Influence of endogenous angiotensin II on control of sympathetic nerve activity in human dehydration

• Published in: The Journal of physiology Vol. 587; no. 22; pp. 5441 - 5449
• Main Authors: Rabbitts, J. A., Strom, N. A., Sawyer, J. R., Curry, T. B., Dietz, N. M., Roberts, S. K., Kingsley‐Berg, S. M., Charkoudian, N.
• Format: Journal Article
• Language: English
• Published: Oxford, UK The Physiological Society 15-11-2009; Blackwell Publishing Ltd; Blackwell Science Inc
• Subjects: Adolescent; Adult; Angiotensin II - physiology; Blood Pressure - physiology; Cardiovascular; Dehydration - physiopathology; Female; Heart Rate - physiology; Humans; Male; Receptor, Angiotensin, Type 1 - physiology; Sympathetic Nervous System - physiology; Water-Electrolyte Balance - physiology; Young Adult
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/jphysiol.2009.176693

Arterial blood pressure can often fall too low during dehydration, leading to an increased incidence of orthostatic hypotension
and syncope. Systemic sympathoexcitation and increases in volume regulatory hormones such as angiotensin II (AngII) may help
to maintain arterial pressure in the face of decreased plasma volume. Our goals in the present study were to quantify muscle
sympathetic nerve activity (MSNA) during dehydration (DEH), and to test the hypothesis that endogenous increases in AngII
in DEH have a mechanistic role in DEH-associated sympathoexcitation. We studied 17 subjects on two separate study days: DEH
induced by 24 h fluid restriction and a euhydrated (EUH) control day. MSNA was measured by microneurography at the peroneal
nerve, and arterial blood pressure, electrocardiogram, and central venous pressure were also recorded continuously. Sequential
nitroprusside and phenylephrine (modified Oxford test) were used to evaluate baroreflex control of MSNA. Losartan (angiotensin
type 1 receptor (AT1) antagonist) was then administered and measurements were repeated. MSNA was elevated during DEH (42 ±
5 vs. EUH: 32 ± 4 bursts per 100 heartbeats, P = 0.02). Blockade of AT1 receptors partially reversed this change in MSNA during DEH while having no effect in the control
EUH condition. The sensitivity of baroreflex control of MSNA was unchanged during DEH compared to EUH. We conclude that endogenous
increases in AngII during DEH contribute to DEH-associated sympathoexcitation.