In this brief review, we have discussed the functional significance of cardiac myosin isoform redistribution. The development of in vitro motility assay techniques has greatly aided the research in this field. The next important step would be the integration of data at molecular or cellular level to account for the pathophysiology of animal or human body. A new conceptual framework that can deal with the complex nature of a biological system may be required for this purpose.

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The present study was designed to investigate whether the limited capacity for concentrating urine in neonatal rats is associated with an immature ability to regulate serum osmolality. During milk deprivation, the percent of reduction in body weight per 10 h (mean±SE) was 4.3±0.2, 3.7±0.1, 4.8±0.2, and 6.0±0.1% in 4-, 7-, 10-, and 14-d-old rats, respectively (n=23-24, each age). The osmolality of urine increased to 718±12 (4d), 741±28 (7d), 792±20 (10d), and 1, 203±41 mosmol/kg H₂O (14d). Free-water absorption (T^c_H2O) Promptly increased after deprivation of milk: It significantly increased from 2.3±0.3 (0-4h) to 3.4±0.1 (4-7h) (4d), from 3.1±0.3 to 4.1±0.3 (7d), from 3.6±0.4 to 5.2±0.3 (10d), and from 5.0±0.4 to 7.9±0.7 μl/min/100g (14d). The raised values were maintained at the later period of dehydration. Thus serum osmolality was unchanged throughout dehydration: 287±1.0 (7d) and 292±0.9 mosmol/kg H₂O (14d). On the other hand, the level of serum sodium concentration slightly but significantly increased (r=0.61) when the body weight reduction was higher than 5% of the control (14-d-old rats). These results indicate that neonatal rats of 4-14d control their serum osmolality by reabsorbing free water in the kidney during the 10 or 12h of milk deprivation.

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Brown adipose tissue (BAT) is a major organ of nonshivering thermogenesis during cold acclimation, overfeeding, and nonthermal restraint stress. An increased unsaturation of fatty acids of membrane phospholipid in BAT has been shown to be closely associated with an enhanced function of this tissue as reported in other tissues. In the previous study, we found that among fatty acids detected, the n-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) in BAT phospholipid is the only fatty acid that altered concomitantly with a change in the in vitro thermogenic capacity for nonshivering thermogenesis of BAT from cold acclimated and restrained rats. To examine the effect of dietary DHA on fatty acid composition of phospholipid and in vitro BAT thermogenic activity, rats were fed a standard diet supplemented with purified DHA for 4 or 16 weeks. Dietary DHA for 4 or 16 weeks increased DHA level in BAT phospholipid, and it also decreased arachidonic acid. The unsaturation index increased and remained unchanged under DHA feeding for 4 and 16 weeks, respectively. In vitro thermogenic activity of BAT remained unchanged and decreased under dietary DHA for 4 and 16 weeks, respectively. These findings indicate that dietary DHA could increase DHA level in phospholipid of BAT, but it could not improve in vitro BAT thermogenic response.

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We measured rat left ventricular pressure, volume, and oxygen consumption (=arteriovenous oxygen content difference×coronary flow) to establish a new evaluation of its mechanoenergetics in the whole heart preparation by using the cross-circulation method. We obtained a curved end-systolic pressure-volume relation in contrast to a linear end-systolic pressure-volume relation in dogs, rabbits, and humans. However, we obtained a linear oxygen consumption per beat (VO₂)-systolic pressure-volume area (PVA, a measure of left ventricular total mechanical energy per beat) relation as in other species. Thus PVA can be a good index for assessing rat left ventricular mechanoenergetics. The VO₂ intercept and slope of the linear VO₂-PVA relation correspond to those in other species. Intracoronary calcium elevated the curved end-systolic pressure-volume relation and significantly increased PVA at 0.15 ml/g of left ventricular end-diastolic volume (PVA_0.15) by 50%. Calcium also significantly increased the VO₂ intercept of the VO₂-PVA relation by 30% without a change in its slope. We conclude that the rat left ventricular end-systolic pressure-volume relation is curved, but the VO₂-PVA relation is linear, and that the VO₂ intercept is mainly composed of PVA-independent VO₂, presumably VO₂ for Ca²⁺ handling in the excitation-contraction coupling and basal metabolism. Therefore we propose PVA at an appropriate left ventricular volume and the VO₂ intercept as good rat left ventricular mechanoenergetic indexes despite the nonlinearity of the end-systolic pressure-volume relation.

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In the membrane stability of human erythrocytes, the role of two cysteine residues (Cys-201 and Cys-317) in the cytoplasmic domain of band 3 is not clear. So we tried to resolve this problem by examining hemolytic properties under high pressure. From SH contents and spin labeling, it was found that Cys-201 and Cys-317 of band 3 were modified with N-ethyl-maleimide (NEM). The hemolysis of intact erythrocytes at 200 MPa was suppressed by the binding of 4, 4'-diisothiocyanostilbene-2, 2'-disulfonate (DIDS), anion transport inhibitor, to band 3. Similarly, the suppressive effect of DIDS was observed in the erythrocyte that Cys-201 and Cys-317 were modified with NEM. These results suggest that the cysteine residues in the cytoplasmic domain of band 3 are not essential for the DIDS-induced membrane stabilization.

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The daily profile of energy expenditures was examined in the new animal model of genetically diabetic obese rats. The diurnal rhythm was observed at 8 weeks of age, with highest and lowest values for energy consumption per hour observed in the dark and light periods, respectively. However, at 24 weeks of age after the manifestation of noninsulin-dependent diabetes mellitus, the rhythm completely disappeared, but it did not in the control rats.

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The hypotensive effects of an angiotensin II type 1 receptor antagonist TCV-116 were accelerated by swimming training in the early period of chronic administration in young rats. In the latter period, however, a severe decrease in blood pressure that appeared during long-term administration of TCV-116 was prevented by swimming training. Therefore exercise may contribute to the stabilization of blood pressure in young rats treated with TCV-116.

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