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Decreased function of voltage-gated potassium channels contributes to augmented myogenic tone of uterine arteries in late pregnancy

Lookup NU author(s): Dr Seva TelezhkinORCiD

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Abstract

Increased pressure-induced (myogenic) tone in small uteroplacental arteries from late pregnant (LP) rats has been previously observed. In this study, we hypothesized that this response may result from a diminished activity of vascular smooth muscle cell (SMC) voltage-gated delayed-rectifier K⁺ (K_v) channels, leading to membrane depolarization, augmented Ca²⁺ influx, and vasoconstriction (tone). Elevation of intraluminal pressure from 10 to 60 and 100 mmHg resulted in a marked, diltiazem-sensitive rise in SMC cytosolic Ca²⁺ concentration ([Ca²⁺]_i) associated with a vasoconstriction of uteroplacental arteries of LP rats. In contrast, these changes were significantly diminished in uterine arteries from nonpregnant (NP) rats. Gestational augmentation of pressure-induced Ca²⁺ influx through L-type Ca²⁺ channels was associated with an enhanced SMC depolarization, the appearance of electrical and [Ca²⁺]_i oscillatory activities, and vasomotion. Exposure of vessels from NP animals to 4-aminopyridine, which inhibits the activity of K_v channels, mimicked the effects of pregnancy by increasing pressure-induced depolarization, elevation of [Ca²⁺]_i, and development of myogenic tone. Furthermore, currents through K_v channels were significantly reduced in myocytes dissociated from arteries of LP rats compared with those of NP controls. Based on these results, we conclude that decreased K_v channel activity contributes importantly to enhanced pressure-induced depolarization, Ca²⁺ entry, and increase in myogenic tone present in uteroplacental arteries from LP rats.

Publication metadata

Author(s): Telezhkin V, Goecks T, Bonev A, Osol G, Gokina NI

Publication type: Article

Publication status: Published

Journal: American Journal of Physiology - Heart and Circulatory Physiology

Year: 2008

Volume: 294

Issue: 1

Pages: H272-H284

Print publication date: 01/01/2008

ISSN (print): 0363-6135

ISSN (electronic): 1522-1539

Publisher: American Physiological Society

URL: https://doi.org/10.1152/ajpheart.00216.2007

DOI: 10.1152/ajpheart.00216.2007

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