Low LBNP tolerance in men is associated with attenuated activation of the renin-angiotensin system

Plasma vasoactive hormone concentrations [epinephrine (p(Epi)), norepinephr ine (p(NE)), ANG II (p(ANG II)), vasopressin (p(VP)), endothelin-1 (p(ET-1) )] and plasma renin activity (p(RA)) were measured periodically and compare d during lower body negative pressure (LBNP) to test the hypothesis that re sponsiveness of the renin-angiotensin system, the latter being one of the m ost powerful vasoconstrictors in the body, is of major importance for LBNP tolerance. Healthy men on a controlled diet (2,822 cal/day, 2 mmol . kg(-1) . day(-1) Na+) were exposed to 30 min of LBNP from -15 to -50 mmHg. LBNP w as uneventful for seven men [25 +/- 2 yr, high-tolerance (HiTol) group], bu t eight men (26 +/- 3 yr) reached presyncope after 11 +/- 1 min [P < 0.001, low-tolerance (LoTol) group]. Mean arterial pressure (MAP) did not change measurably, but central venous pressure and left atrial diameter decreased similarly in both groups (5-6 mmHg, by approximate to 30%, P < 0.05). Contr ol (0 mmHg LBNP) hormone concentrations were similar between groups, howeve r, pRA differed between them (LoTol 0.6 +/- 0.1, HiTol 1.2 +/- 0.1 ng ANG I . ml(-1) . h(-1), P < 0.05). LBNP increased (P < 0.05) p(RA) and p(ANG II) , respectively, more in the HiTol group (9.9 +/- 2.2 ng ANG I . ml(-1) . h( -1) and 58 +/- 12 pg/ml) than in LoTol subjects (4.3 +/- 0.9 ng ANG I . ml( -1) . h(-1) and 28 +/- 6 pg/ml). In contrast, the increase in p(VP) was hig her (P < 0.05) in the LoTol than in the HiTol group. The increases (P < 0.0 5) for p(NE) were nonsignificant between groups, and p(ET-1) remained uncha nged. Thus there may be a causal relationship between attenuated activation of p(RA) and p(ANG II) and presyncope, with p(VP) being a possible cofacto r. Measurement of resting p(RA) may be of predictive value for those with l ower hypotensive tolerance.