T-type voltage gated calcium channels and vascular function

Termin i miejsce

08.01.2016 − Sala Ateńska w budynku A Parku Life Science, Bobrzyńskiego 14, Kraków, woj. małopolskie

Komitety

Przewodniczący komitetu naukowego:
Prof. Pernille Hansen (Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark)

Organizatorzy

Jagiellońskie Centrum Rozwoju Leków(JCET) Uniwersytet Jagielloński

Tematyka

Serdecznie zapraszamy na wykład JCET pt. "T-type voltage gated calcium channels and vascular function", który wygłosi Prof. Pernille Hansen (Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark).

Wykład odbędzie się w piątek 8.01.2016 r. o godz. 9.00, w Sali Ateńskiej w budynku A Parku Life Science (Bobrzyńskiego 14).

T-type channels play an important role in renal hemodynamics, contractility of resistance vessels
and pacemaker activity in the heart. At least two types of T-type channels, Cav3.1 and Cav3.2, are
expressed in blood vessels, the kidney and the heart. They contribute to both vasoconstriction and
vasodilatation. T-type (Cav3.1) channels are involved in an endothelial cell-dependent dilatation and
Cav3.1 T-type channels in endothelial cells co-localize with endothelial nitric oxide synthase
(eNOS). In particular, during depolarization of mesenteric resistance arteries of young mice, the
opening of Cav3.1 T-type channels modulates the influx of calcium ions which in turn stimulate
eNOS, and increase production of nitric oxide (NO) and thereby affect the NO-dependent
dilatation. Clinical studies suggest that T-type calcium channel blockers improve endothelial
dysfunction and it was hypothesized that T-type channels contribute to the endothelial dysfunction
during ageing. The NO-dependent relaxations of aortae and mesenteric arteries were significantly
diminished in arteries of one year old Wt but not old Cav3.1-/- mice. Furthermore, DAF fluorescent
imaging showed significantly lower NO levels in mesenteric arteries of old Wt compared to old
Cav3.1-/-mice.
In conclusion, T-type channels contribute to contraction of human and mouse blood vessels.
Furthermore, Cav3.1 and Cav3.2 T-type calcium channels contribute to vasodilatation through
different mechanisms. Since T-type channel deficient mice are protected against age-dependent
endothelial dysfunction, T-type blockers might protect against such dysfunction.