Sympathovagal balance and baroreflex control of heart rate (HR) were evaluated during the development (1 and 4 wk) 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 ANG 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 they exhibited elevated sympathetic and reduced vagal tone. The intrinsic HR was elevated only 1 wk after clipping. Systolic AP variability was elevated, while HR variability and baroreflex sensitivity were reduced 1 and 4 wk after clipping. Renal ANG II staining and PRA were elevated only 1 wk after clipping. Concentric cardiac hypertrophy was observed at 1 and 4 wk, while cardiac fibrosis was observed only at 4 wk after clipping. In conclusion, these data further support previous findings in the literature and provide new features of neurohumoral 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 nondependent ANG II hypertension in transgenic mice. renovascular hypertension; sympathetic tone; vagal tone; intrinsic heart rate; baroreflex THE UNDERSTANDING OF THE PATHOPHYSIOLOGY of hypertension has been greatly advanced because of studies performed in several species, including dog, rabbit, and rat (9,12,14). Among the experimental models of hypertension, the renovascular model has brought considerable insights to studies of the pathophysiology of hypertension (4,33,45). In particular, it is well recognized that the onset and development of one-kidney, one clip (1K1C) hypertension have complex mechanisms involving humoral and autonomic aspects.The renin-angiotensin system (RAS) plays a key role in the onset of 1K1C hypertension and its biologically active hormone, ANG II, has important hemodynamic effects, leading to rise in arterial pressure (AP) (9). Studies from our laboratory (24,26) demonstrated that the 1st wk of 1K1C hypertension in rats is accompanied by a transient tachycardia and increased intrinsic heart rate (HR). Other studies performed on 1K1C hypertensive rats have indicated that sympathetic drive is involved in the development and maintenance of this model of hypertension (4, 17). It was observed that 1K1C hypertension is accompanied by an increased cardiac sympathetic drive from the 1st wk after clipping and a reduced cardiac vagal activity after 4 wk of the onset of 1K1C hypertension (4). It has also been demonstrated that the baroreflex gain was reduced 1 day after clipping, while the major baroreflex impairment occurred after 30 days (30). A number of studies...