Does acute hyperglycemia alter rat aortic depressor nerve function?

Abstract

Because it is not known where in the reflex arch, i.e., afference, central nervous system or efferences, hyperglycemia affects baroreflex function, the present study examined the effect of short-term (30 min) hyperglycemia on aortic depressor nerve function measured by a mean arterial pressure vs aortic depressor nerve activity curve, fitted by sigmoidal regression, or by cross-spectral analysis between mean arterial pressure and aortic depressor nerve activity. Anesthetized male Wistar rats received an intravenous bolus (0.25 mL) injection, followed by 30 min of infusion (1 mL/h) of 30% glucose (N = 14). Control groups received a bolus injection and infusion of 0.9% saline (N = 14), or 30% mannitol (N = 14). Glucose significantly increased both blood glucose and plasma osmolarity (P < 0.05). Mean arterial pressure did not change after glucose, saline or mannitol infusion. Mean arterial pressure vs nerve activity curves were identical before and 10 and 30 min after the beginning of glucose, saline or mannitol infusion. Slow (0.3 Hz) oscillations of arterial pressure were induced by controlled bleeding, and cross-spectral analysis was applied to arterial pressure and aortic nerve activity. Transfer function magnitude (aortic depressor nerve activity/mean arterial pressure ratio in the frequency domain) was calculated as an index of gain of the aortic depressor nerve. Transfer function magnitude was similar in all groups during induced or spontaneous oscillations of arterial pressure. In conclusion, the present study demonstrates, by means of two different approaches for assessing baroreceptor function, that aortic depressor nerve activity was not altered by short-term (30 min) hyperglycemia.

Improved glucose homeostasis in male obese Zucker rats coincides with enhanced baroreflexes and activation of the nucleus tractus solitarius

“…Although the present study cannot delineate the cellular mechanisms underlying diminished baroreceptor-mediated activation of the NTS in OZR or its reversal by treatments that normalize glucose homeostasis, these changes are consistent with the impact of hyperglycemia upon the afferent limb of the baroreflex. In the absence of obesity, hypertension, or hyperinsulinemia, the presence of elevated blood glucose is accompanied by diminished phenylephrine-induced c-Fos expression in the NTS (26) and impaired baroreflexes without altering the relationship between aortic depressor nerve activity and AP (17,20,38). Likewise, adult male OZR develop impaired activation of the NTS with no overt changes in aortic depressor nerve activity at an age when they are chronically hyperglycemic with access to food (31,39).…”

Attenuated baroreflex control of sympathetic nerve activity in obese Zucker rats by central mechanisms

“…Ganglionic blockade silenced SNA because recordings were from postganglionic nerves and silenced ADNA because AP was reduced below threshold for firing (Sapru & Wang, 1976). As previously described (Huber et al 2007), the sensitivity of the ADN to changes in AP and baroreflex‐mediated changes in SNA were assessed by generating a MAP–nerve activity curve fitted by a 4‐parameter sigmoid regression (Sigma‐Plot software) and the equation model: y = A1/1 + exp([A2(MAP − A3)]+ A4), where A1 is the range of the nerve activity, A2 is the gain coefficient, A3 is the MAP at the midpoint of the curve (MAP 50 ) and A4 is the lower plateau.…”

“…The left greater splanchnic nerve was exposed retroperitoneally, placed on two Teflon‐coated silver wires bared at the tips, and surrounded by dental impression material (Superdent, Darby Dental) as previously described (Mandel & Schreihofer, 2006; Schreihofer et al 2007). The left ADN was identified as it joined the cervical vagus nerve near the superior laryngeal nerve and isolated from connective tissue (Huber et al 2007). The ADN was placed on two Teflon‐coated silver wires bared at the tips and surrounded by silicone elastomers (Kwik‐Sil, World Precision Instruments).…”

Acute glucose influx-induced mitochondrial hyperpolarization inactivates myosin phosphatase as a novel mechanism of vascular smooth muscle contraction

“…A temporary spike in BP in response to acute stress has been well-documented, while the observations of postprandial BP are not consistent. Both postprandial hypertension and postprandial hypotension have been reported, but most of these data are collected in aging or patients [29][30][31] . As the metabolic disturbance following feeding is more complex than the glucose challenge, changes in postprandial BP in healthy individuals need to be further investigated.…”