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Cardiac nicotinic receptors show beta-subunit-dependent compensatory changes

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00179906%3A_____%2F21%3A10432082" target="_blank" >RIV/00179906:_____/21:10432082 - isvavai.cz</a>

  • Result on the web

    <a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=y2o7DzIULg" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=y2o7DzIULg</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1152/ajpheart.00995.2020" target="_blank" >10.1152/ajpheart.00995.2020</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Cardiac nicotinic receptors show beta-subunit-dependent compensatory changes

  • Original language description

    Nicotinic receptors (NRs) play an important role in the cholinergic regulation of heart functions, and converging evidence suggests a diverse repertoire of NR subunits in the heart. A recent hypothesis about the plasticity of beta NR subunits suggests that beta 2-subunits and beta 4-subunits may substitute for each other. In our study, we assessed the hypothetical beta-subunit interchangeabil- ity in the heart at the level of mRNA. Using two mutant mice strains lacking beta 2 or beta 4 NR subunits, we examined the relative expression of NR subunits and other key cholinergic molecules. We investigated the physiology of isolated hearts perfused by Langendorffs method at basal conditions and after cholinergic and/or adrenergic stimulation. Lack of beta 2 NR subunit was accompanied with decreased relative expression of beta 4-subunits and alpha 3-subunits. No other cholinergic changes were observed at the level of mRNA, except for increased M3 and decreased M4 muscarinic receptors. Isolated hearts lacking beta 2 NR subunit showed different dynamics in heart rate response to indirect cholinergic stimulation. In hearts lacking beta 4 NR subunit, increased levels of beta 2-subunits were observed together with decreased mRNA for acetylcholine-synthetizing enzyme and M1 and M4 muscarinic receptors. Changes in the expression levels in beta 4(-/-) hearts were associated with increased basal heart rate and impaired response to a high dose of acetylcholine upon adrenergic stimulation. In support of the proposed plasticity of cardiac NRs, our results confirmed subunit-dependent compensatory changes to missing cardiac NRs subunits with consequences on isolated heart physiology. NEW &amp; NOTEWORTHY In the present study, we observed an increase in mRNA levels of the beta 2 NR subunit in beta 4(-/-) hearts but not vice versa, thus supporting the hypothesis of beta NR subunit plasticity that depends on the specific type of missing beta-subunit. This was accompanied with specific cholinergic adaptations. Nevertheless, isolated hearts of beta 4(-/-) mice showed increased basal heart rate and a higher sensitivity to a high dose of acetylcholine upon adrenergic stimulation.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30105 - Physiology (including cytology)

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2021

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    American Journal of Physiology - Heart and Circulatory Physiology

  • ISSN

    0363-6135

  • e-ISSN

  • Volume of the periodical

    320

  • Issue of the periodical within the volume

    5

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    10

  • Pages from-to

    "H1975"-"H1984"

  • UT code for WoS article

    000661571000006

  • EID of the result in the Scopus database

    2-s2.0-85105254009