January 1, 2021Clinical ScienceOpen Access

No evidence for brain renin–angiotensin system activation during DOCA-salt hypertension

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Why the study?

Brain renin-angiotensin system activation is thought to mediate DOCA-salt hypertension, but whether brainstem angiotensin II is generated from locally synthesized angiotensinogen to mediate this hypertension remained to be determined.

Does brain renin-angiotensin system activation mediate DOCA-salt hypertension in rats?

Population

Chronic DOCA-salt-hypertensive rats (n = 6-8/group) and rats without DOCA-salt

Comparison

Liver-directed siRNA targeted to angiotensinogen vs valsartan vs spironolactone

Design

Animal experimental study

Authors

EUEstrellita UijlErasmus MC LRLiwei RenJinan University KCKatrina M. Mirabito ColafellaDiscovery Institute

Discussion

Member takes

Implication

Questions brain RAS mediation of DOCA-salt hypertension; leaves open mechanisms in primary aldosteronism models.

Structured PICO

Does brain renin-angiotensin system activation mediate DOCA-salt hypertension in rats?

Population

Chronic DOCA-salt-hypertensive rats (n=6-8/group)

Intervention

Liver-directed siRNA targeted to angiotensinogen, valsartan (angiotensin II type 1 receptor antagonist), or spironolactone (mineralocorticoid receptor antagonist)

Comparator

Rats without DOCA-salt

Outcome

Mean arterial pressure, circulating angiotensinogen and renin, tissue angiotensinogen, and angiotensin metabolites (including brainstem angiotensin II)surrogate

Contrary to previous hypotheses, DOCA-salt hypertension is not mediated by brain renin-angiotensin system activation, as brain angiotensin II depends on circulating angiotensinogen.

Cite This Study

Uijl et al. (2021) studied this question.

synapsesocial.com/papers/6a719c58f44fa9f079df6068 https://doi.org/10.1042/cs20201239

Topics

Hypertension management

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