自发性高血压大鼠中脑导水管周围灰质nNOS阳性神经元的变化

目的观察自发性高血压大鼠(spontaneously hypertensiverats,SHR)中脑导水管周围灰质内神经元型一氧化氮合酶(neuronal nitric oxide synthase,nNOS)阳性神经元的变化。方法取SHR和京都种威斯特大鼠(Wistar-Koytorats,WKY)大鼠各30只,分别于3月(14周)龄,6月龄和12月龄测血压并处死,ABC免疫细胞化学方法显示nNOS阳性神经元。结果SHR血压随鼠龄的增长逐渐升高,于12～14周龄时血压在高位稳定,且均高于WKY大鼠(P<0.05)维持在[(20.8±1.1)～(26.3±1.0)]kPa(P<0.05);WKY大鼠各时期血压无明显差异,维持在[(13.7±1.6)～(15.1±1.7)]kPa。中脑导水管周围灰质nNOS阳性神经元以小细胞为主,突起有2-4个,许多朝中脑水管方向延伸。定量结果显示,SHR大鼠nNOS阳性神经元随着血压升高呈逐渐减少的趋势,12月龄与3月龄和6月龄相比均有显著差异(P<0.01),而各个时期WKY大鼠PAGnNOS阳性神经元均无明显变化。结论SHR中脑导水管周围灰质nNOS阳性神经元的减少可能通过影响延髓的血压调节中枢调控高血压的发生,并有可能与高血压的痛觉过敏有关。     

Cardiovascular and sympathetic nervous system responses to an acute stressor in borderline hypertensive rats (BHR)

The present study examined cardiovascular and plasma catecholamine responses to acute footshock stress in adult male Wistar-Kyoto (WKY) normotensive, borderline hypertensive (BHR), and spontaneously hypertensive (SHR) rats. Basal mean arterial pressure and heart rate were equivalent for SHRs and BHRs, and levels for both groups were elevated compared to WKYs. Following transfer to the footshock chamber, blood pressure increased to a greater degree in SHRs than in WKYs or BHRs. However, the tachycardia was exaggerated in both BHRs and SHRs compared to WKYs. In response to intermittent footshock stress, all groups had comparable heart rate increases while maintaining blood pressure near baseline levels. SHRs demonstrated a sympathetic hyperresponsiveness to footshock stress, with greater increases in plasma norepinephrine and epinephrine levels than WKYs immediately following footshock. At 5 minutes postfootshock, plasma catecholamines remained elevated in SHRs over both WKYs and BHRs. Plasma catecholamine increases following footshock were comparable at all time points between WKYs and BHRs. The present results demonstrate that sympathetic responsiveness of BHRs to acute footshock stress is more similar to normotensive WKYs than to hypertensive SHRs.     

Angiotensin converting enzyme inhibition prevents polyploidization of cardiomyocytes in spontaneously hypertensive rats with left ventricular hypertrophy

Polyploidization of cardiomyocyte nuclei is a physiological phenomenon that increases in pathological conditions such as myocardial hypertrophy. The purpose of this study was to evaluate the potential benefit of the angiotensin converting enzyme (ACE) inhibitor quinapril in reversing the polyploidization of cardiomyocyte nuclei in spontaneously hypertensive rats (SHR) with established left ventricular hypertrophy (LVH). Sixteen week-old male SHR were treated with oral quinapril (average dose 10 mg/kg per day) for 20 weeks. Sixteen- and 36-week-old untreated SHR and 16- and 36-week-old normotensive Wistar-Kyoto (WKY) rats were used as controls. Nuclear polyploidization was determined by DNA flow cytometry of frozen tissues from the left ventricle, at least 20 000 nuclei being measured in each sample. The rates of tetraploidy in the 16- and 36-week-old SHR groups were 2·8 per cent (range 2·16-3 per cent) and 5·4 per cent (range 4·9–5·9 per cent), respectively. Treated SHR had a similar rate of DNA tetraploidy to the 16- and 36-week-old WKY rat groups: 1·8 per cent (range 1·5–2·3 per cent), 1·55 per cent (range 1·5–1·6 per cent), and 1·5 per cent (range 1·4–1·6 per cent), respectively. The differences in the percentage of tetraploid cardiomyocytes between the SHR untreated groups and the SHR treated group were statistically significant (P<0·05). Regression of LVH and normalization of blood pressure were observed in treated rats. These results indicate that DNA tetraploidy in the myocardium of SHR increases with hypertrophy and decreases on quinapril treatment. It is suggested that ACE inhibition modifies nuclear processes involved in myocyte growth in arterial hypertension.     

