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We have shown that lack of the inhibitory G-protein isoform G\u03b1<jats:sub>i3<\/jats:sub> improves cardiac outcome and survival in a murine heart-failure model of cardiac \u03b2<jats:sub>1<\/jats:sub>-adrenoceptor (\u03b2<jats:sub>1<\/jats:sub>-AR) overexpression (\u03b2<jats:sub>1<\/jats:sub>-tg), while lack of the G\u03b1<jats:sub>i2<\/jats:sub> isoform was detrimental in the same heart-failure model. Given the potential role of LTCC and their modulation by \u03b2-adrenergic signalling, we now analysed ventricular <jats:italic>I<\/jats:italic>\n            <jats:sub>CaL<\/jats:sub> in \u03b2<jats:sub>1<\/jats:sub>-tg mice and in \u03b2<jats:sub>1<\/jats:sub>-tg mice lacking either G\u03b1<jats:sub>i2<\/jats:sub> or G\u03b1<jats:sub>i3<\/jats:sub>. Using the patch-clamp technique, we recorded whole-cell <jats:italic>I<\/jats:italic>\n            <jats:sub>CaL<\/jats:sub> in ventricular myocytes freshly isolated from adult mice. Compared to age-matched wild-type littermates, basal <jats:italic>I<\/jats:italic>\n            <jats:sub>CaL<\/jats:sub> was reduced in myocytes from \u03b2<jats:sub>1<\/jats:sub>-tg mice both under basal conditions (\u2212 8.1 \u00b1 1.6 vs. \u2212 5.5 \u00b1 1.5 pA\/pF) and upon \u03b2-adrenergic stimulation with 1 \u00b5M isoproterenol (\u2212 14.3 \u00b1 5.6 vs. \u2212 7.4 \u00b1 1.9 pA\/pF). Lack of G\u03b1<jats:sub>i3<\/jats:sub> normalised basal <jats:italic>I<\/jats:italic>\n            <jats:sub>CaL<\/jats:sub> to nearly wild-type levels (\u2212 7.5 \u00b1 1.6 pA\/pF), while \u03b2-adrenergic response remained attenuated (\u2212 9.5 \u00b1 3.6 pA\/pF). In contrast, the absence of G\u03b1<jats:sub>i2<\/jats:sub> did not restore basal <jats:italic>I<\/jats:italic>\n            <jats:sub>CaL<\/jats:sub> (\u2212 5.7 \u00b1 1.8 pA\/pF), but restored the \u03b2-adrenergic response of <jats:italic>I<\/jats:italic>\n            <jats:sub>CaL<\/jats:sub>, with the difference from basal current even exceeding that in wild-type mice (\u2212 12.2 \u00b1 2.9 pA\/pF).We propose that by restoring basal <jats:italic>I<\/jats:italic>\n            <jats:sub>CaL<\/jats:sub>, G\u03b1<jats:sub>i3<\/jats:sub> deficiency might contribute to the restoration of contractility in \u03b2<jats:sub>1<\/jats:sub>-tg mice, while maintaining attenuation of the <jats:italic>I<\/jats:italic>\n            <jats:sub>CaL<\/jats:sub> response upon \u03b2-adrenergic stimulation protects against deleterious effects mediated by enhanced \u03b2-AR signalling. In contrast, restored and even enhanced <jats:italic>I<\/jats:italic>\n            <jats:sub>CaL<\/jats:sub> response to \u03b2-adrenergic stimulation might contribute to detrimental effects of G\u03b1<jats:sub>i2<\/jats:sub> deficiency observed in \u03b2<jats:sub>1<\/jats:sub>-tg mice previously.<\/jats:p>","DOI":"10.1007\/s00210-025-03999-y","type":"journal-article","created":{"date-parts":[[2025,4,1]],"date-time":"2025-04-01T22:16:35Z","timestamp":1743545795000},"page":"12543-12549","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Opposite effects of G\u03b1i2 or G\u03b1i3 deficiency on reduced basal density and attenuated \u03b2-adrenergic response of ventricular Ca2+ currents in myocytes of mice overexpressing the cardiac \u03b21-adrenoceptor"],"prefix":"10.1007","volume":"398","author":[{"given":"Nour","family":"Katnahji","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2754-1555","authenticated-orcid":false,"given":"Jan","family":"Matthes","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,3,31]]},"reference":[{"key":"3999_CR1","doi-asserted-by":"publisher","first-page":"1139","DOI":"10.1007\/s00424-014-1491-5","volume":"466","author":"AJ Baker","year":"2014","unstructured":"Baker AJ (2014) Adrenergic signaling in heart failure: a balance of toxic and protective effects. 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