Literature DB >> 8616612

Sodium and potassium current in neonatal rat carotid body cells following chronic in vivo hypoxia.

S C Hempleman1.   

Abstract

Chronic hypoxic acclimatization modifies ventilatory reflexes arising from carotid body stimulation. To explore this, the effects of in vivo chronic hypoxia on membrane currents were quantified in chemoreceptive carotid body glomus cells. Pregnant rats were maintained in either normoxia (NORM: inspired oxygen tension 141 mmHg), or hypoxia (CHX: inspired oxygen tension 80 mmHg) from day 3 of gestation, to day 5-10 postpartum. Whole cell patch clamp recordings were then made from the mechanically and enzymatically dissociated carotid body glomus cells of the rat pups (NORM: 41 cells, CHX: 36 cells) and comparisons of means +/- S.E.M. were made with unpaired t-tests. Glomus cells were bright under phase contrast illumination, formed clusters, were histochemically positive for catecholamines and possessed voltage-gated potassium currents that were depressed by acute hypoxia. Acclimatization to chronic hypoxia did not affect rat pup whole body mass (CHX: 12.0 +/- 0.7 g vs. NORM: 11.0 +/- 0.2 g), but it significantly increased blood hematocrit (CHX: 48.7 +/- 0.9% vs. NORM: 37.8 +/- 0.5%, P < 0.05). Sodium current was not uniformly present in glomus cells from either group, but sodium current was observed in a greater proportion of glomus cells isolated from the chronically hypoxic pups (CHX: 72% vs. NORM: 46%, P < 0.05). The mean peak tetrodotoxin-sensitive sodium current evoked by -70 mV to +10 mV depolarizations was greater after hypoxic acclimatization (CHX: -100 +/- 25 pA vs. NORM: -38 +/- 15 pA, P < 0.05), but the sodium current density (pA/pF) was unchanged. In contrast, the mean peak voltage-gated potassium current (pA) evoked by -70 mV to 0 mV depolarizations was unchanged by acclimatization, but the potassium current density (pA/pF) was reduced (P < 0.05). Unchanged sodium current density coupled with decreased potassium current density may make glomus cells more excitable during exposure to chronic in vivo hypoxia.

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Year:  1995        PMID: 8616612     DOI: 10.1016/0006-8993(95)00850-p

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


  5 in total

Review 1.  Hypoxia. 4. Hypoxia and ion channel function.

Authors:  Larissa A Shimoda; Jan Polak
Journal:  Am J Physiol Cell Physiol       Date:  2010-12-22       Impact factor: 4.249

Review 2.  The influence of chronic hypoxia upon chemoreception.

Authors:  Frank L Powell
Journal:  Respir Physiol Neurobiol       Date:  2007-01-20       Impact factor: 1.931

3.  Chronic hypoxia reduces adenosine A2A receptor-mediated inhibition of calcium current in rat PC12 cells via downregulation of protein kinase A.

Authors:  S Kobayashi; D Beitner-Johnson; L Conforti; D E Millhorn
Journal:  J Physiol       Date:  1998-10-15       Impact factor: 5.182

Review 4.  Tetrodotoxin as a tool to elucidate sensory transduction mechanisms: the case for the arterial chemoreceptors of the carotid body.

Authors:  Asuncion Rocher; Ana Isabel Caceres; Ana Obeso; Constancio Gonzalez
Journal:  Mar Drugs       Date:  2011-12-15       Impact factor: 6.085

5.  Carotid Body Type-I Cells Under Chronic Sustained Hypoxia: Focus on Metabolism and Membrane Excitability.

Authors:  Raúl Pulgar-Sepúlveda; Rodrigo Varas; Rodrigo Iturriaga; Rodrigo Del Rio; Fernando C Ortiz
Journal:  Front Physiol       Date:  2018-09-19       Impact factor: 4.566

  5 in total

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