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Part of the book series: Progress in Experimental Cardiology ((PREC,volume 2))

Summary

An intrinsic tissue renin-angiotensin system (RAS) has been described in the brain. This review provides an overview of the localization of the enzymes, peptides, and receptors of the brain RAS and the organization of angiotensinergic pathways involved in cardiovascular regulation. Centrally administered exogenous angiotensin (Ang) II increases sympathetic neuronal activity, decreases the gain of the baroreflex, and induces vasopressin release. Ang II generated by the brain can cause similar changes through effects in nuclei from the forebrain to the brainstem. In salt-sensitive hypertension, both brain ouabain-like compounds (“ouabain”) and the brain RAS appear to play an essential role. Both central and high sodium intake activate brain “ouabain” followed by stimulation of the brain RAS and sympathoexcitatory and hypertensive responses. The actual pathways involved have not yet been established, but appear to involve the ventral anteroventral third ventricle region, the anterior hypothalamic area, and the paraventricular nucleus of the hypothalamus.

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Veerasingham, S.J., Leenen, F.H. (1998). The Brain Renin-Angiotensin System And Salt-Sensitive Hypertension. In: Dhalla, N.S., Zahradka, P., Dixon, I.M.C., Beamish, R.E. (eds) Angiotensin II Receptor Blockade Physiological and Clinical Implications. Progress in Experimental Cardiology, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5743-2_2

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  • DOI: https://doi.org/10.1007/978-1-4615-5743-2_2

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-7631-6

  • Online ISBN: 978-1-4615-5743-2

  • eBook Packages: Springer Book Archive

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