ArticleHeart and vessels2012
L/N-type calcium channel blocker suppresses reflex aldosterone production induced by antihypertensive action.
Article in Heart and vessels, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Long-term effects of L- and N-type calcium channel blocker on uric acid levels and left atrial volume in hypertensive patients.Heart and vessels · 2016Trial
- L/N-type calcium channel blocker cilnidipine reduces plasma aldosterone, albuminuria, and urinary liver-type fatty acid binding protein in patients with chronic kidney disease.Heart and vessels · 2013Trial
- On the top of ARB N/L type Ca channel blocker leads to less elevation of aldosterone.Bioscience reports · 2016Article
- GABAB receptors are expressed in human aortic smooth muscle cells and regulate the intracellular Ca(2+) concentration.Heart and vessels · 2015Article
- Suppression of aldosterone synthesis and secretion by ca(2+) channel antagonists.International journal of endocrinology · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The L/N-type calcium channel blocker cilnidipine has been shown to suppress aldosterone production induced by angiotensin II (Ang II) in vitro. In addition, cilnidipine also suppresses the reflex tachycardia induced by its antihypertensive action in vivo. We investigated the effects of cilnidipine on the reflex aldosterone production induced by its antihypertensive action, to identify the differences in the effects of cilnidipine from those of the L-type calcium channel blocker nifedipine. Male SHR/Izm rats were anesthetized by intraperitoneal injection of pentobarbital sodium, and administered an intravenous infusion of saline supplemented or not with Ang II for 30 min. Blood pressure was monitored continuously in the femoral artery. Each of the calcium channel blockers under study was administered intravenously as a bolus through the femoral vein 1 min after the start of the Ang II infusion, and blood samples were collected 30 min after the start of the Ang II infusion. Following administration at nonhypotensive doses, all calcium channel blockers tended to decrease the plasma aldosterone. In particular, cilnidipine significantly suppressed the plasma aldosterone levels. On the other hand, under the condition of Ang II-induced hypertension, administration of a hypotensive dosage of cilnidipine showed no effect on the plasma aldosterone levels, whereas a hypotensive dosage of nifedipine significantly increased the plasma aldosterone levels. Our results suggest that the L/N-type calcium channel blocker cilnidipine reduces the plasma aldosterone level by suppressing the aldosterone production induced by reflex upregulation of the renin-angiotensin-aldosterone system associated with reduction of the blood pressure.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.