Key result
Chronic hypotension produced by myocardial infarction in rats resulted in complete resetting of baroreceptors without changes in gain sensitivity (1.67 %/mmHg at 30 days vs 1.47 %/mmHg for SHAM).
Why the study?
Does chronic hypotension produced by myocardial infarction alter aortic baroreceptor gain sensitivity in rats?
Does chronic hypotension produced by myocardial infarction alter aortic baroreceptor gain sensitivity in rats?
Absolute Event Rate: 1.67% vs 1.47%
In a rat model of MI-induced chronic hypotension, aortic baroreceptors reset to lower pressures without a decrease in gain sensitivity, maintaining normal baroreflex control of heart rate.
Preserved baroreflex gain despite resetting in rat MI model; leaves open applicability to clinical post-MI baroreflex assessment.
In chronic hypertension, the baroreceptors reset to hypertensive levels with a decrease in gain sensitivity, but only a few studies have evaluated baroreceptor resetting during chronic hypotension and, under these conditions, no consistent information is available concerning changes in baroreceptor gain sensitivity. Therefore, in the present study, the aortic baroreceptor function curve and the baroreflex control of heart rate (HR) were evaluated in chronic hypotension produced by myocardial infarction (MI) with no heart failure. 2. Aortic baroreceptor function curves were studied in anaesthetized three groups of rats: (i) MI-7, six rats 7 days after MI; (ii) MI-30, nine rats 30 days after MI; and (iii) five control animals (SHAM). The pressure-nerve activity relationship was measured during rapid changes in blood pressure by integrating the whole-nerve activity of the baroreceptors in a computerized beat-to-beat analysis. 3. Both long-term periods (7 or 30 days) of hypotension were accompanied by complete resetting of the baroreceptor in rats (the leftward displacement of the baroreceptor curve matched the decrease in blood pressure). Moreover, the resetting of the baroreceptor function curve was not accompanied by changes in gain sensitivity (1.47, 1.64 and 1.67%/mmHg for SHAM, MI-7 and MI-30 groups, respectively) and the baroreflex control of HR was normal comparing SHAM and MI-30 groups (bradycardic 1.62 +/- 0.18 vs 1.99 +/- 0.52 b.p.m./mmHg, respectively; tachycardic 3.6 +/- 0.5 vs 4.1 +/- 0.4 b.p.m./mmHg for, respectively). 4. The data indicate that the resetting of baroreceptors in chronic hypotension is stable and is not accompanied by changes in gain sensitivity, as observed in hypertension. This may account for the normal baroreflex control of HR observed in non-anaesthetized rats.
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Koike et al. (2006) studied Chronic hypotension produced by myocardial infarction (n=20). Chronic hypotension produced by myocardial infarction vs. SHAM (control animals) was evaluated on Baroreceptor gain sensitivity. Chronic hypotension produced by myocardial infarction in rats resulted in complete resetting of baroreceptors without changes in gain sensitivity (1.67 %/mmHg at 30 days vs 1.47 %/mmHg for SHAM).
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