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Does the 1K1C hypertension model induce changes in arterial pressure variability, baroreflex sensitivity, and cardiac hypertrophy in conscious mice?
Does the 1K1C hypertension model induce changes in arterial pressure variability, baroreflex sensitivity, and cardiac hypertrophy in conscious mice?
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The 1K1C hypertension model in mice successfully induces reduced baroreflex sensitivity, increased arterial pressure variability, and cardiac hypertrophy, providing a useful model for studying hypertensive end-organ damage.
This study aimed to evaluate arterial pressure variability (APV), baroreflex sensitivity (BRS) and end‐organ damage in conscious one kidney, one clip (1K1C) hypertensive mice. Under tribromoethanol anesthesia, Swiss mice received a silver clip around the right renal artery associated with contralateral nephrectomy (n=17). Sham operated mice (n=22) were submitted to left nephrectomy. After 4 weeks mice were equipped with catheters placed into the left carotid artery, and had the arterial pressure (AP) recorded. Standard deviation of systolic AP was defined as systolic APV while BRS was calculated using the sequence method. Mice were killed by decapitation and the hearts submitted to histological analysis. 1K1C hypertensive mice exhibited marked cardiac hypertrophy characterized by increase of the diameter of left ventricular myocyte (13.58±0.84 vs 15.37±1.54 μm) and septum myocyte (10.55±0.65 vs 12.10±0.42 μm). Left ventricular (1.49±0.019 vs 1.23±0.16 mm) and septum (1.35±0.21 vs 1.11±0.09 mm) wall thickness were also increased in 1K1C hypertensive mice. 1K1C hypertension was associated with decreased BRS (0.96±0.13 vs 0.32±0.05 bpm/mmHg) and elevated systolic APV (3.9±0.2 vs 5.4±0.5 mmHg). There were no alterations in the collagen content of the groups studied. In conclusion, 1K1C hypertension in mice displayed reduced BRS, increased APV, and cardiac hypertrophy. Support: FAPESP and CNPq.
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Borges et al. (2008) studied this question.
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