Changes in blood glucose concentration in the carotid body-sinus modify brain glucose retention
Centro Universitario de Investigaciones Biomédicas, Universidad de Colima, Col. México, Mexico. Brain Research
(Impact Factor: 2.84).
09/1994; 654(1):167-70. DOI: 10.1016/0006-8993(94)91585-7
To test whether blood glucose concentration in the carotid body-sinus may influence the amount of glucose retained by the brain, the isolated carotid sinus was perfused with glucose-rich blood or glucose-poor blood from a second animal. The circulation of the right carotid body-sinus was temporarily isolated in rat A, and perfused with blood coming from rat B. Blood glucose in rat B was modified by injections of glucose or insulin. Changes in glucose retention by the brain were measured in rat A. When the isolated carotid body-sinus in rat A was perfused with hyperglycemic blood (16.7 mM), brain glucose retention in rat A decreased significantly from 0.14 +/- 0.02 mumol/g/min (t = 0) to 0.08 +/- 0.01 mumol/g/min at 4 min after the beginning of perfusion. In contrast, the perfusion of the isolated carotid body-sinus of rat A with hypoglycemic blood (2.7 mM) from rat B, had the opposite effect. Brain glucose retention in rat A increased (0.23 +/- 0.03 mumol/g/min) at t = 4 min in comparison to control values (0.13 +/- 0.01 mumol/g/min). Chemoreceptor activity was also manipulated by the injection of cyanide (NaCN) in rat B, under these conditions, brain glucose retention in rat A increased from 0.13 +/- 0.01 mumol/g/min to 0.28 +/- 0.03 mumol/g/min between 4 to 8 min after the beginning of perfusion. These results indicate that chemosensory activity within the carotid body-sinus, superfused in vivo with different glucose concentrations, modify glucose retention by the brain.
Available from: Valery Melnikov
- "Using a thin-slice preparation that retains the structure of the carotid body and preserves the response of the glomus cells to hypoxia, it has been shown that low glucose levels and hypoxia converge in these cells to raise cytosolic calcium concentration to release transmitters, especially dopamine which, in turn, stimulates afferent sensory fibers . Furthermore, decreased or increased plasma glucose concentration in the carotid sinus elicits a rapid neuroendocrine response to correct glycemic levels . Local NaCN carotid chemoreceptor stimulation increases cephalic glucose retention, as well as induces peripheral hyperglycemia by sympathoadrenal activation  to counteract hypoglycemia . "
[Show abstract] [Hide abstract]
ABSTRACT: Previous work has shown that the carotid body glomus cells can function as glucose sensors. The activation of these chemoreceptors, and of its afferent nucleus in the brainstem (solitary tract nucleus - STn), induces rapid changes in blood glucose levels and brain glucose retention. Nitric oxide (NO) in STn has been suggested to play a key role in the processing of baroreceptor signaling initiated in the carotid sinus. However, the relationship between changes in NO in STn and carotid body induced glycemic changes has not been studied. Here we investigated in anesthetized rats how changes in brain glucose retention, induced by the local stimulation of carotid body chemoreceptors with sodium cyanide (NaCN), were affected by modulation of NO levels in STn. We found that NO donor sodium nitroprusside (SNP) micro-injected into STn completely blocked the brain glucose retention reflex induced by NaCN chemoreceptor stimulation. In contrast, NOS inhibitor N(ω)-nitro-L-arginine methyl ester (L-NAME) increased brain glucose retention reflex compared to controls or to SNP rats. Interestingly, carotid body stimulation doubled the expression of nNOS in STn, but had no effect in iNOS. NO in STn could function to terminate brain glucose retention induced by carotid body stimulation. The work indicates that NO and STn play key roles in the regulation of brain glucose retention.
Nitric Oxide 11/2011; 25(4):387-95. DOI:10.1016/j.niox.2011.09.003 · 3.52 Impact Factor
Available from: Sergio Montero
- "Brain glucose uptake was calculated in Amol/g/min by multiplying the arterio-venous glucose differences (A – V) glu by the CBF  . Brain (A – V) glu were determined between glucose concentration in the abdominal aorta and glucose concentration in the jugular sinus  ; blood glucose levels in the abdominal aorta were indistinguishable from those in carotid artery. "
[Show abstract] [Hide abstract]
ABSTRACT: It is well established that the carotid body receptors (CBR), at the bifurcation of the carotid artery, inform the brain of changes in the concentration of CO(2) and O(2) in arterial blood. More recent work suggests that these receptors are also extremely sensitive to blood glucose levels suggesting that they may play an important role as sensors of blood components important for brain energy metabolism. Much less is known about changes in brain glucose metabolism in response to CBR activation. Here we show that 2-8 min after local injection of sodium cyanide (NaCN) into the CBR or after electrical stimulation of the carotid sinus nerve in dogs and rats, brain glucose uptake increased fourfold. Cerebrospinal fluids (CSF) transferred from dogs, 2-8 min after CBR stimulation, into the cisterna magna of non-stimulated dogs or rats induced a similar increase in brain glucose uptake. CSF from stimulated dogs was also active when injected intravenously in anesthetized or awake rats. The activity was destroyed when the stimulated CSF was heated to 100 degrees C or treated with trypsin. We conclude that a peptide important for brain glucose regulation appears in the CSF shortly after CBR stimulation.
Brain Research 01/2004; 994(1):124-33. DOI:10.1016/j.brainres.2003.09.030 · 2.84 Impact Factor
Advances in Experimental Medicine and Biology 02/2000; 475:749-60. DOI:10.1007/0-306-46825-5_75 · 1.96 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.