The Japan Aerospace Exploration Agency recently performed a mouse experiment in the International Space Station in which mice were raised for 35 days, retrieved using the Dragon spacecraft, and then harvested for analysis 2 days after splashdown. However, the impact of the retrieval procedure, which exposed mice to 5-10 g for 2 min during atmospheric reentry and splashdown, was unknown. Therefore, the purpose of this study was to examine the impact of a 10 g load for 2 min (using a gondola-type centrifuge with a 1.5-m arm installed at Gifu University) on conscious mice. Plasma corticosterone increased at 30 min after load application and recovered at 90 min. Significant Fos expression was observed in the vestibular nuclei (VeN), paraventricular hypothalamic nucleus (PVN), and central nucleus of the amygdala (CeA). Rearing behavior and food intake were suppressed. Mice with vestibular lesions demonstrated increased corticosterone and Fos expression in the PVN, but neither suppression of food intake and rearing behavior nor increased Fos expression in the VeN and CeA. These results suggest that the simulated gravity load induced a transient stress response, hypoactivity, and a vestibular-mediated suppression of food intake.
Decreased carotid arterial compliance has been reported in obese subjects and animals. Carotid baroreceptors are located at the bifurcation of the common carotid artery, and respond to distension of the arterial wall, suggesting that higher pressure is required to obtain the same distension in obese subjects and animals. A hyperosmotic NaCl solution induces circulatory volume expansion and arterial pressure (AP) increase, which reflexively augment renal excretion. Thus, we hypothesized that sodium regulation via the baroreflex might be impaired in response to chronic hyperosmotic NaCl infusion in rats fed a high-fat diet. To examine this hypothesis, we used rats fed a high-fat (Fat) or normal (NFD) diet, and measured mean AP, water and sodium balance, and renal function in response to chronic infusion of hyperosmotic NaCl solution via a venous catheter. Furthermore, we examined arterial baroreflex characteristics with static open-loop analysis and distensibility of the common carotid artery. Significant positive water and sodium balance was observed on the 1st day of 9% NaCl infusion; however, this disappeared by the 2nd day in Fat rats. Mean AP was significantly higher during 9% NaCl infusion in Fat rats compared with NFD rats. In the open-loop analysis of carotid sinus baroreflex, a rightward shift of the neural arc was observed in Fat rats compared with NFD rats. Furthermore, distensibility of the common carotid artery was significantly reduced in Fat rats. These results indicate that a reduced baroreceptor distensibility-induced rightward shift of the neural arc might contribute to impairment of sodium regulation in Fat rats.
Previous study from our laboratory demonstrated that the renal sensory afferent fibers responded to NaCl concentration in the renal artery, i.e., the renal afferent nerve activity was increased by an intrarenal arterial infusion of hypertonic NaCl solution in a dose dependent manner. However, a physiological significance of the increased renal afferent nerve activity was still unclear. We hypothesized that the renal afferent nerves may contribute to body fluid homeostasis through controlling arginine vasopressin (AVP) release. To examine this, plasma AVP was measured, while intrarenal NaCl receptors were selectively stimulated by a small dose infusion of hypertonic NaCl in conscious rats. Under a gas anesthesia, a PE‐10 catheter for NaCl infusion was inserted into the right renal artery via the suprarenal artery and a PE‐50 catheter for blood sampling was inserted into the abdominal aorta via the left femoral artery; these catheters were exteriorized from the back of the neck and connected to a swivel. One day was elapsed to recover from anesthesia and the surgery. Hyperosmotic NaCl solution (616 mmol/L) was infused into the renal artery at a rate of 50 μL/min for 10 min. Plasma Na+ concentration was not affected by this infusion (from 142.8 ± 0.6 to 143.6 ± 0.4 mmol/L), while plasma K+ concentration was significantly decreased (4.3 ± 0.1 to 4.1 ± 0.1 mmol/L). The hypertonic NaCl infusion significantly increased plasma AVP concentration from 2.8 ± 0.2 to 3.4 ± 0.4 pg/mL. This response was completely abolished by renal denervation. These data indicate that the renal sensory afferent fibers might sense changes in the intrarenal arterial NaCl concentration and alter AVP release.
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