Cardiac conditioning ameliorates cardiac dysfunction associated with renal hypertension in rats.

Abstract

Abstract. To explore the effect of physiologic hypertrophy superimposed on pathologic hypertrophy, hearts from female control rats (C), renal hypertensive rats (H), rats conditioned with a 10-12 wk swimming program (Sw), and hypertensive rats trained by the swimming program (H-Sw) were perfused in an isolated working rat-heart apparatus. Systolic blood pressure was -100 mmHg in C and Sw and was 160 mmHg in H and HSw. The swimming program had no effect on blood pressure. Compared with C, heart weight was increased by 30% in Sw, 47% in H, and 77% in H-Sw. At high preload and afterload, cardiac output (milliliters per gram dry LV weight) was decreased in H, increased in Sw, and partially restored towards normal in H-Sw. Ejection fraction, percent fractional shortening, and mean velocity of circumferential fiber shortening were enhanced in Sw, depressed in H, and normalized in H-Sw when compared with C. Coronary flow and myocardial oxygen consumption in this series of hearts were depressed in H, with no restoration in H-Sw, but coronary effluent lactate/ pyruvate ratios were only elevated in the hearts of H-Sw. Coronary vascular responses were examined in a second series of experiments which used microspheres. In this series, the depressed coronary flow observed in H was partially restored towards normal in H-Sw and the inner/ outer myocardial flow ratio was normal when hearts were

The cardiac beta-myosin heavy chain isogene is induced selectively in alpha 1-adrenergic receptor-stimulated hypertrophy of cultured rat heart myocytes.

“…Induction of early developmental isogenes is not found in all types of hypertrophy in vivo, such as hypertrophy produced by exercise training or thyroid hormone excess (7,(14)(15)(16)49). Similarly, hypertrophied cardiac myocytes in culture have different MHC isoform phenotypes which depend on the specific hypertrophic stimulus.…”

“…Furthermore, it has been shown that fl-MHC induction in pathological hypertrophy produced by pressure overload can be reversed by exercise training, a stimulus for physiological hypertrophy (14)(15)(16). This observation has raised the possibility that the molecular mechanisms mediating fl-MHC expression are activated only in certain types of hypertrophy.…”

Analysis of differentially expressed genes in hyperthyroid-induced hypertrophied heart by cDNA microarray

“…Although it is reported that thyroid hormone influences cardiac growth and metabolism via the signaling pathway distinct from other hypertrophic stimuli, the molecular mechanisms underlying hyperthyroid-induced versus pathological hypertrophy remain uncertain (Scheuer et al 1982, Schaible et al 1984, Izumo et al 1987. Some of the unique features of thyroid hormone-induced gene expression in cardiac muscle are induction of alpha myosin heavy chain (MHC-), sarco-endoplasmic reticulum Ca 2+ ATPase (SERCA) and repression of beta MHC (MHC-) (Dillmann 1990, Kinugawa et al 2001, Klein & Ojamaa 2001.…”

Thyroid hormone improves function and Ca2+ handling in pressure overload hypertrophy. Association with increased sarcoplasmic reticulum Ca2+-ATPase and alpha-myosin heavy chain in rat hearts.

“…Although the molecular mechanisms underlying physiological versus pathological hypertrophy remain uncertain, one potential therapeutic strategy might be to convert a pathological growth process to a physiological one. Indeed, Scheuer and colleagues showed that swimming exercise improved cardiac function in rats with pressure overload hypertrophy, even though heart weight was increased (7)(8)(9).…”