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Acute effects of empagliflozin on open-loop baroreflex function and urinary glucose excretion in rats with chronic
Toru Kawada1, Meihua Li2, Akitsugu Nishiura2
1Department of Cardiovascular Dynamics, National Cerebral and Cardiovascular Center, Osaka, 564-8565, Japan. torukawa@ncvc.go.jp.
Abstract:
Sodium-glucose cotransporter 2 (SGLT2) inhibitors have exerted cardioprotective effects in clinical trials, but underlying mechanisms are not fully understood. As mitigating sympathetic overactivity is of major clinical concern in the mechanisms of heart failure treatments, we examined the effects of modulation of glucose handling on baroreflex-mediated sympathetic nerve activity and arterial pressure regulations in rats with chronic myocardial infarction (n = 9). Repeated 11-min step input sequences were used for an open-loop analysis of the carotid sinus baroreflex. An SGLT2 inhibitor, empagliflozin, was intravenously administered (10 mg/kg) after the second sequence. Neither the baroreflex neural nor peripheral arc significantly changed during the last observation period (seventh and eighth sequences) compared with the baseline period although urinary glucose excretion increased from near 0 (0.0089 ± 0.0011 mg min-1 kg-1) to 1.91 ± 0.25 mg min-1 kg-1. Hence, empagliflozin does not acutely modulate the baroreflex regulations of sympathetic nerve activity and arterial pressure in this rat model of chronic myocardial infarction.
Insights
Sodium-glucose cotransporter 2 (SGLT2) inhibitors like empagliflozin did not acutely affect baroreflex control of sympathetic activity or blood pressure in rats with heart damage. This suggests SGLT2 inhibitors
Area of Science:
- Cardiovascular Physiology
- Pharmacology
- Metabolic Disease Research
Background:
- Sodium-glucose cotransporter 2 (SGLT2) inhibitors show cardioprotective effects, but mechanisms remain unclear.
- Sympathetic overactivity is a key concern in heart failure treatment.
- Understanding SGLT2 inhibitors' impact on autonomic regulation is crucial.
Purpose of the Study:
- To investigate the acute effects of an SGLT2 inhibitor on baroreflex control of sympathetic nerve activity and arterial pressure.
- To determine if modulating glucose handling impacts autonomic regulation in chronic heart failure.
Main Methods:
- Utilized an open-loop analysis of the carotid sinus baroreflex in rats with chronic myocardial infarction.
- Administered empagliflozin (an SGLT2 inhibitor) intravenously.
- Measured sympathetic nerve activity and arterial pressure responses to baroreflex stimulation.
Main Results:
- Empagliflozin administration increased urinary glucose excretion significantly.
- Neither the neural nor the peripheral components of the baroreflex were acutely altered.
- No significant changes in baroreflex regulation of sympathetic nerve activity or arterial pressure were observed.
Conclusions:
- Empagliflozin does not acutely modulate baroreflex regulation in this rat model of chronic myocardial infarction.
- The cardioprotective effects of SGLT2 inhibitors may involve mechanisms beyond acute autonomic modulation.
- Further research is needed to elucidate the precise mechanisms of SGLT2 inhibitor-induced cardioprotection.
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