Alterations in Skeletal Muscle Oxygen Consumption and Functional Hyperemia in Renal Hypertensive Rats

Results from in situ hemodynamic studies in the hindlimbs of renal hypertensive rats (two-kidney, one-clip Goldblatt hypertension) and age-matched normotensive rats show that both resting hindlimb blood flow and resting hindlimb 0₂ consumption are significantly lower (P < .OS) in the hypertensive group than in the normotensive group by about 40 to 50 %. Contraction of hindlimb muscles reduces vascular resistance of hindlimb and increases both hindlimb blood flow and hindlimb 0₂ consumption in a frequency dependent manner. Hindlimb blood flow during muscle contraction is significantly lower (P < .OS) in the renal hypertensive group than in the normal control group, at the same degree of muscular activity. This is also true for the peak of reactive hyperemia following the period of ischemia produced by 5 to 25 sec. of arterial occlusion. Similarly, hindlimb 0₂ consumption during exercise is also found to be significantly reduced (P < .OS) in renal hypertensive rats when compared to that of age-matched normotensive rats. The linear relationship between hindlimb blood flow and hindlimb 0₂ consumption, however, is not altered by hypertension. When maximal vasodilation is produced in hindlimb vascular bed, the minimum vascular resistance is about 2-fold greater in renal hypertensive group than in the age-matched normotensive group (P < .01). This increase in minimum resistance is very likely to be due to structural adaptive changes of the vasculature such as the narrowing of the lumen of resistance vessels and the reduction in number of arterioles open to flow. These anatomical changes, however, do not restrict blood flow to the hindlimb at all degrees of muscular activity tested due to the fact that 0₂ extractions in the hindlimbs of hypertensive and normotensive rats, under the same conditions, are virtually the same. In addition, the increase in 0₂ extraction from arterial blood can be demonstrated in either type of rats when hindlimb blood flow is slightly decreased.

According to the results of active hyperemia studies, it is postulated that the lower hindlimb blood flow observed in renal hypertensive rats is a result of the reduction in oxygen consumption of the hindlimb muscles. The decrease in 0₂ usage and 0₂ demand of skeletal muscle in hypertensive rats is speculated to be due to the induced changes in the metabolic pathway for generating ATP, and/or impairment of mechanical function of skeletal muscle. Skeletal muscle cells in hypertension might develop a decrease in oxidative enzyme capacity, a reduction in density or growth of mitochondria, or an increase in the anaerobic metabolism. Functionally, skeletal muscle in hypertensive animals may develop less force than the muscle in normotensive animals, thereby require less energy, oxygen, or blood supply. Results from in situ measurements of maximum isometric tetanic force (P₀) in SOL and EDL muscles of renal hypertensive rats and age-matched normotensive rats, however, show that, under the conditions which the muscles are tetanized for 1 second, the maximal force generating capacity (P₀) of skeletal muscle in both types of animals are virtually the same. Whether the rate of energy production and expenditure during muscle contraction, and the endurance of mechanical performance of skeletal muscle is altered by renal hypertension or not, remains to be investigated.