ArticlePflugers Archiv : European journal of physiology2004
Effects of angiotensin II on sustained outward currents in rat ventricular myocytes.
Article in Pflugers Archiv : European journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Impact of Impaired Kidney Function on Arrhythmia-Promoting Cardiac Ion Channel Regulation.International journal of molecular sciences · 2023Review
- Angiotensin-converting enzyme gates brain circuit-specific plasticity via an endogenous opioid.Science (New York, N.Y.) · 2022Article
- Angiotensin II Type 1 Receptor-Mediated Electrical Remodeling in Mouse Cardiac Myocytes.PloS one · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the effects of angiotensin II (Ang II) on the sustained outward current ( I(sus)) and action potential of rat ventricular myocytes using the whole-cell patch-clamp technique. Ang II at 30 nM-3 microM inhibited I(sus) with an IC(50) of 240 nM, a Hill coefficient of 1.0 and maximum inhibition of 19.4%. Ang II-mediated inhibition of I(sus) was voltage independent, was due to a decrease in the K(+) current and was abolished by the Ang II type-I (AT(1)) receptor blocker, valsartan. The protein kinase C (PKC) inhibitors PKC19-36 or calphostin C, abolished Ang II-mediated inhibition of I(sus). In contrast, pretreatment with the protein kinase A (PKA) inhibitor PKA6-22 (100 microM) significantly enhanced the suppression of I(sus) by 1 microM Ang II: (33.7+/-5.1% vs. control 17.1+/-2.3%). These results indicate that Ang II inhibits I(sus) via the AT(1) receptor and activation of PKC. Ang II significantly prolonged action potential duration (APD) when the control APD was lengthened by a Ca(2+) channel activator, BAY K8644. In myocytes with a relatively long APD, Ang II may prolong APD by inhibiting I(sus).
Indexed as
Identifiers
What OpenQuestion holds
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.