Cardiovascular autonomic regulation in subjects with normal blood pressure, high-normal blood pressure and recent-onset hypertension.

1. In the present study, we tested the hypothesis that heart rate variability (HRV) is reduced in recent-onset hypertension and that pressor responses to standard autonomic reflex tests are not any different in hypertensives compared with normotensives. We also hypothesized that subjects with high-normal blood pressure (BP) would be distinguishable from normotensives on the basis of short-term HRV indices. 2. Three groups of subjects, each consisting of 15 men and 10 women, were examined. The first group consisted of subjects with recent-onset hypertension who were not taking antihypertensive medication (mean (+/-SD) age 50 +/- 12 years; BP >/= 140/90 mmHg), the second group consisted of subjects with high-normal BP (mean age 46 +/- 13 years; BP 130-139/85-89 mmHg) and the third group consisted of subjects with normal BP (mean age 48 +/- 12 years; BP < 120/80 mmHg). The aim was to characterize the autonomic state in each group. 3. Blood pressure, heart rate (HR), indices of short-term HRV during supine rest and quiet standing, HR variation during timed deep breathing (HRVdb) and pressor responses to the cold pressor test and sustained isometric handgrip were compared between the groups. 4. Although the three groups were comparable (P > 0.1) in terms of mean HR and low-frequency (LF) power expressed in normalized units at rest and during quiet standing, the standard deviation of normal-to-normal RR intervals (SDNN) during supine rest, LF and high-frequency spectral powers during supine rest and HRVdb were lowest in hypertensives (P </= 0.05 for each), indicating diminished baroreflex modulation of RR intervals in hypertensives. 5. In contrast, LF power was highest in subjects with high-normal BP (P </= 0.05) during supine rest and this is possibly because of higher BP variability. 6. The results suggest that HRVdb provides a simple measure of cardiac vagal effects in hypertensives, the rate-pressure product provides a simple measure of overall HRV in hypertensives and, in clinical hypertension, the arterial baroreflex mechanism is reset to maintain a higher BP through diminished vagal modulation of HR and possibly heightened sympathetic outflow to the heart and resistance vessels.