Modulation of angiotensin II binding sites in neuronal cultures by mineralocorticoids.

@article{Sumners1989ModulationOA,
  title={Modulation of angiotensin II binding sites in neuronal cultures by mineralocorticoids.},
  author={C. Sumners and Melvin J. Fregly},
  journal={The American journal of physiology},
  year={1989},
  volume={256 1 Pt 1},
  pages={
          C121-9
        }
}
Previous studies have determined that mineralocorticoid hormones are able to increase the number of angiotensin II (ANG II)-specific binding sites in rat diencephalon and in neuronal cultures and also increase the drinking response elicited by centrally injected ANG II. In the present study, we have examined the specificity and mechanisms of this mineralocorticoid action. In neuronal cultures from the hypothalamus and brain stem (H/BS), both D-aldosterone and deoxycorticosterone acetate (DOCA… Expand
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TLDR
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Regulation of Corticotropin and Adrenal Steroid Feed-Back
Mineralocorticoids, such as deoxycorticosterone acetate (DOCA), and angiotensin II (AngII) act synergistically in the brain to elicit salt appetite. Glucocorticoids, such as dexamethasone (DEX), alsoExpand
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TLDR
Aldosterone may potentiate the pressor responses of angiotensin II via effects on angiotENSin II receptors, and prevented angiotsin II-induced downregulation and desensitization. Expand
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TLDR
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Mineralocorticoid treatment attenuates activation of oxytocinergic and vasopressinergic neurons by icv ANG II.
TLDR
DOCA attenuates the responsiveness of OT and VP neurons to ANG II without completely suppressing the activity of these neurons and, therefore, support the hypothesis that attenuation of OT neuronal activity is one mechanism by which mineralocorticoids enhance NaCl intake. Expand
Angiotensin II receptor subtype antagonists can both stimulate and inhibit salt appetite in rats
TLDR
Evidence is provided for a complex action of Ang II on the At-1 receptor mediating the generation of salt appetite that appears to involve either at least two functional subtypes of this AT- 1 receptor, as already suggested by previous electrophysiological experiments, or one AT-1 receptors with several activation states. Expand
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