The renin–angiotensin system in cardiovascular autonomic control

recent developments and clinical implications

Amanda J. Miller, Amy Arnold

Research output: Contribution to journalReview article

3 Citations (Scopus)

Abstract

Complex and bidirectional interactions between the renin–angiotensin system (RAS) and autonomic nervous system have been well established for cardiovascular regulation under both physiological and pathophysiological conditions. Most research to date has focused on deleterious effects of components of the vasoconstrictor arm of the RAS on cardiovascular autonomic control, such as renin, angiotensin II, and aldosterone. The recent discovery of prorenin and the prorenin receptor have further increased our understanding of RAS interactions in autonomic brain regions. Therapies targeting these RAS components, such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers, are commonly used for treatment of hypertension and cardiovascular diseases, with blood pressure-lowering effects attributed in part to sympathetic inhibition and parasympathetic facilitation. In addition, a vasodilatory arm of the RAS has emerged that includes angiotensin-(1–7), ACE2, and alamandine, and promotes beneficial effects on blood pressure in part by reducing sympathetic activity and improving arterial baroreceptor reflex function in animal models. The role of the vasodilatory arm of the RAS in cardiovascular autonomic regulation in clinical populations, however, has yet to be determined. This review will summarize recent developments in autonomic mechanisms involved in the effects of the RAS on cardiovascular regulation, with a focus on newly discovered pathways and therapeutic targets for this hormone system.

Original languageEnglish (US)
Pages (from-to)231-243
Number of pages13
JournalClinical Autonomic Research
Volume29
Issue number2
DOIs
StatePublished - Apr 1 2019

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Cardiovascular System
Renin
Blood Pressure
Baroreflex
Angiotensin Receptor Antagonists
Autonomic Nervous System
Angiotensins
Vasoconstrictor Agents
Aldosterone
Angiotensin-Converting Enzyme Inhibitors
Angiotensin II
Cardiovascular Diseases
Therapeutics
Animal Models
Hormones
Hypertension
Brain
Research
Population

All Science Journal Classification (ASJC) codes

  • Endocrine and Autonomic Systems
  • Clinical Neurology

Cite this

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abstract = "Complex and bidirectional interactions between the renin–angiotensin system (RAS) and autonomic nervous system have been well established for cardiovascular regulation under both physiological and pathophysiological conditions. Most research to date has focused on deleterious effects of components of the vasoconstrictor arm of the RAS on cardiovascular autonomic control, such as renin, angiotensin II, and aldosterone. The recent discovery of prorenin and the prorenin receptor have further increased our understanding of RAS interactions in autonomic brain regions. Therapies targeting these RAS components, such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers, are commonly used for treatment of hypertension and cardiovascular diseases, with blood pressure-lowering effects attributed in part to sympathetic inhibition and parasympathetic facilitation. In addition, a vasodilatory arm of the RAS has emerged that includes angiotensin-(1–7), ACE2, and alamandine, and promotes beneficial effects on blood pressure in part by reducing sympathetic activity and improving arterial baroreceptor reflex function in animal models. The role of the vasodilatory arm of the RAS in cardiovascular autonomic regulation in clinical populations, however, has yet to be determined. This review will summarize recent developments in autonomic mechanisms involved in the effects of the RAS on cardiovascular regulation, with a focus on newly discovered pathways and therapeutic targets for this hormone system.",
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The renin–angiotensin system in cardiovascular autonomic control : recent developments and clinical implications. / Miller, Amanda J.; Arnold, Amy.

In: Clinical Autonomic Research, Vol. 29, No. 2, 01.04.2019, p. 231-243.

Research output: Contribution to journalReview article

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