{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T06:44:02Z","timestamp":1789627442238,"version":"build-2803163510"},"reference-count":51,"publisher":"The Company of Biologists","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:p>Recent investigations have reported that T-type Ca2+ channels (CaV3.x) are expressed in rat cerebral arterial smooth muscle. In this study, we isolate the T-type conductance, differentiate the current into the CaV3.1\/CaV3.2 subtypes and determine whether they are subject to protein kinase regulation. Using patch clamp electrophysiology, whole-cell Ba2+ current was monitored and initially subdivided into nifedipine-sensitive and -insensitive components. The latter conductance was abolished by T-type Ca2+ channel blockers and displayed faster and leftward shifted activation\/inactivation properties, reminiscent of T-type channel. Approximately 60% of this T-type conductance was blocked by 50\u2005\u00b5M Ni2+, a concentration that selectively interferes with CaV3.2 channels. Subsequent work revealed that the whole-cell T-type conductance was subject to protein kinase A (PKA) modulation. Specifically, positive PKA modulators (db-cAMP, forskolin, isoproterenol) suppressed T-type currents and evoked a hyperpolarized shift in steady-state inactivation. Blocking PKA (KT5720) masked this suppression without altering the basal T-type conductance. A similar effect was observed with stHt31, a peptide inhibitor of A-kinase anchoring proteins. A final set of experiments revealed that PKA-induced suppression targeted the CaV3.2 subtype. In closing, this study revealed that a T-type Ca2+ channel conductance can be isolated in arterial smooth muscle, and differentiated into a CaV3.1 and CaV3.2 component. It also showed that vasodilatory signaling cascades inhibit this conductance by targeting CaV3.2. Such targeting will impact Ca2+ dynamics and consequent tone regulation in the cerebral circulation.<\/jats:p>","DOI":"10.1242\/jcs.128363","type":"journal-article","created":{"date-parts":[[2013,4,24]],"date-time":"2013-04-24T03:37:18Z","timestamp":1366774638000},"source":"Crossref","is-referenced-by-count":34,"title":["Protein kinase a regulation of T-type Ca2+ channels in rat cerebral arterial smooth muscle"],"prefix":"10.1242","author":[{"given":"Osama F.","family":"Harraz","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donald G.","family":"Welsh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","published-online":{"date-parts":[[2013,1,1]]},"reference":[{"key":"2021042612581691800_b2","doi-asserted-by":"crossref","first-page":"141","DOI":"10.1113\/jphysiol.1989.sp017754","article-title":"Low-voltage-activated calcium current in rat aorta smooth muscle cells in primary culture.","volume":"416","author":"Akaike","year":"1989","journal-title":"J. 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