Introduction
Exercising can increase heart rate, blood pressure, ventilation, and peripheral vasoconstriction. Renal vasoconstriction is a phenomenon that is seen during exercise in humans and results in increased sympathetic flow. The mechanism helps control renal blood pressure and redistribution of blood supply to active sites. This article provides insights into renal reflex vasoconstriction and its impact on cardiovascular health.
What Is Peripheral Arterial Disease?
Peripheral arterial disease is a cardiac condition that affects ten percent of the population worldwide. The disorder is characterized by the narrowing of blood vessels due to atherosclerosis, causing a reduced ankle-brachial index. It commonly affects ten to 20 percent of the population over 70 years. The risk factors for peripheral arterial disease are hypertension, smoking, diabetes, and hyperlipidemia. Patients who develop peripheral arterial disease are at higher risk for mortality.
A lower ankle-brachial index correlates with severe disease and an increased risk for cardiovascular events. The symptoms of peripheral artery disease are intermittent claudication and limb pain or pain during physical activity that is relieved by rest. Most of the time, the disorder can be asymptomatic and leave individuals unaware of the condition, making them susceptible to myocardial infarction or stroke.
What Is Heart Failure?
Heart failure develops when heart muscles are unable to pump blood efficiently. This can lead to fluid accumulation in the lungs, leading to shortness of breath. Reduced exercise capacity and sympathoexcitation are cardinal features of heart failure. Early fatigue in heart failure patients during exercise can be attributed to diminished blood perfusion to active skeletal muscle.
What Is Renal Blood Flow and Its Regulation?
Renal arteries are end arteries that supply the kidneys—around 1000 milliliters of blood flow to the kidneys every minute. Almost 95 percent of this blood goes to the cortex, and the remaining reaches the medulla. Renal blood flow is constant with a mean arterial pressure of 75 to 160 mm Hg (millimeter of mercury).
Renal blood flow can be autoregulated or by sympathetic mechanism. Renal blood flow autoregulation is achieved through myogenic response, tubuloglomerular feedback, and mechanisms involving angiotensin II and nitric oxide. Sympathetic tone can induce an effect on renal autoregulation of blood flow.
How Does Exercise Induce an Effect on Reflex Renal Vasoconstriction?
In healthy individuals, exercising redistributes blood from inactive vascular beds like kidneys to active regions like skeletal muscle. It causes an increase in heart rate, blood pressure, and ventilation in response to the feedforward and feedback mechanism. Kidneys tend to receive 25 percent of the resting cardiac output. The reflex renal vasoconstriction mechanism is an important mechanism that helps maintain blood pressure within the kidneys depending on the exercise intensity.
The factors affecting reflex renal vasoconstriction are muscle mechanoreflex and metaboreflex activation. When exercises cause mechanical distortion of muscle fibers, they stimulate groups III and IV of muscle afferent nerve fibers. This mechanical distortion causes the generation of metabolic by-products within active skeletal muscle. The combination of these factors could affect the level of renal vasoconstriction in humans. Muscle mechanoreflex plays an important role in reflex renal vasoconstriction in humans and animals.
How Does Reflex Renal Vasoconstriction Affect Cardiac Patients?
Heart Failure: In heart failure patients, reflex renal vasoconstriction is augmented during exercise due to an exaggerated muscle mechanoreflex activation. These findings could be demonstrated in animal models with peripheral vascular disease, heart failure, and hypertension. Studies have revealed that the response of muscle metaboreceptors to vasoconstriction is stunted in heart failure patients.
The renal vasculature is vasoconstrictive at rest in heart failure patients. Despite an increase in basal renal vasoconstriction, there was a significant increase in reflex renal vasoconstriction during exercise. The peak renal reflex vasoconstriction was greater in heart failure patients than normal. In normal patients, reflex renal vasoconstriction returned to normal within two to five minutes after exercise. However, in heart failure patients, the time taken was prolonged, and 20 minutes was required to return to baseline after exercise.
Peripheral Artery Disease: Patients with peripheral arterial disease had augmented blood pressure increases during lower-limb exercise. However, it is still unknown if general renal vasoconstriction occurs during exercise in patients with peripheral artery disease.
The mechanism of increased mechanoreflex activity that augments renal vasoconstriction during exercise has to be evaluated. The atherosclerotic narrowing in patients' lower limb blood vessels causes reduced blood flow. Initially, there might be an increase in muscle metaboreceptors sensitivity, but gradually, their sensitivity might be reduced due to overstimulation. There is a gradual increase in muscle mechanoreceptor sensitivity as a compensatory response.
In peripheral artery disease patients, the augmented blood pressure was attenuated by infusing antioxidant ascorbic acid. Many risk factors of atherosclerosis increase oxidants like reactive oxygen species production. Oxidative stress induced by reactive oxygen species leads to endothelial dysfunction and atherosclerotic plaque formation. It could lead to turbulent blood flow in narrowed blood vessels and further increase the production of oxidants.
Peripheral arterial disease patients have higher oxidative stress markers and lower ascorbic acid levels. Oxidative stress could augment blood pressure and increase renal sympathetic nerve activity to static muscular contraction in animal models. The sensitization of muscle mechanoreceptors likely causes it. Therefore, it can be concluded that exercise-induced renal vasoconstriction is enhanced in patients with peripheral artery disease.
Conclusion
Renal reflex vasoconstriction is a mechanism that occurs in the kidneys while exercising. It helps regulate the blood pressure and renal flow to the kidney depending on the exercise intensity. Animal studies have shown impaired reflex renal vasoconstriction in heart failure and peripheral artery disease models. However, further research on this mechanism in humans is necessary to benefit cardiac patients.
