Basal sympathetic nerve activity is enhanced with augmentation of baroreceptor reflex in Wistar fatty rats: a model of obesity-induced NIDDM

Aim Wistar fatty rats (WFR) develop mild hypertension associated with obesity, hyperglycaemia and hyperinsulinaemia, and are thus assumed to be a good model of insulin resistance-related hypertension. We determined whether the activity of the sympathetic nervous system and its baroreflex-mediated regulation are involved in the development of hypertension in this strain. Methods Renal sympathetic nerve activity (RSNA) was recorded in pre-hypertensive WFR (n = 8, age 12 weeks) and Wistar lean rats (WLR) (n = 8) during changes in arterial pressure by phenylephrine and nitroprusside infusion in the conscious state. Baroreflex control of RSNA and heart rate were examined by logistic function analysis. Results The mean arterial pressure (MAP) of WFR was similar to that of WLR (108 +/- 4 versus 101 +/- 2 mmHg, not significant). Basal RSNA was elevated in WFR compared with WLR (86 +/- 2 versus 51 +/- 2% maximum, P < 0.01). Baroreflex control of RSNA was shifted to higher pressure levels (mid-range, 119 +/- 4 versus 99 +/- 4 mmHg, P< 0.05) in WFR compared with WLR in spite of similar MAP. However, baroreflex sensitivity concerning RSNA was greater in WFR than WLR (3.07 +/- 0.15 versus 1.63 +/- 0.12% maximum/mmHg, P < 0.01). Baroreflex control of heart rate was also shifted to higher pressure levels (mid-range 129 +/- 4 versus 100 +/- 5 mmHg, P < 0.01) and its sensitivity was increased in WFR compared with WLR (4.62 +/- 0.51 versus 3.16 +/- 0.10 bpm/mmHg, P< 0.05). Conclusion These results suggest that baroreflex is not impaired in spite of elevation of blood pressure and that the raised sympathetic nerve activity may contribute to the development of hypertension in WFR. I Hypertens 1999, 17:959-964 (C) Lippincott Williams & Wilkins.