Calcium regulation of membrane fusion during hormone secretion.
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Adrenal Medulla↗
Biomedical subjects
A Stutzin
Publications and source records attributed to A Stutzin.
Effects of guanethidine on electron transport and proton movements in rat heart, brain and liver mitochondria.
Guanethidine at 5-25 mM concentrations was found to induce up to 79% inhibition of ADP-stimulated (state III) oxygen consumption in isolated rat heart, brain or liver mitochondria, when the added substrate was glutamate or succinate, but the inhibition was considerably lower (24% or less) when respiration was supported by ascorbate plus tetramethylphenylenediamine (TMPD). Comparable results were seen regarding ADP-stimulated proton uptake, where even greater inhibition (up to 94% with glutamate or succinate, but not ascorbate plus TMPD) was found. Similar but somewhat less marked effects were also seen in resting (state IV) respiration and on the acceptor control ratio (state III/state IV respiration). 2,4-Dinitrophenol was unable to relieve guanethidine-induced inhibition of electron transport. These results indicate that guanethidine inhibits primarily mitochondrial electron transport itself, and that the site where such inhibition is more marked is located in the span between ubiquinone and cytochrome c of the respiratory chain. It is, therefore, suggested that active guanethidine uptake by noradrenergic neurons can lead to a high drug concentration in their cytoplasm and hence to mitochondrial alterations that can contribute to the pharmacological effect of this drug. Our results demonstrate the interaction between guanethidine and the electron transport chain of mitochondria derived from different tissues and, therefore, support this hypothesis.
Adenosine Diphosphate↗
Guanethidine effects on the guinea pig vas deferens are antagonized by the blockers of calcium-activated potassium conductance, apamin, methylene blue, and quinine.
The blocking effects of guanethidine on electrically induced, neurally mediated, contractions of the guinea pig vas deferens in vitro could be markedly antagonized by the bee venom polypeptide apamin (20-60 nM), by 0.1 mM methylene blue, and (less regularly) by 0.1-0.15 mM quinine, three substances known to inhibit calcium-activated potassium conductance in a variety of cells. Guanethidine (20 microM) was also found to inhibit (by 88%) the release of [3H]norepinephrine induced by electrical stimulation (20-Hz, 2-msec, biphasic pulses of supramaximal voltage). Such inhibition was decreased to 39% when 20 nM apamin was present together with guanethidine, thus showing that the effect of this polypeptide is presynaptic. On the basis of these findings, we suggest that guanethidine may block adrenergic neurons by activating their calcium-activated potassium conductance, presumably by releasing intracellular calcium.
Animals↗
Swelling-activated ion channels: functional regulation in cell-swelling, proliferation and apoptosis.
Cell volume regulation is one of the most fundamental homeostatic mechanisms and essential for normal cellular function. At the same time, however, many physiological mechanisms are associated with regulatory changes in cell size meaning that the set point for cell volume regulation is under physiological control. Thus, cell volume is under a tight and dynamic control and abnormal cell volume regulation will ultimately lead to severe cellular dysfunction, including alterations in cell proliferation and cell death. This review describes the different swelling-activated ion channels that participate as key players in the maintenance of normal steady-state cell volume, with particular emphasis on the intracellular signalling pathways responsible for their regulation during hypotonic stress, cell proliferation and apoptosis.
Animals↗