Essential hypertension results from the interaction among multiple genes and the environment. A post-pubertal high-salt diet (AIN-76A, 4% NaCl, 4 weeks) induces hypertension in SS/JrHsd/Mcwi rats after pre-pubertal environmental priming (low-salt AIN-76 diet to the breeder and offspring from weaning) (Mattson, Physiol. Genomics, 2004, 16:194-203). Introgression of chromosome 13 from Brown Norway rats into the SS/JrHsd/Mcwi genome confers protection from salt-sensitive hypertension to the SS-13BN/Mcwi consomic rat strain (Cowley, Hypertension, 2001, 37[part 2]:456-461). We assessed whether a post-pubertal dietary challenge is sufficient to induce salt-sensitive hypertension in SS/JrHsd/Mcwi rats, adopting SS-13BN/Mcwi rats as a control strain. SS/JrHsd/Mcwi and SS-13BN/Mcwi breeders and their offspring were maintained on a grain-based low-salt diet. Rats under study (n = 4 males per strain) were subjected to a massive dietary challenge (AIN 76-A, 8% NaCl, 4 weeks) from the end of puberty, implanted with electrodes for sleep-state identification and an arterial catheter for pressure measurement, and studied during spontaneous episodes of wakefulness (W), rapid-eye-movement sleep (REMS), and non-rapid-eye-movement sleep (NREMS). Data are analyzed by ANOVA and reported as grand means ± SEM. In SS/JrHsd/Mcwi rats, mean arterial pressure (MAP) was 131±4, 123±3 and 121±4 mmHg in W, NREMS and REMS, respectively. In SS-13BN/Mcwi rats, MAP was 127±3, 120±3 and 117±3 mmHg in W, NREMS and REMS, respectively. MAP significantly differed among wake-sleep states (p<0.001), being significantly higher in W than either in NREMS (p<0.001) or REMS (p<0.001). Neither the main effect of the rat strain (p=0.47) nor the interaction between strain and wake-sleep state (p=0.92) were statistically significant. With our dietary protocol, the difference in MAP between salt-sensitive SS/JrHsd/Mcwi and SS-13BN control rats was substantially less robust than the physiological MAP differences among wake-sleep states. Our data thus indicate that the lack of a pre-pubertal environmental priming prevented salt-sensitive hypertension in this consomic rat model.
Silvani A, Asti V., Berteotti C., Ferrari V., Franzini C., Lenzi P., et al. (2006). Lack of pre-puberal environmental priming prevents salt-sensitive hypertension in a consomic rat model.
Lack of pre-puberal environmental priming prevents salt-sensitive hypertension in a consomic rat model
SILVANI, ALESSANDRO;ASTI, VALENTINA;BERTEOTTI, CHIARA;FERRARI, VERA;FRANZINI, CARLO;LENZI, PIERLUIGI;ZOCCOLI, GIOVANNA
2006
Abstract
Essential hypertension results from the interaction among multiple genes and the environment. A post-pubertal high-salt diet (AIN-76A, 4% NaCl, 4 weeks) induces hypertension in SS/JrHsd/Mcwi rats after pre-pubertal environmental priming (low-salt AIN-76 diet to the breeder and offspring from weaning) (Mattson, Physiol. Genomics, 2004, 16:194-203). Introgression of chromosome 13 from Brown Norway rats into the SS/JrHsd/Mcwi genome confers protection from salt-sensitive hypertension to the SS-13BN/Mcwi consomic rat strain (Cowley, Hypertension, 2001, 37[part 2]:456-461). We assessed whether a post-pubertal dietary challenge is sufficient to induce salt-sensitive hypertension in SS/JrHsd/Mcwi rats, adopting SS-13BN/Mcwi rats as a control strain. SS/JrHsd/Mcwi and SS-13BN/Mcwi breeders and their offspring were maintained on a grain-based low-salt diet. Rats under study (n = 4 males per strain) were subjected to a massive dietary challenge (AIN 76-A, 8% NaCl, 4 weeks) from the end of puberty, implanted with electrodes for sleep-state identification and an arterial catheter for pressure measurement, and studied during spontaneous episodes of wakefulness (W), rapid-eye-movement sleep (REMS), and non-rapid-eye-movement sleep (NREMS). Data are analyzed by ANOVA and reported as grand means ± SEM. In SS/JrHsd/Mcwi rats, mean arterial pressure (MAP) was 131±4, 123±3 and 121±4 mmHg in W, NREMS and REMS, respectively. In SS-13BN/Mcwi rats, MAP was 127±3, 120±3 and 117±3 mmHg in W, NREMS and REMS, respectively. MAP significantly differed among wake-sleep states (p<0.001), being significantly higher in W than either in NREMS (p<0.001) or REMS (p<0.001). Neither the main effect of the rat strain (p=0.47) nor the interaction between strain and wake-sleep state (p=0.92) were statistically significant. With our dietary protocol, the difference in MAP between salt-sensitive SS/JrHsd/Mcwi and SS-13BN control rats was substantially less robust than the physiological MAP differences among wake-sleep states. Our data thus indicate that the lack of a pre-pubertal environmental priming prevented salt-sensitive hypertension in this consomic rat model.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
