BAROREFLEX DYSFUNCTION IN DIABETES-MELLITUS .2. SITE OF BAROREFLEX IMPAIRMENT IN DIABETIC RABBITS

In our companion paper [T. S. McDowell, M. W. Chapleau, G. Hajduczok, and F. M. Abboud, Am. J. Physiol. 266 (Heart Circ. Physiol. 35): H235- H243, 1994] we report that baroreflex-mediated bradycardia is impaired in diabetic rabbits. The purpose of the present study was to identify the site of impairment. Diabetes was induced in rabbits by alloxan (9 0-100 mg/kg iv; n = 7). Alloxan-treated rabbits that remained normogly cemic (n = 8) and rabbits given saline instead of alloxan (n = 4) serv ed as controls. Twenty-four weeks after administration of alloxan or s aline, rabbits were anesthetized with alpha-chloralose. Aortic barorec eptor and renal sympathetic nerve activity (RSNA) were recorded during phenylephrine- and nitroglycerin-induced changes in arterial pressure . The slope of the baroreceptor pressure-activity relation was not sig nificantly different in diabetic rabbits (1.3 +/- 0.3%/mmHg, n = 7) co mpared with either alloxan-treated (1.3 +/- 0.1%/mmHg) or saline-treat ed normoglycemic rabbits (1.2 +/- 0.2%/mmHg). The slope of the arteria l pressure-RSNA relation was not significantly different in diabetic r abbits (-3.5 +/- 0.3%/mmHg, n = 7) compared with the alloxan-treated n ormoglycemic rabbits (-3.0 +/- 0.4%/mmHg, n = 8) and was greater than that in saline-treated normoglycemic rabbits (-1.9 +/- 0.3%/mmHg, n = 4; P < 0.05). The decreases in heart rate in response to electrical st imulation (10 V, 2 ms, 0.5-16 Hz) of the cut peripheral end of the rig ht cervical vagus were similar in diabetic and alloxan-treated normogl ycemic rabbits. The results suggest that a defect in the activation of central parasympathetic pathways is responsible for the selective imp airment of baroreflex control of heart rate in diabetes; baroreflex co ntrol of RSNA is preserved in this model of diabetes.