Chronic hypoxia selectively augments rat pulmonary artery Ca2+ and K+ channel-mediated relaxation.

Title

Chronic hypoxia selectively augments rat pulmonary artery Ca2+ and K+ channel-mediated relaxation.

Creator

Rodman DM

Publisher

The American Journal Of Physiology

Date

1992

Subject

Male; Animals; Rats; Chronic disease; Inbred Strains; Anoxia/me [Metabolism]; Calcium Channels/ph [Physiology]; Potassium Channels/ph [Physiology]; Pulmonary Artery/me [Metabolism]; Vasoconstriction; Anoxia/pp [Physiopathology]; Calcium/me [Metabolism]; Cyclic AMP/ph [Physiology]; Cyclic GMP/ph [Physiology]; Endothelium; Extracellular Space/me [Metabolism]; Pulmonary Artery/de [Drug Effects]; Pulmonary Artery/pp [Physiopathology]; Vascular/ph [Physiology]; Vasodilator Agents/pd [Pharmacology]

Description

The initiating event in hypoxic pulmonary hypertension is felt to be sustained hypoxic vasoconstriction, ultimately leading to vascular remodeling and fixed pulmonary hypertension. During the initial vasospastic phase endogenous vasodilatory pathways may serve to ameliorate the development of pulmonary hypertension. However, various studies in the systemic and pulmonary circulations have shown that chronic hemodynamic stress alters both endothelial and smooth muscle cell function. The effect of chronic hypoxia in rats was therefore tested on three major vasodilatory pathways: 1) endothelium-dependent relaxation (using endothelium-derived relaxing factor agonists and antagonists); 2) smooth muscle cell cyclic nucleotide-mediated relaxation [using guanosine and adenosine 3',5'-cyclic monophosphate (cGMP and cAMP) agonists]; and 3) ion channel-dependent relaxation (using K+ channel agonists and Ca2+ channel antagonists). It was found that short-term exposure (72 h) to hypoxia caused augmentation of K+ and Ca2+ channel-dependent relaxation with no effect on endothelium-dependent or cyclic nucleotide-mediated relaxation. More prolonged exposure (4-5 wk) was additionally associated with inhibition of endothelium-dependent relaxation and smooth muscle cell cGMP-mediated relaxation. There was no effect on either basal modulation of tone by the endothelium, cAMP-mediated relaxation, or systemic vessel relaxation. It is concluded that an early response to hemodynamic stress in the pulmonary circulation is alteration in smooth muscle cell ion channel function and/or Ca2+ homeostasis.
1992

Rights

Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).

Type

Journal Article

Citation List Month

Backlog

Pages

L88-94

Issue

1

Volume

263

Citation

Rodman DM, “Chronic hypoxia selectively augments rat pulmonary artery Ca2+ and K+ channel-mediated relaxation.,” Pediatric Palliative Care Library, accessed October 25, 2021, https://pedpalascnetlibrary.omeka.net/items/show/11886.

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