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Exercise Pressor Reflex in UC Davis Type‐2 Diabetes Mellitus (UCD‐T2DM) Rats Prior to the Onset of Diabetes
Author(s) -
Huo Yu,
Grotle Ann-Katrin,
Lee Junghoon,
Ybarbo Kai M.,
Graham James,
Stanhope Kimner L.,
Havel Peter J.,
Harison Michelle L.,
Stone Audrey J.
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.05847
Subject(s) - medicine , reflex , blood pressure , diabetes mellitus , endocrinology , type 2 diabetes mellitus , type 2 diabetes
Both the exercise pressor reflex and mechanoreflex are exaggerated after the development of T2DM in UCD‐T2DM rats. Whether the pressor reflex is also exaggerated before UCD‐T2DM rats developed diabetes is not known. Therefore, the purpose of this study was to determine if both the exercise pressor reflex and mechanoreflex are exaggerated in the UCD‐T2DM rats before the onset of diabetes. Methods For this study, we used young (8–12 wk old), male (n=12) and female (n=10), non‐diabetic UCD‐T2DM rats and age‐matched, male (n=11) and female (n=7), healthy Sprague Dawley rats. The exercise pressor reflex was evoked by statically and intermittently contracting the hindlimb muscle for 30s, and the mechanoreflex was evoked by passively stretching the Achilles tendon for 30s. Changes in mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) were continuously measured during both contraction and stretch. Results We found that fasting blood glucose for both groups was below the threshold for diagnosis of diabetes (200mg/dl). Statically contracting the muscle did not significantly increase peak MAP (CTL: 11 ± 1 mmHg, n=12; UCD‐T2DM: 14 ± 2 mmHg, n=13, p>0.05), HR (CTL: 12 ± 4 bpm, n=12; UCD‐T2DM: 14 ± 5 bpm, n=13, p>0.05), or RSNA (CTL: 40 ± 20 %, n=4; UCD‐T2DM: 39 ± 23 %, n=3, p>0.05) in UCD‐T2DM rats compared to control rats with similar developed tensions. Likewise, intermittently contracting the muscle did not significantly increase peak MAP (CTL: 14 ± 2 mmHg, n=13; UCD‐T2DM: 14 ± 2 mmHg, n=6, p>0.05), HR (CTL: 16 ± 3 bpm, n=13; UCD‐T2DM: 14 ± 5 bpm, n=6, p>0.05), or RSNA (CTL: 73 ± 42 %, n=5; UCD‐T2DM: 34 ± 14 %, n=2, p>0.05) in UCD‐T2DM rats compared to control rats with similar developed tensions. Moreover, stretching the Achilles tendon did not significantly increase peak MAP (CTL: 15 ± 3 mmHg, n=11; UCD‐T2DM: 13 ± 1 mmHg, n=14, p>0.05), HR (CTL: 11 ± 4 bpm, n=11; UCD‐T2DM: 14 ± 2 bpm, n=14, p>0.05), or RSNA (CTL: 60 ± 12 %, n=3; UCD‐T2DM: 24 ± 19 %, n=4, p>0.05) in UCD‐T2DM rats compared to control rats with similar developed tensions. Conclusion We conclude that both the exercise pressor reflex and the mechanoreflex are not exaggerated in UCD‐T2DM rats before the onset of diabetes. This study suggests that young UCD‐T2DM rats have similar MAP, HR, and RSNA responses to both muscle contraction and tendon stretch as seen in age‐matched Sprague Dawley rats prior to the onset of diabetes. Support or Funding Information This project was supported by NIH R01 HL144723.