Spontaneously hypertensive rats exhibit altered cardiovascular and neuronal responses to muscle contraction

We examined the cardiovascular and ventrolateral medullary neuronal responses to muscle contraction in the spontaneously hypertensive rat (SHR) and normotensive Wistar-Kyoto rat (WKY) control. Cardiovascular, respiratory and ventrolateral medullary neuronal responses to muscle contraction evoked by tibial nerve stimulation were recorded. SHRs exhibited significantly larger drops in arterial pressure compared to WKYs in response to muscle contraction (P < 0.05). Basal ventrolateral medulla neuronal discharge rates were similar between the SHR and the WKY groups. A majority of neurons recorded responded to muscle contraction in both the WKY (77 %; n = 53) and the SHR groups (68 %; n = 62). There was no difference in the percentage of neurons that responded with an increase (approximately 60 %) or decrease (approximately 40 %) in firing rate between hypertensive and normotensive rats. Pulse wave-triggered averaging techniques showed that most neurons that responded to muscle contraction also possessed a basal firing rhythm temporally related to the cardiac cycle (85 % in WKYs, 83 % in SHRs). However, decreases in neuronal firing rates in response to muscle contraction were significantly greater in SHRs than WKYs. Therefore, we conclude that muscle contraction unmasks a hyperexcitability of neurons in the ventrolateral medulla of SHRs that parallels the heightened blood pressure responses.     

Differential expression of α-enolase in the normal and pathological cardiac growth

Objectives

It was found that α-enolase was dramatically up-regulated in the hypertrophic hearts of SHR in our previous study. The purposes of this study were to examine the expression pattern of α-enolase in pre- and postnatal myocardium of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, and to explore the relationship between the overexpression of α-enolase and left ventricular hypertrophy.

Methods

HE staining was used for the measurement of cardiac hypertrophy. Immunohistochemical technique was used to evaluate the location of α-enolase. The expressions of α-enolase in the left cardiac ventricles at different development times were examined by Real-time RT-PCR and Western blot.

Results

Cardiac hypertrophy was found in SHR rats at 4 weeks of age and remained up to 24 weeks of age. The signals of α-enolase protein were strong and existed extensively in hypertrophic myocardium in SHR, while in the normal myocardium of WKY, the signals were scarcely found and weak. The levels of α-enolase mRNA and protein in SHR and WKY hearts during fetal stage and newborn stage were similar, while from 4 weeks of age to 24 weeks of age, accompanied by the cardiac hypertrophy, the levels of α-enolase mRNA and protein in left ventricle of SHR were significantly higher than that in WKY.

Conclusions

The expressions of α-enolase in the left ventricle of the rats during normal and pathological cardiac development were different. This phenomenon provides the potential clues to understanding pathophysiological mechanisms in cardiac hypertrophy of SHR.     

自发性高血压大鼠淋巴微循环功能受损

目的:观察自发性高血压大鼠(SHRs)淋巴微循环功能变化.方法:8周龄雄性SHR大鼠(SHR组)和WKY大鼠(WKY组),每组各10只.应用VasT rack测量两组大鼠微淋巴管自律运动;取胸导管分离原代淋巴管内皮细胞(LECs).应用免疫荧光和Western Blot检测LECs血管内皮生长因子受体3(VEGFR3)...     

Cardiac muscle mechanics from Doca- and aging spontaneously hypertensive rats

Contractile properties of isolated papillary muscles from three age groups of spontaeously hypertensive rats (SHRs) were compared to those from age-matched Wistar-Kyoto rats (WKYs) to assess whether there were differences between the strains preceding and during the course of the hypertension. In all three age groups (7, 12, and 50 wk), the mechanical refractory periods (MRP) were longer and aftercontractions more prominent after paired pulse stimulation in preparations from SHRs than from age-matched WKYs. Other isometric twitch properties of SHR papillary muscles at Lmax were not different from WKYs, with the exception of a shorter half-relaxation time in the youngest SHR group. Although hypertension and cardiac hypertrophy increased in SHRs with age, aging had similar influences on most cardiac contractile properties in both strains. None of the isometric properties of papillary muscles from rats made hypertensive by Doca treatment were different from those in normotensive control preparations. This suggests that differences seen between SHRs and WKYs probably represent genetic differences between these strains and are not directly caused by the hypertension.     

