Mastoparan blockade of currents through Ca2+-activated K+ channels in bovine chromaffin cells

Glavinović, M.I.; Joshi, Amey; Trifaró, J. M.

doi:10.1016/0306-4522(92)90456-c

Cited by 5 publications

(4 citation statements)

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“…12 This effect did not contribute to contraction in the current studies, however, since indomethacin did not alter the response to mastoparan. In addition, mastoparan has been shown to modulate Ca 2+ -sensitive K + channels (0.5 to l x l f r 5 mol/L) 25 and increase L-channel-independent Ca 2+ permeability of cell membranes (>10~5 mol/L), 26 two effects that may have contributed to the mastoparan contraction at high concentrations (10~5 J mol/L), since nifedipine did not totally block the contraction at this concentration. However, since nifedipine totally blocked the contraction to lower concentrations of mastoparan, our observations do not support a contribution by these mechanisms at lower mastoparan concentrations.…”

Section: Discussionmentioning

confidence: 99%

Enhanced vascular reactivity to mastoparan, a G protein activator, in genetically hypertensive rats.

Kanagy

Webb

1994

Hypertension

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Vascular smooth muscle from stroke-prone spontaneously hypertensive rats has an increased responsiveness to the vasoconstrictors angiotensin II and serotonin. This abnormality is postulated to contribute to the hypertension characteristic of this strain of rats. We hypothesized that a portion of the increased responsiveness may be due to altered function of G proteins. This hypothesis was tested using mastoparan, a peptide that mimics ligand-bound receptors to stimulate G proteins directly. In addition, we investigated the mechanism of mastoparan-induced contraction of vascular smooth muscle. Changes in isometric tension were recorded in denuded carotid artery strips from hypertensive and normotensive (Wistar-Kyoto) rats. Vascular strips from the hypertensive rats had a significantly greater response to mastoparan at all concentrations between 10~8 and 10" 5 mol/L. A G protein inhibitor, A^-ethylmaleimide (10~3 mol/L), attenuated the response to mastoparan (10~7 mol/L) (67±4% of control re-H ypertension is associated with altered vascular reactivity to many agonists. The inbred strain of stroke-prone spontaneously hypertensive rats (SHRSP) specifically exhibits increased sensitivity to vasoconstrictors and a decreased response to vasodilators.1 Presently, the mechanisms responsible for this augmented responsiveness are not clear. Potential sites of modification in vascular tissue that could lead to increased responsiveness include increased number or affinity of agonist receptors, altered function or number of intramembrane signal transduction molecules (ie, G proteins), elevated function of intracellular secondmessenger-generating enzymes, and enhanced sensitivity of contractile proteins to second-messenger signals.Previous studies have shown that although receptor upregulation occurs in some models of hypertension, it is not sufficient to explain the differences in contractility.2 Furthermore, the sensitivity of contractile proteins to calcium is not elevated in genetic hypertension in the rat, 3 nor is there a difference in the function of secondmessenger-generating enzymes 4 -5 or in the amount of G proteins present in vascular smooth muscle of hypertensive rats.6 ' 7 However, the function of G proteins in vascular tissue has not been compared between hypertensive and normotensive animals.The purpose of this study was to examine the function of G proteins in isolated vascular tissue from hypertenFrom the Department of Physiology, University of Michigan Medical School, Ann Arbor.Correspondence to Nancy L. Kanagy, PhD, Department of Physiology, University of Michigan Medical School, Ann Arbor, MI 48109-0622. sponse), whereas pertussis toxin treatment did not. Inhibition of phospholipase C also significantly decreased the mastoparan-induced response (23 ±12% of control), and nifedipine (10~3 mol/L), a calcium channel blocker, completely blocked the mastoparan-induced contraction. Indomethacin treatment did not affect the mastoparan contraction even though mastoparan has been shown to stimulate phosphol...

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Section: Discussionmentioning

confidence: 99%

Enhanced vascular reactivity to mastoparan, a G protein activator, in genetically hypertensive rats.

