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2.
Radiat Res ; 137(1): 52-8, 1994 Jan.
Article in English | MEDLINE | ID: mdl-8265788

ABSTRACT

Sprague-Dawley rats (200-250 g) were exposed 30 min/day for 4 days to thermogenic levels (rectal temperature increase of 2.2 degrees C) of microwave radiation [2.45 GHz, 80 mW/cm2, continuous-wave mode (CW)] or to a radiant heat source resulting in an equivalent increase in body temperature of 2.2 degrees C. On the fifth day after the 4 days of exposure to microwave radiation, the animals were sacrificed and their livers removed. The canalicular membranes were isolated and evaluated for adenosinetriphosphatase (ATPase) activity, total fatty acid composition and membrane fluidity characteristics. Mg(++)-ATPase activity (Vmax) decreased by 48.5% in the group exposed to microwave radiation, with no significant change in the group exposed to radiant heat. The decrease in Mg(++)-ATPase was partially compensated by a concomitant increase in Na+/K(+)-ATPase activity (170% increase in Vmax over control) in animals exposed to microwave radiation, while no change occurred in the group exposed to radiant heat. This alteration in ATPase activity in the group exposed to microwave radiation is associated with a large decrease in the ratio of saturated to unsaturated fatty acids. Conversely, the group exposed to radiant heat had an increase in the ratio of saturated to unsaturated fatty acids. The most dramatic changes were found in the levels of arachidonic acid. Finally, the electron paramagnetic resonance (EPR) spin label technique used to measure the fluidity of the canalicular membranes of the animals in the three groups (sham, microwave radiation and radiant heat) indicated that the results were different in the three groups, reflecting the changes found in their fatty acid composition. The physiological response to "equivalent" thermal loads in rats is expressed differently for different types of energy sources. Possible mechanisms producing these divergent thermogenic responses are discussed.


Subject(s)
Bile Canaliculi/radiation effects , Ca(2+) Mg(2+)-ATPase/radiation effects , Cell Membrane/radiation effects , Microwaves , Sodium-Potassium-Exchanging ATPase/radiation effects , Animals , Bile Canaliculi/enzymology , Body Temperature/radiation effects , Body Temperature Regulation/radiation effects , Ca(2+) Mg(2+)-ATPase/metabolism , Cell Membrane/enzymology , Electron Spin Resonance Spectroscopy , Fatty Acids/metabolism , Hyperthermia, Induced , Male , Rats , Rats, Sprague-Dawley , Sodium-Potassium-Exchanging ATPase/metabolism
3.
Circ Res ; 69(3): 800-9, 1991 Sep.
Article in English | MEDLINE | ID: mdl-1651818

ABSTRACT

Previous studies show that angiotensin II (Ang II) increases phosphoinositide turnover in cultured neonatal heart cells. Ang II has also been shown to transiently increase spontaneous beating behavior in these cells. In this study we seek to identify the molecular mechanism underlying this rapid (3-5-minute) desensitization. Time-course studies on the accumulation of [3H]inositol phosphates indicate that the loss in functional responsiveness correlates with reduced efficacy of Ang II to activate the phosphoinositide path. Binding studies with 125I-Ang II revealed that there was no change in surface receptor binding capacity during the time in which desensitization developed. Normal phosphoinositide and functional responses are observed when desensitized cells are treated with probes that activate the cardiac phosphoinositide pathway at discrete steps. These studies reveal that the functional status of the major components of the phosphoinositide signaling pathway, including G proteins, phospholipase C, and protein kinase C (PKC), are normal during maintained Ang II desensitization. To study the potential role of PKC in Ang II desensitization, the cells are treated with TPA for 24 hours, which downregulates PKC activity. PKC-depleted cells rapidly desensitize after Ang II application. We conclude that the selective Ang II-evoked biochemical/functional desensitization involves inhibition at the level of the receptor, rather than at a component downstream in the path, and that this process is independent of PKC and loss of surface binding capacity.


Subject(s)
Angiotensin II/pharmacology , Myocardium/metabolism , Phosphatidylinositols/metabolism , Receptors, Angiotensin/drug effects , Angiotensin II/metabolism , Animals , Animals, Newborn , Culture Techniques , GTP-Binding Proteins/metabolism , Inositol Phosphates/metabolism , Myocardium/cytology , Phenylephrine/pharmacology , Protein Kinase C/metabolism , Rats , Rats, Inbred Strains , Receptors, Angiotensin/metabolism , Type C Phospholipases/metabolism
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