Abstract
Summary
To evaluate the role of the renin-angiotensin system in the aldosterone response to sodium depletion in the conscious rabbit, angiotensin blockade was achieved with [Sar 1 , Ala 8 ] angiotensin II and SQ 20881. After infusion of [Sar 1 , Ala 8 ] angiotensin II (1 μg/kg/min) for 60 min into sodium-depleted animals, PAC was unchanged (33.3 ± 7.4 ng% compared with a control sodium-deplete value of 41.1 ± 8.2 ng%). When the dose was increased to 50 μg/kg/min for an additional 60 min, PAC fell to 15.4 ± 3.7 ng% (P < 0.0125), a value similar to the sodium replete value. In a second group of animals, SQ 20881 was given initially as a 7 mg/kg bolus and followed by an infusion of 60 μg/kg/min for 30 min; PAC fell from a sodium-deplete level of 86.6 ± 21.0 to 63.9 ± 18.2 ng% (P < 0.025). The infusion was extended to 60 min in five of the seven animals and PAC remained significantly reduced (63.3 ± 16.2 ng%, P < 0.01). These studies demonstrate that attenuation of the aldosterone response to sodium depletion occurred with both [Sar 1 , Ala 8 ] angiotensin II and SQ 20881 in the conscious rabbit indicating a role for the renin-angiotensin system in this model.
We thank Mssrs. D. Welch, C. Gay, D. Early, K. Lohman, and Ms. M. Flood for very able technical assistance.
The gifts of SQ 20881 from Squibb and [Sar 1 , Ala8] angiotensin II from Eaton Laboratories are gratefully acknowledged.
This work was supported by U.S. Public Health Service Grant HL10610 and the senior author was supported by a Wellcome Trust travel grant.
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