Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prior results from this laboratory have demonstrated that the respiratory response to hypercapnia is enhanced by microinjection of GABA antagonists or GABA synthesis inhibitors into the caudal hypothalamus of both cats and rats. However, no evidence was found for modulation of the respiratory response to hypoxia by a hypothalamic GABAergic mechanism. The purpose of the present study was to determine if synaptic input other than GABAergic onto caudal hypothalamic neurons affects the respiratory responses to hypoxia. The respiratory (diaphragmatic EMG) responses to hypoxia (10% O2) and hypercapnia (5% CO2) were recorded in anesthetized rats before and after bilateral microinjection of a blocker of synaptic transmission (CoCl2, 100 mM) or an excitatory amino acid receptor antagonist (kynurenic acid, 50 mM) into the caudal hypothalamus. Both hypoxia and hypercapnia elicited increases in tidal diaphragmatic activity and respiratory frequency prior to the microinjections. The respiratory response to hypercapnia was increased (+10.5%) after CoCl2 microinjections, which is consistent with prior results obtained with blockade of GABAergic input. Kynurenic acid did not alter the respiratory response to hypercapnia. A new finding was that the respiratory response to hypoxia was diminished after both CoCl2 (-13.0%) and kynurenic acid (-25.0%) microinjections. The results of this study support our prior findings that neurons in the caudal hypothalamus modulate the respiratory response to hypercapnia. In addition, our findings suggest that an excitatory input acting through excitatory amino acid receptors in the caudal hypothalamus modulates the respiratory responses to hypoxia.
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PMID:Modulation of the respiratory responses to hypoxia and hypercapnia by synaptic input onto caudal hypothalamic neurons. 789 38

The area postrema (AP) is the most caudal circumventricular organ in the central nervous system and contains arginine vasopressin (AVP) receptors. To investigate that AVP receptors in the AP might participate in the modulation of respiration, the adult rat was anesthetized with urethane (1.2 g/kg, i.p.), paralyzed, ventilated artificially, and maintained at normocapnia in hyperoxia. The phrenic nerve was separated at C4 level. Phrenic burst was amplified, filtered, integrated, and then stored in the hard disc via the PowerLab system. Three doses of AVP and an AVP V(1A) receptor antagonist, [beta-mercapto-beta,beta-cyclopentamethylenepropionyl1,-O-Me-Tyr2,Arg8]-vasopressin, were microinjected into the AP through a pair of microelectrodes. The moderate and high doses of AVP reduced the PNA to 72% and 45% of the control (P < 0.05), extended the mean TE from 1.4 s before AVP to 4.0 s and 7.6 s, (P < 0.05), and decrease in BP by 26 and 37 mmHg (P < 0.05), respectively. These significant reductions in PNA and BP and elongation of TE were totally abolished by the pre-treatment of the AVP V(1A) receptor antagonist and by application of lidocaine or CoCl2 at the nucleus tractus solitarius (NTS). Moreover, pulmonary inhibition caused by AVP was significantly attenuated by hypercapnia. These results strongly suggest that AVP V(1A) receptors in the AP may participate in the modulation of cardiopulmonary functions through the activation of V(1A) receptors and the pathway connected to the NTS. They may also indicate that a putative vasopressinergic pathway has a projection to the AP to alter the excitability of neurons having AVP V(1A) receptors and results in an inhibition of cardiopulmonary functions via the connection between the AP and NTS.
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PMID:Vasopressin produces inhibition on phrenic nerve activity and apnea through V(1A) receptors in the area postrema in rats. 1735 38