Key result
Restoring ADMA-NO balance prevents progression from prehypertension to hypertension in animal models.
Why the study?
Does restoring the ADMA-NO balance prevent the development of hypertension in experimental models?
Does restoring the ADMA-NO balance prevent the development of hypertension in experimental models?
Targeting the ADMA-NO pathway prior to clinical hypertension represents a promising experimental therapeutic strategy to halt disease progression, though clinical translation is pending.
Answers are grounded in this paper and cite their sources.
Supports ADMA-NO targeting to prevent hypertension in animal models; hypothesis-generating for humans and should not yet change practice.
Despite the use of extensive antihypertensive therapy in patients with hypertension, little attention has been paid to early identification and intervention of individuals at risk for developing hypertension. The imbalance between nitric oxide (NO) and reactive oxygen species (ROS) resulting in oxidative stress has been implicated in the pathophysiology of hypertension. NO deficiency can precede the development of hypertension. Asymmetric dimethylarginine (ADMA) can inhibit nitric oxide synthase (NOS) and regulate local NO/ROS balance. Emerging evidence supports the hypothesis that ADMA-induced NO-ROS imbalance is involved in the development and progression of hypertension. Thus, this review summarizes recent experimental approaches to restore ADMA-NO balance in order to prevent the development of hypertension. Since hypertension might originate in early life, we also discuss the putative role of the ADMA-NO pathway in programmed hypertension. Better understanding of manipulations of the ADMA-NO pathway prior to hypertension in favor of NO will pave the way for the development of more effective medicine for the treatment prehypertension and programmed hypertension. However, more studies are needed to confirm the clinical benefit of these interventions.
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Tain et al. (2014) conducted a review in Hypertension and Prehypertension. Restoration of ADMA-NO balance (e.g., L-citrulline, melatonin, N-acetylcysteine) was evaluated. Restoring the ADMA-NO balance through experimental approaches prevented the transition from prehypertension to hypertension in animal models.
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