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DOCA‐salt hypertension persists in mice with ouabain‐resistant α1 and α2 Na, K‐ATPase (NKA)
Author(s) -
Loreaux Elizabeth L,
Oshiro Naomi,
Lingrel Jerry B,
Lorenz John N
Publication year - 2008
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.22.1_supplement.1210.18
Subject(s) - ouabain , blood pressure , medicine , endocrinology , saline , chemistry , endogeny , basal (medicine) , sodium , organic chemistry , insulin
It has been proposed that endogenous cardiac glycosides may play an important role in the development of various forms of human and experimental hypertension, including DOCA‐salt hypertension and ACTH‐induced hypertension. We have previously shown that ACTH‐induced hypertension is blunted in mutant mice that express a ouabain‐resistant isoform of the α2NKA. In the present study, therefore, we sought to explore whether the development of DOCA salt hypertension is altered in mutant mice variably expressing ouabain‐resistant and ‐sensitive α1 and α2 NKA isoforms. Mice were uninephrectomized and instrumented with telemetry implants for the continuous measurement of blood pressure. After recovery, DOCA pellets were implanted and animals were given saline to drink. Mean arterial pressure increased comparably in α1‐resistant/α2‐sensitive mice (wild type, 110±1 to 149±5 mmHg) vs α1‐resistant/α2‐resistant mice (108±4 to 146±3 mmHg). In separate groups of DOCA‐salt‐treated mice instrumented with indwelling arterial catheters, treatment with digoxin antibody (digibind) had no effect on blood pressure in either α1‐resistant/α2‐sensitive or α1‐resistant/α2‐resistant mice. We also evaluated DOCA‐salt hypertension by telemetry in α1‐sensitive/α2‐resistant mice, and found that blood pressure increased similarly to the other two genotypes (106±3 to 153±9). These data suggest that the elevated pressure in DOCA‐salt treated mice is not dependent on the interaction of endogenous cardiotonic steroids with α1 or α2 NKA.