PubMed · 11791021
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Michael Stowasser. 2002. Hyperaldosteronism: primary versus tertiary.. https://doi.org/10.1097/00004872-200201000-00004
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This study was conducted on unanesthetized rainbow trout equipped with two ECG electrodes and with an intracerebroventricular (i.c.v.) micro-guide. The ECG signal was recorded during three experimental sessions of 30 min and the heart rate variability (HRV) spectral analysis was performed during stabilized periods of recording. The first recording session was conducted during the control period and the mean heart rate (HR) of the trout was 44+/-2 bpm. The total power spectral density (PSD) of the R-R interval signal of the ECG was 21233+/-4400 ms(2)/Hz. A major high frequency (HF) spectral band centered at 0.16 Hz and a minor low frequency (LF) spectral band centered at 0.04 Hz were the two main components of the PSD. An i.c.v. injection of 0.5 microl of vehicle during the second session had no significant statistical effect, either on the mean HR (43+/-2 bpm), the total PSD (24693+/-6394 ms(2)/Hz) or on the center frequency and power of the two main spectral bands. Conversely, an i.c.v. injection of ANGII (1.5, 6.25 and 50 pmol) during the third recording session induced a significant increase in the mean HR (+3%, +15%, +30%, respectively) but the effect of the peptide was more obvious on the total PSD which was profoundly decreased (-27%, -65%, -76%, respectively). The two main spectral bands of the PSD were totally blunted after the injection of 50 pmol of ANGII. In another group of control trout, intraperitoneal (i.p.) injection of atropine abolished the PSD of the R-R interval signal of the ECG demonstrating that the parasympathetic system is the main contributor of HRV in trout. Our results have thus demonstrated for the first time, at least in a non-mammalian species, that i.c.v. injection of native ANGII profoundly reduces HRV. We hypothesize that ANGII in the brain of the trout alters the pattern of the electrical activity along preganglionic cardiac vagal motoneurons.
We previously identified the gene expression of renin-angiotensin system in human monocyte-derived dendritic cells (DCs). This study was conducted to examine the mechanisms by which angiotensin II and captopril, the inhibitor of the angiotensin-converting enzyme (ACE), affect human DCs. In DCs, lipopolysaccharide (LPS)-induced production of tumor necrosis factor-alpha (TNF-alpha), interleukin-(IL)-1alpha, IL-10, IL-12, and IL-18 was significantly inhibited by captopril. In contrast, angiotensin II treatment resulted in a significant increase in TNF-alpha and IL-6 protein biosynthesis by DCs. In addition, we have studied the global expression of 2400 genes in DCs from two donors. Here, we demonstrated the specific down-regulation of the ACE gene expression in captopril-treated DCs. Our finding indicates the possible activation of NF-kappaB through the up-regulation of expressions of MEFV gene (encoding PYRIN protein) and heterogeneous nuclear ribonucleoprotein R in DCs. This is the first study on the modulation of cytokine and gene expression by angiotensin II and captopril in DCs.
OBJECTIVES: The rapid induction of heat shock proteins (HSPs) by cardiac overload has been shown using in vivo models and it is assumed that HSPs are involved in myocardial protection against cardiac overload. However, the mechanisms for the induction of heat shock response by cardiac overload remain unclear. We examined whether increased preload as mechanical stress directly induces heat shock gene expression. METHODS: Rat hearts were isolated and perfused with Krebs-Henseleit buffer by the Langendorff method. Whole-cell extracts were prepared for gel mobility shift assay using oligonucleotides containing the heat shock element. We examined the induction of the DNA-binding activity of heat shock transcription factor (HSF), by which the transcription of heat shock genes is mainly regulated, during increased preload of left ventricle (LV) or perfusion with the buffer containing epinephrine, norepinephrine, angiotensin II, or vasopressin. RESULTS: In preloaded hearts, with LVEDP of both 30 and 50 mmHg, the DNA-binding activity of HSF1 was detected at 10 min, and increased at 20 and 60 min. At any time point, the activity with LVEDP of 50 mmHg was stronger than that with LVEDP of 30 mmHg. However, none of these hypertensive agents activated the DNA-binding activities of HSF. In afterloaded hearts, with the perfusion of norepinephrine, the activation of HSF was not induced. CONCLUSION: Our findings demonstrate that increased preload as mechanical stress directly induces the activation of HSF1 in the LV-overloaded heart.