{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,5,2]],"date-time":"2024-05-02T21:54:22Z","timestamp":1714686862016},"reference-count":42,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2012,1]]},"abstract":"<jats:p> Ca<jats:sup>2+<\/jats:sup> currents ( I<jats:sub>Ca<\/jats:sub>) recorded from adrenal chromaffin cells (CCs) of spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats are similar to one another, but different from those recorded in other rodent species. I<jats:sub>Ca<\/jats:sub> in WKY\/SHR CCs comprises an early, transient ( I<jats:sub>Ca<jats:sub>e<\/jats:sub><\/jats:sub>) and a late, sustained component ( I<jats:sub>Ca<jats:sub>s<\/jats:sub><\/jats:sub>). In Wistar CCs, I<jats:sub>Ca<jats:sub>e<\/jats:sub><\/jats:sub> is absent, and I<jats:sub>Ca<jats:sub>s<\/jats:sub><\/jats:sub> is of greater amplitude. Activation and steady-state inactivation of I<jats:sub>Ca<jats:sub>e<\/jats:sub><\/jats:sub> and I<jats:sub>Ca<jats:sub>s<\/jats:sub><\/jats:sub> in WKY\/SHR CCs suggest the recruitment of at least two populations of Ca<jats:sup>2+<\/jats:sup> channels with different voltage dependence and kinetics. In WKY\/SHR CCs, I<jats:sub>Ca<jats:sub>e<\/jats:sub><\/jats:sub> is inhibited by nifedipine, enhanced by BAY K 8644, is not blocked by the mibefradil analog NNC 55\u20130396, and displays Ca<jats:sup>2+<\/jats:sup>-dependent inactivation and fast deactivation kinetics, suggesting that it results from the opening of L-type rather than T-type Ca<jats:sup>2+<\/jats:sup> channels. I<jats:sub>Ca<jats:sub>e<\/jats:sub><\/jats:sub> properties suggest that it originates from the opening of Ca<jats:sup>2+<\/jats:sup> channels formed with the short splice variant (Ca<jats:sub>V<\/jats:sub>1.3<jats:sub>42A<\/jats:sub>). RT-PCR showed that expression of Ca<jats:sub>V<\/jats:sub>1.3<jats:sub>42A<\/jats:sub> mRNA is similar in both Wistar and WKY\/SHR, but that the long variant (Ca<jats:sub>V<\/jats:sub>1.3<jats:sub>42<\/jats:sub>) is virtually absent in WKY\/SHR. Thus I<jats:sub>Ca<jats:sub>e<\/jats:sub><\/jats:sub> corresponds to the recruitment of Ca<jats:sub>V<\/jats:sub>1.3<jats:sub>42A<\/jats:sub> channels, unmasked by the absence of Ca<jats:sub>V<\/jats:sub>1.3<jats:sub>42<\/jats:sub> channels. Studies in WKY CCs do not report major functional alterations, despite the unusual expression pattern of Ca<jats:sub>V<\/jats:sub>1.3 splice variants. It remains to be established if more subtle functional alterations exist, and if the atypical splicing pattern of Ca<jats:sub>V<\/jats:sub>1.3 could be related to the functional and behavioral alterations reported in WKY\/SHR rats, including their susceptibility to develop hypertension. <\/jats:p>","DOI":"10.1152\/ajpheart.00849.2011","type":"journal-article","created":{"date-parts":[[2011,11,12]],"date-time":"2011-11-12T08:33:32Z","timestamp":1321086812000},"page":"H467-H478","source":"Crossref","is-referenced-by-count":6,"title":["Atypical Ca<sup>2+<\/sup> currents in chromaffin cells from SHR and WKY rat strains result from the deficient expression of a splice variant of the \u03b1<sub>1D<\/sub> Ca<sup>2+<\/sup> channel"],"prefix":"10.1152","volume":"302","author":[{"given":"Pedro","family":"Segura-Chama","sequence":"first","affiliation":[{"name":"Divisi\u00f3n de Neurociencias, Departamento de Neurociencia Cognitiva 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