the progression of Parkinson's. Inhibition of Cav1.3 can be achieved using calcium channel blockers, such as dihydropyridines (DHPs). These drugs are used since decades to treat arterial hypertension and angina. This is due to their potent vasorelaxant properties, which are mediated by the inhibition of Cav1.2 L-type calcium channels in arterial smooth muscle. Therefore, hypotensive reactions (and leg edema) are regarded dose-limiting side effects when using DHPs for inhibiting Cav1.3 channel in the brain. In the face of this issue, attempts have been made to discover selective Cav1.3 channel blockers. One candidate has been claimed to be a potent and highly selective inhibitor of Cav1.3. This compound, 1-(3-chlorophenethyl)-3-cyclopentylpyrimidine-2,4,6-(1H,3H,5H)-trione was therefore put forward as a candidate for the future treatment of Parkinson's. However, its selectivity and potency could not be confirmed in two independent studies from two other groups. One of them even reported gating changes induced by this drug., which indicate channel activating rather than blocking effects. Prostate cancer Recent evidence from immunostaining experiments shows that CACNA1D is highly expressed in prostate cancers compared with benign prostate tissues. Blocking L-type channels or knocking down gene expression of CACNA1D significantly suppressed cell-growth in prostate cancer cells. It is important to recognise that this association does not represent a causal link between high levels of α1D protein and prostate cancer. Further investigation is needed to explore the role of CACNA1D gene overexpression in prostate cancer cell growth. Aldosteronism De novo somatic mutations in conserved regions within the channel's activation gate of its pore-forming α1-subunit (CACNA1D) cause excessive aldosterone production in aldosterone-producing adenomas (APA) resulting in primary aldosteronism, which causes treatment - resistant arterial hypertension. These mutations allow increased Ca2+ influx through Cav1.3, which in turn triggers Ca2+ - dependent aldosterone production. The number of validated APA mutations is constantly growing. In rare cases, APA mutations have also been found as germline mutations in individuals with neurodevelopmental disorders of different severity, including autism spectrum disorder. See also Calcium channel References Further reading External links Ion channels