Key result
Central nervous system interactions between angiotensin II, mineralocorticoids, and medullary centers drive neurogenic hypertension.
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A large body of evidence indicates that the central nervous system plays an essential role in the pathogenesis of hypertension. However, in many cases the specific brain regions involved and the mechanisms by which these regions promote hypertension are not known. In recent years, research in this and other laboratories has attempted to determine the mechanisms by which neural and humoral signals arising in response to pathological conditions (often occurring in the periphery) interact with the central nervous system to produce hypertension. In this article, we illustrate the coupling of peripheral and central factors in the pathogenesis of hypertension by examining the central actions of angiotensin II and mineralocorticoids in the expression of renal hypertension and mineralocorticoid-salt hypertension, respectively. We also review recent data from this laboratory illustrating the involvement of medullary vasomotor centers in the development of neurogenic hypertension after sinoaortic deafferentation and in the maintenance of hypertension in the spontaneously hypertensive rat.
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Brody et al. (1991) conducted a review in Hypertension. Angiotensin II, mineralocorticoids, and sinoaortic deafferentation was evaluated on Pathogenesis and maintenance of renal, mineralocorticoid-salt, and neurogenic hypertension. Angiotensin II, mineralocorticoids, and medullary vasomotor centers interact with peripheral signals in the central nervous system to drive renal, salt, and neurogenic hypertension.
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