Kanagy

Webb

1994

Hypertension

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“…Potential cancer biomarker (Slaby et al 2009;van de Sande et al 2006) Is the target of various anticancer drugs and so it could be used as a potential target for therapy (Tuynder et al 2004 Mast cell degranulation (Hirai et al 1979 Activation of G-protein-mediated mechanisms (Higashijima et al 1988;Perianin and Snyderman 1989;Ozaki et al 1990) Inhibition of calmodulin-mediated mechanisms (Wheeler-Jones et al 1992;Joyce-Brady et al 1991) Stimulation of phospholipases A 2 and C (Wallace and Carter 1989; Perianin and Snyderman 1989) Stimulation or inhibition of cation-specific channels (Glavinovic et al 1992) Hemolytic activity (Souza et al 2009)…”

Section: Venommentioning

confidence: 98%

“…Mastoparan is a 14-amino-acid amphipathic peptide obtained from wasp venom (Zimmerberg and Parsegian 1986). It have a wide spectrum of pharmacological activities including mast cell degranulation (Hirai et al 1979), activation of G-protein-mediated mechanisms (Ozaki et al 1990), inhibition of calmodulin-mediated mechanisms (Wheeler-Jones et al 1992), stimulation of phospholipases A 2 and C (Wallace and Carter 1989), and stimulation or inhibition of cation-specific channels (Glavinovic et al 1992). Mastoparan have been reported to have anti-cancer effect by inducing potent mitochondrial permeability transition in the concentration range between 5 and 100 mM, by forming a permeability transition pore (Pfeiffer et al 1995).…”

Section: Waspmentioning

confidence: 99%

Helminthes and insects: maladies or therapies

El-Tantawy

2014

Parasitol Res

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By definition, parasites cause harm to their hosts. But, considerable evidence from ancient traditional medicine has supported the theory of using parasites and their products in treating many diseases. Maggots have been used successfully to treat chronic, long-standing, infected wounds which failed to respond to conventional treatment by many beneficial effects on the wound including debridement, disinfection, and healing enhancement. Maggots are also applied in forensic medicine to estimate time between the death and discovery of a corpse and in entomotoxicology involving the potential use of insects as alternative samples for detecting drugs and toxins in death investigations. Leeches are segmented invertebrates, famous by their blood-feeding habits and used in phlebotomy to treat various ailments since ancient times. Leech therapy is experiencing resurgence nowadays in health care principally in plastic and reconstructive surgery. Earthworms provide a source of medicinally useful products with potential antimicrobial, antiviral, and anticancer properties. Lumbrokinases are a group of fibrinolytic enzymes isolated and purified from earthworms capable of degrading plasminogen-rich and plasminogen-free fibrin and so can be used to treat various conditions associated with thrombotic diseases. Helminth infection has been proved to have therapeutic effects in both animal and human clinical trials with promising evidence in treating many allergic diseases and can block the induction of or reduce the severity of some autoimmune disorders as Crohn's disease or ulcerative colitis. What is more, venomous arthropods such as scorpions, bees, wasps, spiders, ants, centipedes, snail, beetles, and caterpillars. The venoms and toxins from these arthropods provide a promising source of natural bioactive compounds which can be employed in the development of new drugs to treat diseases as cancer. The possibility of using these active molecules in biotechnological processes can make these venoms and toxins a valuable and promising source of natural bioactive compounds. The therapeutic use of helminthes and insects will be of great value in biomedicine and further studies on insect toxins will contribute extensively to the development of Biomedical Sciences.

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“…Other than interacting specifi cally with heteromeric and monomeric G-proteins, Mastoparan also has an effect on calcium-and calcium/potassium regulated events (Glavinovic et al 1992;Yule and Williams 1991), phosphoinositide -regulated cellular events (Nakahata et al 1990) and inositol phospholipid metabolism, the latter resulting in fl agella abscission in Chlamydomonas rheinhardtii (Quarmby et al 1992). Futhermore, release of arachidonic acid via phosphoinositide-independent pathways upon Mastoparan treatments have also been observed (Gil et al 1991), as have been effects that are known to Figure 10.4 Effects of G-protein and protein kinase C modulating drugs on bioluminescence in Pyrocystis lunula .…”

Section: Effects Of G-protein and Protein Kinase C Modulatorsmentioning

confidence: 99%

10 Algal cell biology – important tools to understand metal and herbicide toxicity

Heimann¹

2012

Advances in Algal Cell Biology

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Mastoparan blockade of currents through Ca2+-activated K+ channels in bovine chromaffin cells

Cited by 5 publications

References 42 publications

Enhanced vascular reactivity to mastoparan, a G protein activator, in genetically hypertensive rats.

Enhanced vascular reactivity to mastoparan, a G protein activator, in genetically hypertensive rats.

Helminthes and insects: maladies or therapies

10 Algal cell biology – important tools to understand metal and herbicide toxicity

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