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Published on: February 14, 2021
Resetting of aortic baroreceptors in response to hypotension does not alter gain sensitivity
Marcia K Koike1, Edson D Moreira, Gustavo J J da Silva
1Hypertension Unit, Heart Institute (InCor), Medical School, University of São Paulo, São Paulo, Brazil.
Insights
Baroreceptors in rats with chronic hypotension reset normally without altered gain sensitivity. This finding explains the preserved baroreflex control of heart rate in hypotension, unlike in hypertension.
Area of Science:
- Cardiovascular Physiology
- Autonomic Nervous System Regulation
Background:
- Baroreceptor resetting is well-documented in chronic hypertension, showing decreased gain sensitivity.
- Limited data exists on baroreceptor function and gain sensitivity during chronic hypotension.
- Myocardial infarction (MI) in rats can induce chronic hypotension without heart failure, serving as a model for study.
Purpose of the Study:
- To investigate aortic baroreceptor function and baroreflex control of heart rate (HR) in a rat model of chronic hypotension induced by MI.
- To determine if baroreceptor resetting in hypotension is associated with changes in gain sensitivity.
- To compare baroreflex control of HR in hypotensive rats with control animals.
Main Methods:
- Aortic baroreceptor function curves were assessed in anesthetized rats 7 and 30 days post-MI, alongside a sham-operated control group.
- Pressure-nerve activity relationships were measured using computerized beat-to-beat analysis of integrated whole-nerve activity.
- Baroreflex control of HR was evaluated by analyzing bradycardic and tachycardic responses.
Main Results:
- Chronic hypotension (7 and 30 days post-MI) resulted in complete baroreceptor resetting, with the function curve shifting leftward to match the reduced blood pressure.
- Baroreceptor resetting was not accompanied by significant changes in gain sensitivity across the groups (SHAM, MI-7, MI-30).
- Baroreflex control of HR remained normal in rats with chronic hypotension compared to controls.
Conclusions:
- Baroreceptor resetting in chronic hypotension is a stable process that does not alter gain sensitivity.
- The preserved gain sensitivity in hypotension contributes to normal baroreflex control of heart rate.
- Findings contrast with hypertension, where baroreceptor resetting involves decreased gain sensitivity.
Abstract:
1. 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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