Acquisition of conditioned suppression and responsivity to thermal stimulation in spontaneously hypertensive,renal hypertensive and normotensive rats

The acquisition of conditioned suppression of instrumental responding and responsivity to thermal stimulation were assessed in spontaneously hypertensive rats of the Okamoto-Aoki strain (SHRs), renal hypertensive rats of the Wistar-Kyoto strain (WKYs), and normotensive WKY rats. Spontaneously hypertensive rats showed significantly faster acquisition of conditioned suppression than age-matched WKY normotensive rats. This acquisition difference between SHRs and normotensive WKYs was maintained even following chronic preexposure to shock alone; a treatment that retarded normal acquisition of conditioned suppression. In contrast, renal hypertensive WKYs acquired conditioned suppression at the same rate as age-matched normotensive WKYs. Spontaneously hypertensive rats and renal hypertensive WKYs both showed significantly longer latencies than normotensive WKYs to respond to thermal stimulation using a hot-plate assay. These outcomes suggest that the relationship between blood pressure and the acquisition of conditioned suppression in SHRs is either pleiotrophic or a consequence of random fixation, and that acquisition of conditioned suppression may serve as a valuable marker variable of hypertension in the SHR. The dissociation between acquisition of conditioned suppression and responsivity to thermal stimulation suggests that different mechanisms may mediate nociceptive responses to shock and thermal stimulation in these models of hypertension.     

Gamma-interferon corrects aberrant protein kinase C levels and immunosuppression in the spontaneously hypertensive rat.

The effects of gamma-interferon (gamma-IFN) on protein kinase C (PKC) levels and immunosuppression in the spontaneously hypertensive rat (SHR) were examined. First, an abnormal PKC distribution was found in spleen, thymus and aorta from SHRs relative to normotensive controls. Biweekly injections of rat recombinant gamma-IFN (1000 U/kg) restored basal or resting PKC levels to those found in normotensive Wistar-Kyoto (WKY) rats. We also examined the effects of in vivo gamma-IFN treatment on nuclear PKC (nPKC) activation in purified, isolated splenocyte nuclei. It was found that basal nPKC levels were higher in untreated SHRs than gamma-IFN SHRs or WKYs. Also, while nuclei from untreated SHRs were relatively unresponsive to various immunoreactive substances and PKC activators, gamma-IFN treatment significantly restored activity. Last, the proliferative response to mitogen challenge of isolated splenocytes from untreated SHRs, gamma-IFN-treated SHRs and WKYs was studied. Although gamma-IFN treatment did not restore the proliferative response to that of WKYs, the mitogen response was significantly enhanced by treatment with gamma-IFN. The data show that gamma-IFN acts to restore normal immune function and corrects aberrant PKC levels and adds to the growing body of knowledge suggesting a role for immune dysfunction in the etiology of hypertension.     

Effects of exercise training on pathological cardiac hypertrophy related gene expression and apoptosis

This study determined whether exercise training prevents pathological hypertrophy in the left ventricle by modulation of myocardial and apoptosis-associated genes. We used spontaneously hypertensive rats (n=15, non-exercise SHR), exercise-trained SHR (n=15, treadmill exercise for 12 weeks), and sedentary Wistar-Kyoto (WKY) rats (n=15). Exercise-trained SHR expressed adaptive changes such as reduced body weight, heart rate, blood pressures, left ventricle wall thickness, lipid profiles, and homocysteine level. The mRNA expression of angiotensin converting enzyme, endothelin-1, and brain natriuretic peptides in the heart was lower in the exercise-trained SHR and in the WKY than in the non-exercise SHR, whereas mRNA expression of caveolin-3 and eNOS in the heart was higher. Bcl-2 protein was higher in the exercise-trained SHR than in the WKY and the non-exercise SHR. In contrast, Bax protein levels were lower in the exercise-trained SHR and in the WKY than in the non-exercise SHR. Furthermore, the levels of the active forms of caspase-3 (20 kDa) were lower in the exercise-trained SHR and in the WKY than in the non-exercise SHR. These findings suggest that exercise training prevents pathological hypertrophy in the left ventricle by modulation of myocardial genes and that it interferes with a signal transduction pathway of apoptosis secondary to the pathological cardiac hypertrophy.     

