PubMed · 12230704
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Anthony Schaeffer, Jeffrey Stern. 2002. Chronic prostatitis.. https://pubmed.ncbi.nlm.nih.gov/12230704/
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Extracellular-signal-regulated protein kinases (ERKs) are activated rapidly and transiently in response to phenylephrine (PE) and endothelin-1 (ET-1) in cardiac myocytes, but whether this is linked to the subsequent development of the hypertrophic phenotype remains equivocal. To investigate this, we examined the dependence of the hypertrophic response on the length of exposure to PE in neonatal myocyte cultures. In addition to the initial transient activation of ERKs (maximum at 5-10 min), PE (10 microM) induced a second, more prolonged peak of activity several hours later. The activity of a transfected atrial natriuretic factor-luciferase reporter gene was increased 10- to 24-fold by PE. This response was inhibited by the alpha(1)-antagonist prazosin (100 nM) and by U0126 (10 microM) and PD184352 (1 microM), inhibitors of ERK activation, irrespective of whether these were added before or up to 24 h after the addition of PE. Prazosin had no effect on ET-1 (50 nM)-stimulated atrial natriuretic factor-luciferase activity. Protein synthesis was enhanced by 35+/-6% by PE, and this was blocked by prazosin added 1 h after the addition of PE, but decreased only by half when added 8 h after PE. Similarly, PE (48 h) increased myocyte area by 49% and this was prevented by prazosin added 1 h after PE, but decreased only by half when added at 24 h. These results demonstrate that prolonged exposure to PE is required to elicit alterations in gene expression, protein synthesis and cell size, characteristic of hypertrophied myocytes, and they confirm that the initial peak of ERK activity is insufficient to trigger hypertrophic responses.
BACKGROUND: The fact that induction of anxiety- and panic-related symptoms is a property common to a range of drugs suggests that common neural substrates underlie their behavioral effects. METHODS: We used Fos immunocytochemistry to test the effects of four anxiogenic drugs (FG-7142, yohimbine, m-chlorophenylpiperazine [mCPP], and caffeine) on anxiety-related circuitry in rat forebrain. RESULTS: All four drugs commonly increased Fos-like immunoreactivity in 7 of 41 brain areas investigated, namely, central nucleus of the amygdala, bed nucleus of the stria terminalis, lateral septum, paraventricular nucleus of the hypothalamus, lateral hypothalamus, infralimbic and prelimbic cortex. All drugs but one (mCPP) also increased Fos expression in the basolateral and medial amygdala, the dorsomedial hypothalamus, cingulate cortex, and parts of the motor cortex. CONCLUSIONS: The results suggest that the anxiogenic drugs selected activate a restricted set of forebrain areas. Most of these areas have previously been shown to be activated by environmentally evoked anxiety and to have anatomic connections with hindbrain regions that are activated by the same drugs and by environmentally evoked anxiety. Together, these data are consistent with the theory of an integrated forebrain and hindbrain neuronal system that is important for anxiety states evoked by both drug and environmental manipulations.
Imidazoline binding sites (IBS) are now accepted as being receptors, however, their physiological functions are not yet clearly understood. Previously, the authors demonstrated that the density of IBS in the human placenta significantly increased throughout gestation. The present study was performed for the identification of imidazoline receptors in the human umbilical cord.