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, 109 (6), 1998-2000; discussion 2015

Counterpoint: Activation of the Intrarenal Renin-Angiotensin System Is the Dominant Contributor to Systemic Hypertension

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Counterpoint: Activation of the Intrarenal Renin-Angiotensin System Is the Dominant Contributor to Systemic Hypertension

L Gabriel Navar. J Appl Physiol (1985).

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Fig. 2.
Fig. 2.
Pressure-natriuresis relationships and the responses to increases in salt intake or activation of the intrarenal renin-angiotensin system (RAS). Each pressure natriuresis relationship represents the acute responses in sodium excretion to changes in arterial pressure with all other systems maintained. The suppressed relationship occurs when there is overactivation of sodium retaining mechanisms such as increased RAS. The steeper curve represents the relationship when sodium retaining mechanisms are suppressed or sodium excretory mechanisms are activated such as with RAS inhibition or increased ANP. In normal individuals, a high salt intake leads to a shift in the pressure-natriuresis curve represented as arrow 1 such that sodium excretion increases with only small increases in arterial pressure. When the RAS is not appropriately suppressed, a high salt intake must lead to an increased arterial pressure to maintain sodium balance represented as arrow 2. If there is an augmented activation of the RAS, then even normal salt intake may require an increase in blood pressure to allow maintenance of sodium balance as depicted by arrow 3. While many other systems can modulate the magnitude of the responses, the final outcome always has to be the blood pressure where sodium balance can be maintained.

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