Pharmacological blockade of blood pressure and heart rate increases following milk ingestion in 15-day-old SHR and WKY rat pups.

The effects of hexamethonium, a ganglionic blocker, on blood pressure (BP) and heart rate (HR) responses to milk ingestion were assessed in awake, 15-day-old spontaneously hypertensive rats (SHR) and their normotensive progenitor strain, Wistar-Kyoto rats (WKY) using two methods of milk delivery. SHRs had larger increases in BP compared to WKYs, but WKYs exhibited larger increases in HR following milk ingestion from an anesthetized dam. BP responses to milk ingestion from a tongue cannula were also larger in SHRs. Administration of hexamethonium prior to milk delivery resulted in a drop in BP following milk ingestion in both milk delivery situations for each strain. The results suggest that SHRs exhibit exaggerated sympathetic activation to milk ingestion compared to WKYs, and that in both strains, cardiovascular responses to feeding are modulated by the presence of the dam.     

螺内酯和缬沙坦对高血压大鼠心肌细胞外信号调节激酶的影响

目的:观察血管紧张素Ⅱ受体拮抗剂缬沙坦和醛固酮受体拮抗剂螺内酯对SHR心肌中活化的ERK的影响。方法:将18只雄性SHR随机分为三组,每组6只。其中两组分别用缬沙坦30mg/kg/天、螺内酯20mg/kg/天溶于饮水灌胃,连续治疗13周;对照组给正常饮水,并与Wist-ar-kyoto大鼠(WKY)比较。用Western-blot方法检测大鼠心肌磷酸化ERK的表达。结果:SHR对照组心肌磷酸化ERK/actin值高于其余三组(P<0.01),螺内酯和缬沙坦组高于WKY组(P<0.01),两用药组之间无差异。结论:血管紧张素Ⅱ受体拮抗剂缬沙坦和醛固酮受体拮抗剂均能通过抑制ERK途径而抑制左室肥厚和心肌纤维化。     

转化生长因子-β_1在自发性高血压大鼠肾小管的表达及作用

目的:研究转化生长因子-β1(TGF-β1)在自发性高血压大鼠(SHR)肾小管的表达及其与肾小管间质纤维化的关系。方法:以同龄雄性正常血压大鼠(WKY)和SHR为研究对象,监测实验前后大鼠尾动脉血压、肾功能及β2-微球蛋白(β2-MG),并采用免疫组织化学方法检测TGF-β1在肾小管中的表达。结果:同WKY组比较,SHR大鼠组24周时β2-MG显著增高,尾动脉血压显著性增高,尿素氮和血肌酐的差异无显著性意义。TGF-β1在WKY组肾小管的表达无或极微量,而在SHR组肾小管的表达明显,且随高血压病程的进展显著性增加。结论:TGF-β1在SHR肾小管的表达显著增加,提示其可能是致肾问质纤维化的重要因素。     

Peritoneal leucocytes from spontaneously hypertensive rats have reduced chemiluminescence response and lowered sensitivity to dexamethasone in vivo

The genetically altered hypothalamo-pituitary-adrenocortical axis in the spontaneously hypertensive rat (SHR) suggests altered phagocyte function in this strain. We therefore compared luminol-amplified chemiluminescence in peritoneal leucocytes from 10- to 12-week-old SHRs and age-matched Wistar–Kyoto rats (WKYs) activated by serum-opsonized zymosan particles (SOZ), N-formyl-l -methionyl-l -leucyl-l -phenylalanine (fMLP) or phorbol 12-myristate 13-acetate (PMA). While the number of peritoneal monocytes/macrophages was increased by 49% in SHRs relative to WKYs, activator-induced chemiluminescence per cell in SHRs was only 14–42% of that in WKYs. FMLP responses were especially low in SHRs. Treatment of rats with dexamethasone in the drinking water for 48 h prior to ex vivo experiments reduced chemiluminescence dose-dependently in WKYs as well as in SHRs. ED₅₀ of dexamethasone in SHRs was, however, increased compared to WKYs, indicating lowered sensitivity to dexamethasone in SHRs. No evidence was found of strain differences in differential distribution of peritoneal cells or in pharmacokinetics of dexamethasone. Plasma ACTH levels were significantly higher in SHRs than in WKYs, while basal plasma corticosterone concentrations in SHRs and WKYs were not significantly different. The results suggest that production of reactive oxygen compounds by peritoneal mononuclear phagocytes is reduced in SHRs compared with WKYs, and that the phagocyte respiratory burst is modulated differently by endogenous glucocorticoids in the two strains. We propose that reduced activity of the phagocyte NADPH oxidase-myeloperoxidase system is a major contributory cause of the altered chemiluminescence responses in SHRs. The data indicate that species differences may also be present at earlier steps in the signal transduction pathways activated by SOZ, fMLP and PMA.     

