Long-term intermittent hypoxia enhanced blood pressure responsiveness to hypoxia in all rats, but increased left ventricular weight and ANP mRNA only in spontaneously hypertensive rats.
Does long-term intermittent hypoxia alter cardiovascular function in Wistar-Kyoto and spontaneously hypertensive rats?
Long-term intermittent hypoxia induces cardiovascular changes such as enhanced hypoxic pressor response and strain-specific ventricular hypertrophy in a rat model.
We investigated whether the effect of long-term intermittent hypoxia (LTIH) on cardiovascular function may be modified by preexisting genetic traits. To induce LTIH experimentally, cycles of 90-s hypoxia (nadir 6%) followed by 90-s normoxia were applied to six Wistar-Kyoto and six spontaneously hypertensive rats during 8 h daily. Comparison with the same number of control animals after 70 days revealed no alteration of intra-arterial blood pressure or heart rate. Blood pressure responsiveness to a brief hypoxic stimulus was enhanced in the LTIH animals, regardless of strain, whereas the hypoxia-induced increase in heart rate was abolished. In the spontaneously hypertensive but not the Wistar-Kyoto rats, LTIH increased left ventricular weight-to-body weight ratio and content of atrial natriuretic peptide mRNA. Expression of B-type natriuretic peptide was unchanged (Northern blot). Slightly increased right ventricular weight-to-body weight ratios in the LTIH animals were associated with higher right ventricular atrial natriuretic peptide and B-type natriuretic peptide mRNA amounts. Consequently, the effects of LTIH on different components of cardiovascular function appear incompletely related to each other and differentially influenced by constitutional traits.
Kraiczi et al. (Wed,) conducted a other in Cardiovascular function under long-term intermittent hypoxia (n=24). Long-term intermittent hypoxia (LTIH) vs. Control animals (normoxia) was evaluated on Cardiovascular function (blood pressure, heart rate, ventricular weight, natriuretic peptide mRNA). Long-term intermittent hypoxia enhanced blood pressure responsiveness to hypoxia in all rats, but increased left ventricular weight and ANP mRNA only in spontaneously hypertensive rats.
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