Changes in hemodynamic and neuro - humoral control cause cardiac damage in 1 kidney , 1 clip hypertensive mice

Sympathovagal balance and baroreflex control of heart rate (HR) were evaluated during the development (one and four weeks) of one kidney, one clip (1K1C) hypertension in conscious mice. The development of cardiac hypertrophy and fibrosis was also examined. Overall variability of systolic arterial pressure (AP) and HR in the time domain and baroreflex sensitivity were calculated from basal recordings. Methyl atropine and propranolol allowed the evaluation of the sympathovagal balance to the heart and the intrinsic HR. Staining of renal angiotensin II in the kidney and plasma renin activity (PRA) were also evaluated. One and four weeks after clipping, the mice were hypertensive and tachycardic, and exhibited elevated sympathetic and reduced vagal tone. The intrinsic HR was elevated only one week after clipping. Systolic AP variability was elevated while HR variability and baroreflex sensitivity were reduced one and four weeks after clipping. Renal angiotensin II staining and PRA were elevated only one week after clipping. Concentric cardiac hypertrophy was observed one and four weeks, while cardiac fibrosis was observed only at 4 weeks after clipping. In conclusion, these data further support previous findings in the literature and provide new features of neuro-humoral changes during the development of 1K1C hypertension in mice. In addition, the 1K1C hypertensive model in mice can be an important tool for studies evaluating the role of specific genes relating to dependent and non-dependent angiotensin II hypertension in transgenic mice.