Locomotor activity, auditory startle and shock thresholds in spontaneously hypertensive rats

A group of SHRs and a group of WKY normotensive controls were compared sequentially on open-field behavior, Y-maze activity, responsiveness and habituation of the auditory startle response, and shock thresholds. In the open field and Y maze the SHRs were more active than the WKYs, but the locomotor activity of the SHRs decreased more within sessions. However, the SHRs could be described as showing more, less or the same between-session habituation depending upon the apparatus and the portion of the session analyzed. The SHRs were less responsive than controls on the auditory startle response measure, and they did not differ from controls on startle-response habituation. The SHRs were less responsive than controls at low shock levels but more responsive at high shock levels. The relationship between SHRs and WKYs on the responsiveness dimension depended upon the modality and intensity of the stimulus, the response characteristics of the test situation, and the time sample of behavior taken.     

Enhanced excitatory junction potentials in mesenteric arteries from spontaneously hypertensive rats

Excitatory junction potentials (EJPs) were examined using intracellular recording techniques in mesenteric arteries isolated from 12- to 15-week-old spontaneously hypertensive (SHR), Wistar Kyoto (WKY) and Sprague Dawley (SD) rats. The amplitudes of EJPs evoked by single supramaximal stimuli were larger in arteries from SHRs (12.9±0.7 mV,n=16) than in arteries from either WKYs (5.2±0.5 mV,n=24) or SDs (8.6±0.8 mV,n=15). The time constant of decay of EJPs did not differ significantly, suggesting that the passive electrical properties of the vascular smooth muscle are similar in the three rat strains. Spontaneous EJPs recorded in tissues from SHRs and WKYs had similar amplitude frequency distributions, suggesting that the quantal size is also similar between strains. In some arteries from SHRs, EJPs evoked by single stimuli triggered muscle action potentials (MAPs). Visible constriction only occurred following a MAP. In tissues from all three strains, summation of EJPs triggered MAPs. As EJPs are generated by the sympathetic co-transmitter adenosine 5-triphosphate (ATP), the findings of the present study indicate that purinergic transmission is enhanced in mesenteric arteries from SHRs, probably as a result of an increase in quantal release. A consequence is that when nerves are activated SHR arteries more readily undergo constriction that is dependent on voltage-activated Ca²⁺ influx.     

短链酰基辅酶A脱氢酶在大鼠心脏发育中的表达及其与心肌肥厚的关系

 目的：研究大鼠心脏发育过程中短链酰基辅酶A脱氢酶(short-chain acyl-CoA dehydrogenase, SCAD)的表达变化规律,并探讨其与高血压大鼠心肌肥厚的关系。方法：观察不同时期Wistar大鼠和不同周龄自发性高血压大鼠心肌组织的SCAD蛋白表达及酶活性变化,检测大鼠的血清和心肌游离脂肪酸含量。结果：与胚胎期19 d Wistar大鼠组比较,出生后1 d、2周、6周及16周龄Wistar大鼠组心肌的SCAD蛋白表达及酶活性增加,血清和心肌游离脂肪酸含量明显减少,二者之间呈负相关,其中,从2周龄Wistar大鼠组开始差异有统计学意义。与周龄匹配的WKY大鼠组比较,2周龄自发性高血压大鼠组收缩压尚未升高,6周龄及16周龄自发性高血压大鼠组收缩压显著增高;各时点自发性高血压大鼠组的左室重量指数均明显增高,提示自发性高血压大鼠在血压升高之前,已经发生了明显的心肌肥厚。与周龄匹配的WKY大鼠组比较,2周、6周及16周龄自发性高血压大鼠组心肌的SCAD蛋白表达及酶活性明显下降,血清和心肌游离脂肪酸含量明显增加,呈显著负相关。结论：(1)SCAD蛋白表达随大鼠心脏的生长发育逐渐上调,可能与心脏对脂肪酸的利用增加密切相关。(2)SCAD的蛋白表达及其酶活性显著下降, 可能是导致自发性高血压大鼠肥厚心肌能量代谢“胚胎型再演”的分子基础。     

