Two inbred rat strains, differing in their resistance to the induction of myocardial lesions by the administration of isoprenaline (ISO), have been developed. The extent of ISO-induced myocardial lesions (IML) was three to five times lower in the ISO-resistant (IR) strain as compared to that in the ISO-sensitive (IS) strain. The two strains differ also in a number of other genetically determined features, e.g., a higher myocardial glycogen content (MGC) and higher adipose tissue weight in IR rats. Between IML extent and MGC a significant negative correlation has been demonstrated in 2nd filial generation of IR and IS hybrids. By contrast, no correlation has been found between the resistance to the development of IML and the other genetically determined features studied. High resistance to the development of IML and a high MGC were also noted in another inbred strain, the hypertriacylglycerolemic (HTG) rats. Comparison of IML extent in HTG, IR and IS rats has revealed that the extent of IML, while depending on MGC, is independent of triacylglycerolemia. MGC can be raised in IR and IS rats by various interventions (e.g., repeated administration of ISD or fasting). Regardless of the intervention used, it entails a simultaneous increase in resistance to the development of IML. In vivo administration of glucose and insulin, however, exerts only a minimal effect on MGC and on the extent of IML. It may be concluded, therefore, that under our experimental conditions the enhanced resistance to the development of IML, whether genetically determined (IR, HTG rats) or induced by some interventions (fasting, repeated ISO administration), is closely related to an increased MGC.

Adrenergic beta-Agonists↗

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[Use of the polydactyly-luxation syndrome in rats for studying the interaction of the genome with teratogenic factors].

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Abnormalities, Drug-Induced↗

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Selective mesentericography as a guide to diagnosis and treatment of acute superior mesenteric artery occlusion.

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Aged↗

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[The stress gene in hypertension].

Thermosensitivity has been demonstrated in hypertensive rats and mice, and hypertension is frequent in hyperthermia-susceptible pigs. We have demonstrated that thermosensitivity segregates with hypertension in mice as a recessive trait in a single locus termed Tms. Since thermosensitivity can be demonstrated in cells obtained from neonatal hypertensive animals and persists after several passages in culture, it was of interest to study its cellular determinants. We undertook studies of candidate genes of cellular thermosensitivity, hsp70 being the major heat stress gene. First, we have observed an enhanced hsp70 mRNA accumulation in the hypertensive rat, mouse and human after heat shock of the whole animal, of its isolated organs or cultured cells. This increased accumulation of hsp70 mRNA in hypertension is due to its increased transcriptional rate. A restriction fragment length polymorphism (RFLP) of hsp70 was documented in hypertensive rats, which allowed the study of the segregation of this locus with hypertension in recombinant inbred strains of rats. At least one copy of hsp70 has been localized in RT1, the major histocompatibility complex of the rat, with polymorphism demonstrated with BamHI outside of the coding region of hsp70. This polymorphism segregates with 15 mmHg of systolic blood pressure. More recently, our studies led us to identify a polymorphism in another heat stress gene, hsp27. This polymorphism has been identified by PCR SSCP and is located in the 3' region, close to the termination translation codon.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