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The hypertensive response to chronic low‐dose Angiotensin II (AngII) is dependent on arterial pressure (AP) measurement method and salt intake
Author(s) -
King Andrew James,
Zorn Courtney,
Fink Gregory
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a754-a
Subject(s) - angiotensin ii , saline , pressor response , endocrinology , medicine , blood pressure , renin–angiotensin system , mean arterial pressure , chemistry , heart rate
It has been reported that when AP is measured by radiotelemetry, low‐dose AngII enhances pressor responses to external stimuli but does not cause sustained hypertension (Hypertension 42:798, 2003). The purpose of this study was to compare the hypertensive response to AngII in chronically tethered rats to rats with radiotelemetry transmitters. We hypothesize that low‐dose AngII infusion will cause a salt dependent increase in AP that will be greater in tethered rats, due to the stress of tethering. Rats were acclimatized to a 2% or 0.4% NaCl diet for 7 days prior to implantation of a radiotelemetry device or femoral arterial catheter for AP measurements. Following 7 days of control an Ang II or physiological saline filled osmotic minipump was implanted subcutaneously to deliver Ang II (150 ng/kg/min) or vehicle for 14 days. In addition, a group of radiotelemetry rats on 2% NaCl were tethered and subjected to a simulation of tether handling on control day 7 and AngII infusion days 7 and 14. Consistent with our hypothesis, we identified a salt‐sensitive pressor response to Ang II in both radiotelemetry and tethered rats, and the magnitude of the AP elevation in tethered rats was significantly larger. Simulating tether handling in telemetry rats also enhanced the pressor response. We conclude that a salt‐sensitive and sustained increase in AP occurs in response to low‐dose AngII irrespective of measurement method. Tethering enhances this hypertensive response, perhaps by sensitizing the rat to external stimuli. Supported by NIH Grant HL 076312.