Responses of renal nerve activity and urinary Na+ and Cl- excretion were examined in chronically instrumented conscious dogs through feedings of boiled rice with or without NaCl. The boiled rice (20 g/kg body wt) without NaCl did not influence plasma Na+ and Cl- concentrations, renal nerve activity, or urinary Na+ excretion but decreased urinary Cl- excretion. On the other hand, boiled rice containing NaCl (0.4 g/kg body wt) increased plasma Na+ (+3.8 +/- 0.7 meq/l) and Cl- (+3.0 +/- 1.5 meq/l) concentrations, then decreased renal nerve activity by 61 +/- 4%, and increased urinary Na+ and Cl- excretions. In dogs with hepatic denervation, a decrease in renal nerve activity, which was observed in intact dogs in response to the high-NaCl food intake, was completely abolished along with significant attenuation of postprandial natriuresis. That is, only 9 +/- 5% of the loaded Na+ and 7 +/- 3% of the loaded Cl- were excreted during 4 consecutive hours in hepatic-denervated dogs, whereas 36 +/- 5% of the loaded Na+ and 36 +/- 4% of the loaded Cl- were excreted in intact dogs. In dogs with renal denervation, postprandial natriuresis was also attenuated. These results indicate that the high-NaCl food intake elicits a decrease in renal nerve activity, the decrease is predominantly mediated by the hepatic nerves, and the decrease in renal nerve activity plays an important role in augmentation of urinary Na+ and Cl- excretion. Thus, the hepatorenal reflex may play an important role in controlling extracellular fluid homeostasis during food intake.
To investigate the influence of age on the process of nerve regeneration, the right common peroneal nerves of 14 2 month old and 14 10 month old rats were transected and resutured. At four and eight weeks after the nerve repair, the motor nerve conduction velocity (MNCV), latency, and amplitude of the evoked potential from the peroneus longus muscle were measured. The number of regenerated myelinated fibres, axon diameter, axon area, axon circumference, and myelin thickness were also measured. Compared with the control side (left common peroneal nerve and muscle), MNCV, latency, and amplitude showed higher recovery rates (recovery rate (%) = operated/control x 100) in 2 month old rats than in 10 month old rats, particularly at four weeks after the operation. In the morphometric study, axon diameter, axon area, and myelin thickness also recovered more quickly (recovery rate (%) = operated/control x 100) in 2 month old rats, particularly four weeks after the operation. Morphologically, myelin remnants were not found in 2 month old rats eight weeks after the operation, though they remained in 10 month old rats. These studies show that the recovery rate was significantly greater in 2 month old rats than in 10 month old rats. The explanation seems to be the difference in the speed of Wallerian degeneration, axonal regeneration, and myelin regeneration.
Neural, humoral, and metabolic effects on coronary vascular resistance were examined during exercise in conscious dogs, chronically instrumented for the measurement of aortic pressure, heart rate, and left circumflex coronary blood flow. Exercise significantly decreased coronary vascular resistance (CVR) in intact (INT) group, in which CVR was controlled by neural, humoral, and metabolic factors. In cardiac denervated (CD) group with pretreatment of alpha blocker (phentolamine, 2 mg/kg), in which CVR was controlled only by metabolic factor, exercise significantly decreased CVR. To eliminate metabolic effect on CVR, CVR was normalized by the product of CVR and double product (DP = mean aortic pressure x heart rate). CVR.DP did not change throughout the exercise in dogs with CD with alpha blocker. Thus, metabolic effect on CVR during exercise can be excluded by the product of CVR and DP. This calculation was applied to INT group with alpha blocker and CD group without blockers. The 12 km/h exercise significantly increased CVR.DP from 4.1 +/- 0.3 x 10(4) to 6.4 +/- 0.9 x 10(4) in INT group with alpha blocker, in which CVR was controlled only by neural factor, and from 2.8 +/- 0.2 x 10(4) to 4.5 +/- 0.5 x 10(4) in CD group, in which CVR was controlled only by humoral factor. These data suggest that 1) neural and humoral coronary vasoconstriction occurs during exercise, 2) neural and humoral vasoconstriction is overwhelmed by metabolic vasodilation, and 3) CVR.DP is a beneficial calculation for excluding metabolic effect on CVR during exercise.
We report on a girl having congenital chloride diarrhea (CCD) who has been followed for 7 years and 6 months sequentially. Dilated intestinal loops, marked enlargement of the abdominal circumference of the fetus and hydramnios were noted by ultrasound examination at 31 weeks of gestation. After delivery by cesarean section for hydramnios, she excreted profuse watery yellow green stools with marked abdominal distension. At 4 months of age, hypochloremia, hyponatremia and a high concentration of chloride in the stool were identified. She was diagnosed as having CCD. Because it was difficult to administer a large volume of potassium chloride (KCl), and sodium chloride (NaCl), we decided to administer spironolactone. After administration of spironolactone, we could generate correct serum electrolytes using less amounts of KCl. At 7 years and 6 months of age, her body size was within normal limits and her intellectual, mental and physical development had been normal. In spite of normal serum electrolytes, blood pH and the presence of chloriduria, secondary hyperaldosteronism was noted. We consider that spironolactone may be useful to decrease the amount of KCl administration in the neonatal period, but frequent measurements of renin, angiotensin and aldosterone would be necessary for adequate control in CCD cases.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.