) and these hearts generated higher right ventricular systolic and diastolic pressure, but similar systolic and diastolic wall stress, indicating a compensated functional state. Hypertrophied hearts demonstrated a prolonged duration of isovolumic contraction (time to 90% decline from peak: 105+/-1 v 89+/-4 ms at 3 m M extracellular Ca(2+) P<0.05), but neither the time to peak pressure (71+/-3 ms) nor time to peak light (25+/-3 ms) were different from controls. The increased duration of contraction correlated with a similar prolongation of the Ca(2+)transient (time to 90% decline from peak: 72+/-4 v 50+/-3 ms P<0.05), indicating a reduced rate of Ca(2+)sequestration in hypertrophic right ventricles. Peak systolic intracellular Ca(2+)was similar in control and hypertrophied hearts (1.04+/-0.02 and 0.99+/-0.02 microM, P>0.05, n=6). ET-1 (1-300 p M) affected neither the time course of right ventricular contraction nor that of the Ca(2+)transient or peak systolic Ca(2+)concentrations. These data are the first measurements of right ventricular Ca(2+)transients in beating normal and hypertrophic hearts. We conclude that ET-1 plays no role in compensated hypertrophy because it affected neither right ventricular function nor intracellular Ca(2+)handling in this model.

Animals↗
PubMed1999

Cellular mechanisms of diabetic vascular hypertrophy.

Mesenteric vascular hypertrophy occurs in experimental diabetes. The present study examines whether this medial hypertrophy originates via cellular hyperplasia or hypertrophy of smooth muscle cells or an increase in collagen content. Male Sprague-Dawley diabetic (streptozotocin, 50 mg/kg, i.v.) rats were compared with control rats after 3 weeks in order to study mesenteric and aortic smooth muscle cell size and degree of cellular polyploidy. Collagen content in the mesenteric vessels was examined via staining with Sirius red. Further groups of control and diabetic animals were studied after 7 and 14 days of diabetes to assess proliferation in the various layers of the vessel wall using incorporation of [3H]thymidine (0.5 mCi/kg, i.p.). Smooth muscle cell size was measured by a Coulter counter and polyploidy assessed using flow cytometry measurement of cellular DNA content. Diabetic smooth muscle cell size was reduced in both the aorta and the mesenteric vessels and polyploidy was increased in these cells. The collagen content of diabetic mesenteric media was proportionally increased. At day 7, diabetic mesenteric endothelial and adventitial layers showed increased [3H]thymidine labeling of cells and this was not observed in the media of these vessels. These findings indicate that increased endothelial and adventitial cell proliferation are early events in diabetes associated vascular hypertrophy. Furthermore, an increase in extracellular matrix within the media is an important feature of diabetes associated vascular hypertrophy.

Animals↗