Key result
In L-NAME-induced hypertensive rats, exercise did not increase cardiac output or skeletal muscle blood flow, but significantly increased arterio-venous oxygen content difference.
Why the study?
Does a bout of exercise alter cardiovascular adjustments in L-NAME-induced hypertensive rats compared to normotensive rats?
Does a bout of exercise alter cardiovascular adjustments in L-NAME-induced hypertensive rats compared to normotensive rats?
Hypertension associated with impaired nitric oxide release alters normal cardiovascular adjustments to exercise, preventing expected increases in cardiac output and muscle blood flow.
Indicates altered exercise hemodynamics in NO-deficient hypertension; hypothesis-generating for human studies.
The objective of the present study was to investigate cardiovascular adjustments at rest, during exercise, and 1 hour after exercise among nitric oxide (NO) blockade-induced hypertensive rats. Male Wistar rats (308 +/- 9 g) assigned as normotensive (n = 9) and hypertensive (N(omega)-nitro-L-arginine methyl ester, n = 11) underwent a bout of exercise. Arterial pressure (AP) and blood oxygen saturation were measured. Colored microspheres were used to evaluate blood flow and cardiac output (CO). Hypertensive rats (143 +/- 5 vs. 102 +/- 4 mmHg in normotensive rats), who presented reduced CO (57 +/- 6 vs. 102 +/- 7 mL/min in normotensive), also presented diminished blood flow in kidney, lung, and muscles at rest in comparison with normotensive rats. Exercise increased AP (20%), heart rate (40%), and CO (32%) among the normotensive rats, whereas the hypertensive rats presented an increased heart rate (40%) accompanied by a reduced venous oxygen saturation (45.5 +/- 2.1% vs. 75 +/- 0.7% in normotensive rats). Muscle vasodilatation, which was observed among the normotensive rats and is considered a hallmark adjustment to exercise, was not observed among the hypertensive rats. After a 1-hour interval from exercise most of the evaluated parameters returned to basal values. In conclusion, exercise did not cause an increase in CO, AP, or blood flow to skeletal muscle in hypertensive rats. However, it was associated with a significant increase in the arterio-venous oxygen content difference in NO-blocked rats, thus suggesting that hypertension associated with impairment in NO release induced different cardiovascular adjustments to exercise.
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Angelis et al. (2006) studied L-NAME-induced hypertension (n=20). L-NAME-induced hypertension (NO blockade) vs. Normotensive rats was evaluated on Cardiovascular adjustments to exercise. In L-NAME-induced hypertensive rats, exercise did not increase cardiac output or skeletal muscle blood flow, but significantly increased arterio-venous oxygen content difference.
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