SHR心肌细胞内钙离子浓度改变与左室肥厚和功能的关系

目的:探讨自发性高血压大鼠(SHR)心肌细胞内钙离子浓度的动态演变规律及其与左室肥厚和功能的相互关系。方法:应用Ca²⁺荧光指示剂Fura-2/AM分别测定了10周龄、22周龄、34周龄SHR心肌细胞内Ca²⁺浓度以及导管法测定了大鼠心功能,并以同龄京都-Wistar(WKY)大鼠作对照。结果:各周龄SHR收缩压(SBP)、心肌细胞内Ca²⁺浓度([Ca⁺]_i)、左室重量/体重(LVM/BW)均明显高于同龄正常血压WKY大鼠,22周龄SHR左室压力最大下降速率(-dp/dt_max)低于、左室松弛时间常数(τ)长于同龄WKY大鼠,34周龄SHR±dp／dt_max和左室收缩指数均显著低于同龄WKY大鼠,τ进一步延长;心肌细胞内[Ca⁺]_i与大鼠LVM/BW、SBP-dp／dt_max、τ呈显著正相关(r=0.47-0.83,P＜0.01),与dp／dt_max和收缩指数呈显著负相关(r=-0.46,P<0.05和-0.81,P<0.01)。结论:SHR心肌细胞内钙离子超负荷不仅介导了心肌肥厚的形成,还导致了心肌的收缩和舒张功能障碍。     

Behavioral reactivity in spontaneously hypertensive rats

Spontaneously hypertensive rats of the Okamoto strain (SHR) were compared with inbred normotensive rats of the Wistar-Kyoto strain (WKY) and with normally bred Wistar rats (NT) in tests on the audiogenic immobility reaction (freezing), open-field behavior in a dark and an enlightened arena respectively, auditory startle response and male sexual behavior. Compared to the WKYs the SHRs showed increased locomotion and rearing in the open-field situations, reduced startle response and shortened immobility reaction. The SHRs differed in the same way from the NT rats with the exception for motor activity in the dark arena, where no differences were observed. The WKY rats showed less motor activity than the NT animals. Both SH and WKY rats showed shorter latency time for ejaculation than the NT rats. The characteristics of the behavior patterns displayed by the SH rats were interpreted as indicating a reduced propensity for fear reactions in this strain of rats compared to the WKY and NT strains used in the present study.     

The effects of beta adrenoceptor blockade with atenolol on myocardial cellular and subcellular hypertrophy in spontaneously hypertensive rats

In this study we investigated the effects of chronic β adrenoreceptor blockade with atenolol on cellular and subcellular hypertrophy in spontaneously hypertensive rats (SHR). Atenolol was injected subcutaneously (20 mg/kg) twice daily commencing in four-week-old rats. The treated animals (SHR-A) were compared to their nontreated controls and normotensive, Wistar-Kyoto (WKY) controls at the age of 16 weeks. A group of atenolol-treated WKY was also studied. Chronic drug treatment was effective in attenuating the rise in systolic blood pressure characteristic of SHR, but did not normalize the values to those of WKY. Cardiac hypertrophy, characteristic of SHR, was modified by drug treatment as evidenced by left ventricular weights as well as myocardial cell size. The cells from the subendocardium underwent selective hypertrophy in SHR which was attentuated by about 50% after atenolol treatment. Stereological analysis of electron micrographs showed that while relative mitochondrial volume was not affected by treatment, relative myofibrillar volume (%) decreased in both subepicardium (SHR = 63.28 ± 1.25; SHR-A = 56.72 ± 1.37) and subendocardium (SHR = 66.53 ± 1.27; SHR-A = 58.30 ± 1.51). This change raised the mitochondrial/myofibrillar volume ratio, which is characteristically low in SHR compared to WKY. Sarcoplasm, which included all cell constituents except mitochondria, increased with atenolol treatment, but water concentration remained unchanged. The data suggest that attenuation of hypertrophy in SHR after β blockade is associated with selective effects on the myocardial cell involving primarily the myofibrillar cell compartment.