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The effect of Cattaneo–Christov heat flux on hydromagnetic flow of non-Newtonian (Maxwell, Jeffrey and Oldroyd-B) fluids filled with Darcy–Forchheimer porous medium with thermal radiation, uneven heat source/sink and variable thermal conductivity is studied numerically. The mathematical problem is developed with the help of momentum, and energy equations using the suitable transformation variables. The numerical results for the transformed highly nonlinear ordinary differential equations are presented for Maxwell, Jeffrey and Oldroyd-B fluid cases. For numerical computations, an effective numerical solver namely bvp4c package is used. Effects of various controlling restrictions on the flow, and thermal fields are examined. Numerical computations for the friction factor and local Nusselt number are executed. [ABSTRACT FROM AUTHOR]

We recently reported that adrenomedullary chromaffin cells (AMC) from neonatal rats treated with intermittent hypoxia (IH) exhibit enhanced catecholamine secretion by hypoxia (Souvannakitti D, Kumar GK, Fox A, Prabhakar NR. J Neurophysiol 101: 2837-2846, 2009). In the present study, we examined whether neonatal IH also facilitate AMC responses to nicotine, a potent stimulus to chromaffin cells. Experiments were performed on rats exposed to either IH (15-s hypoxia-5rain normoxia; 8 h/day) or to room air (normoxia; controls) from ages postnatal day 0 (P0) to P5. Quantitative RT-PCR analysis revealed expression of mRNAs encoding [[alpha].sub.3]-, [[alpha].sub.5]-, [[alpha].sub.7]-, and [[beta].sub.2]- and [[beta].sub.4]nicotinic acetylcholine receptor (nAChR) subunits in adrenal medullae from control P5 rats. Nicotine-elevated intracellular [Ca.sup.2+] concentration ([[[Ca.sup.2+]].sub.i]) in AMC and nAChR antagonists prevented this response, suggesting that nAChRs are functional in neonatal AMC. In IH-treated rats, nAChR mRNAs were downregulated in AMC, which resulted in a markedly attenuated nicotine-evoked elevation in [[[Ca.sup.2+]].sub.i] and subsequent catecholamine secretion. Systemic administration of antioxidant prevented IH-evoked downregulation of nAChR expression and function. P35 rats treated with neonatal IH exhibited reduced nAChR mRNA expression in adrenal medullae, attenuated AMC responses to nicotine, and impaired neurogenic catecholamine secretion. Thus the response to neonatal IH lasts for at least 30 days. These observations demonstrate that neonatal IH downregulates nAChR expression and function in AMC via reactive oxygen species signaling, and the effects of neonatal IH persist at least into juvenile life, leading to impaired neurogenic catecholamine secretion from AMC. adrenal medullary chromaffin cells; nicotinic cholinergic receptors; recurrent apneas; reactive oxygen species; catecholamine secretion doi: 10.1152/ajpcell.00530.2009.

We previously reported that intermittent hypoxia (IH) augments hypoxic sensory response (HSR) and increases the number of glomus cells in neonatal carotid bodies. In the present study, we tested the hypothesis that recruitment of endothelin-1 (ET-1) signaling by reactive oxygen species (ROS) plays a critical role in IH-evoked changes in neonatal carotid bodies. Experiments were performed on neonatal rats exposed either to I0 days of IH (P0-P10; 8 h/day) or to normoxia. IH augmented HSR of the carotid bodies ex vivo and resulted in hyperplasia of glomus cells. The effects of IH were associated with enhanced basal release of ET-l under normoxia, sensitization of carotid body response to exogenous ET-1, and upregulation of [ET.sub.A] but not an [ET.sub.B] receptor mRNA without altering the ET-1 content. An ETA but not [ET.sub.B] receptor antagonist prevented augmented HSR by IH. ROS levels were elevated in carotid bodies from IH-treated rat pups as evidenced by increased levels of malondialdehyde. Systemic administration of manganese (III) tetrakis(1-methyl-4-pyridyl)porphyrin pentachloride (MnTMPyP; 5 mg/kg ip), a scavenger of [O.sub.2.sup.x-], prevented IH-induced elevation of ROS, basal release of ET-1, up-regulation of [ET.sub.A] mRNA, and augmented HSR. In striking contrast, MnTMPyP treatment had no significant effect on IH-induced hyperplasia of glomus cells. These results demonstrate that IH-evoked increase in HSR involve a ROS-mediated increase in basal ET-1 release and upregulation of [ET.sub.A] receptor mRNA. recurrent apneas; premature infants; chemoreflex; arterial chemoreceptors; chronic intermittent hypoxia