Abstract

We previously reported that maternal separation, rat model of early life stress, enhances pressor responses to acute and chronic stressors. The aims of this study were to determine whether Dahl salt-sensitive (DS) rats subjected to maternal separation (MatSep-DS) as compared to normally reared DS (Ctl-DS) rats show exaggerated blood pressure responses to acute behavioral stressors, such as restraint stress or air jet stress (AJS), or, hypertensive stimuli including chronic high-salt diet (4% NaCl) and angiotensin II (AngII) infusion (200 ng/Kg/min) during 1 week. MatSep was performed in male DS rats for 3 h/day from postnatal days 2-14. At 8 weeks of age, rats were implanted with telemetry transmitters and allowed to recover. Mean arterial pressure (MAP) was not different between MatSep-DS and Ctl-DS rats at baseline (120 ± 2 mmHg vs. 118 ± 1 mmHg, n = 4-8). Blood pressure responses during AJS and restraint stress were not different between MatSep-DS and Ctl-DS at 3 min. However, blood pressure recovery from AJS was significantly impaired in MatSep-DS rats compared to Ctl-DS rats (P < 0.05). 3-h stress-induced similar responses in MatSep and Ctl-DS rats. Chronic blood pressure responses to AngII infusion in rats fed a high-salt diet displayed enhanced MAP in MatSep-DS when compared with Ctl-DS rats (167 ± 5 mmHg vs. 152 ± 2 mmHg, pinteraction <0.05). However, MAP increased similarly in both groups in response to AngII infusion or high-salt diet separately. Renal parameters such as proteinuria, urine flow rate, and urine electrolytes were not different between groups in response to each treatment. In summary, salt sensitivity induces exaggerated blood pressor responses only in presence of AngII due to early life stress.

Document Type

Article

Publication Date

5-21-2015

Notes/Citation Information

Published in Physiological Reports, v. 3, no. 5, article e12408, p. 1-9.

© 2015 The Authors. Physiological Reportspublished by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Digital Object Identifier (DOI)

http://dx.doi.org/10.14814/phy2.12408

Funding Information

This study was supported by grants from the National Institutes of Health National Heart, Lung, and Blood Institute (J.S. Pollock and D.M. Pollock: P01 HL69999, P01 HL95499, and A. S. Loria: K99 HL111354).

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