Toshiyoshi Matsukawa

Muscle sympathetic nerve activity (MSNA) was measured directly along with blood pressure at rest in 69 healthy women (20-79 yr old) and 76 age-matched healthy men (16-80 yr old). All were nonobese and normotensive. In the women and men the MSNA was positively correlated with age (women: y = 0.788x - 5.418, r = 0.846, P < 0. 0001; men: y = 0.452x + 12.565, r = 0.751, P < 0.0001). The regression intercept of y was significantly lower (P < 0.0001) in the women than in the men, and the regression slope was significantly steeper (P < 0.0001) in the women. The MSNA was lower in women than in men among those <30 (P = 0.0012), 30-39 (P = 0. 0126), and 40-49 yr old (P = 0.0462) but was similar in women and men among those 50-59 (P = 0.1911, NS) and >/=60 yr old (P = 0.1739, NS). The results suggest that MSNA increases with age in women and men and that the activity is markedly lower in young women than in men but is markedly accelerated with age.

To determine whether the baroreflex control of sympathetic nerve activity is altered in patients with essential hypertension, muscle sympathetic nerve activity (MSNA) was recorded microneurographically from the tibial nerves of 23 normotensive subjects and 23 patients with essential hypertension. When phenylephrine (2 micrograms/kg) was injected intravenously, although the pressor response of mean arterial blood pressure (MAP) was significantly enhanced in the hypertensives as compared with the normotensives, the reflex decrease in MSNA was significantly smaller in the hypertensives. Furthermore, the baroreflex slope for MSNA, used as an index of baroreflex sensitivity and calculated by relating the change in MSNA to the change in MAP, was significantly less in the hypertensives. Following the injection of nitroglycerin (2 micrograms/kg), there were no significant differences between the normotensives and hypertensives in the depressor response, the reflex increase in MSNA or the baroreflex slope for MSNA. These observations suggest that the baroreflex change in sympathetic nerve activity is reduced during phenylephrine-induced blood pressure elevation but not during nitroglycerin-induced hypotension in the hypertensives, and that the blunted response of sympathetic nerve activity occurring during hypertension in these hypertensive patients may underlie the maintenance of high blood pressure in essential hypertension.

To evaluate the baroreflex changes and basal sympathetic vasomotor tone among three groups of adolescent normotensives or borderline hypertensives with and normotensives without a family history of hypertension, we continuously recorded muscle sympathetic nerve activity, arterial pressure and heart interval. Baroreflex slopes were calculated either by plotting the heart interval against the preceding peak systolic arterial pressure, or by relating the percentage changes in muscle sympathetic nerve activity to the mean changes in systolic arterial pressure produced by intravenous phenylephrine. The baroreflex slopes for the heart interval were significantly smaller in borderline hypertensive offspring (14 +/- 2 ms/mmHg) than in control normotensives (23 +/- 2 ms/mmHg) or normotensive offspring (19 +/- 3 ms/mmHg), whereas those for muscle sympathetic nerve activity were significantly smaller both in normotensive offspring (-8.3 +/- 1.0%/mmHg) and borderline hypertensive offspring (-7.9 +/- 0.5%/mmHg) than in control normotensives (-16.3 +/- 1.4%/mmHg). Baseline muscle sympathetic nerve activity was higher in borderline hypertensive offspring (20.1 +/- 3.0 bursts/min) than in control normotensives (10.1 +/- 1.2 bursts/min) or normotensive offspring (12.8 +/- 1.4 bursts/min), and also the depressor responses to trimethaphan were significantly enhanced in borderline hypertensive offspring [-19.2 +/- 2 versus 14 +/- 1 (normotensive offspring) or 12 +/- 2 (control normotensives)]. These results indicate that baroreflex inhibition of muscle sympathetic nerve activity was reduced in adolescents with a family history of hypertension even when they were normotensive. This reduced reflex sympatho-inhibition could lead to the development of hypertension by increasing sympathetic vasomotor tone.