Post-exercise hypotension is an important event for blood pressure regulation, especially in hypertensive individuals. Although post-exercise hypotension is a well-known phenomenon, the mechanism responsible is still unclear. The kallikrein-kinin system is involved in blood pressure control, but its role in post-exercise hypotension has not yet been investigated. Thus, the purpose of this study was to investigate the involvement of the vasodilators bradykinin and des-Arg(9)-BK and kallikrein activity in post-exercise hypotension promoted by 35 min of cycle ergometer (CE) or circuit weight-training (CWT) bouts in normotensive and hypertensive individuals. A significant decrease in mean arterial pressure at 45 and 60 min after CE and 45 min after CWT was observed in normotensive individuals. Hypertensive values of mean arterial pressure were significantly reduced at 45 and 60 min after CE and at 60 min after CWT. Before exercise, plasma bradykinin concentrations and kallikrein activity were higher in hypertensive compared to normotensive volunteers. Kinin levels increased in the groups evaluated at the end of the training period and 60 min post-exercise. These data suggest that the kallikrein-kinin system may be involved in post-exercise hypotension in normotensive and hypertensive individuals subjected to CE and CWT bouts.

To investigate the antihypertensive effects of conventional resistance exercise (RE) on the blood pressure (BP) of hypertensive subjects, 15 middle-aged (46 ± 3 years) hypertensive volunteers, deprived of antihypertensive medication (reaching 153 ± 6/93 ± 2 mm Hg systolic/diastolic BP after a 6-week medication washout period) were submitted to a 12-week conventional RE training program (3 sets of 12 repetitions at 60% 1 repetition maximum, 3 times a week on nonconsecutive days). Blood pressure was measured in all phases of the study (washout, training, detraining). Additionally, the plasma levels of several vasodilators or vasoconstrictors that potentially could be involved with the effects of RE on BP were evaluated pre- and posttraining. Conventional RE significantly reduced systolic, diastolic, and mean BP, respectively, by an average of 16 (p < 0.001), 12 (p < 0.01), and 13 mm Hg (p < 0.01) to prehypertensive values. There were no significant changes of vasoactive factors from the kallikrein-kinin or renin-angiotensin systems. After the RE training program, the BP values remained stable during a 4-week detraining period. Taken together, this study shows for the first time that conventional moderate-intensity RE alone is able to reduce the BP of stage 1 hypertensive subjects free of antihypertensive medication. Moreover, the benefits of BP reduction achieved with RE training remained unchanged for up to 4 weeks without exercise.

Patients that develop rhabdomyolysis of different causes are at high risk of acute renal failure. Efforts to minimize this risk include volume repletion, treatment with mannitol, and urinary alkalinization as soon as possible after muscle injury. This is a retrospective analysis (from January 1, 1992, to December 31, 1995) of therapeutic response to prophylactic treatment in patients with rhabdomyolysis admitted to an intensive care unit (ICU). The diagnosis of rhabdomyolysis was based on creatinine kinase (CK) level (> 500 Ui/L) and the criteria for prophylaxis were: time elapsed between muscle injury to ICU admission < 48 h and serum creatinine < 3 mg/dL. Fifteen patients were treated with the association of saline, mannitol, and sodium bicarbonate (S + M + B group) and 9 patients received only saline (S group). Serum creatinine at admission was similar in both groups: 1.6 +/- 0.6 mg/dL in the S + M + B group and 1.5 +/- 0.6 mg/dL in the S group (p > 0.05). Maximum serum CK measured was 3351 +/- 1693 IU/L in the S + M + B group and 1747 +/- 2345 IU/L in the S group (p < 0.05). However the measurement of CK was earlier in S + M + B patients (1.7 vs 2.7 days after rhabdomyolysis). APACHE II scores were 16.9 +/- 7.4 and 13.4 +/- 4.9 in the S + M + MB and S groups, respectively (p > 0.05). Despite the treatment protocol the serum levels of creatinine had similar behavior and reached normal levels in all patients in 2 or 3 days. The saline infusion during the first 60 h on the ICU was 206 mL/h in the S group and 204 mL/h in S + M + B (p > 0.05). Mannitol dose was 56 g/day, and bicarbonate 225 mEq/day during 4.7 days. Our data show that progression to established renal failure can be totally avoided with prophylactic treatment, and that once appropriate saline expansion is provided, the association of mannitol and bicarbonate seems to be unnecessary.