Both Nitric Oxide and Endothelin-1 Influence Cerebral Blood Flow Velocity at Rest and after Hyper- and Hypocapnic Stimuli in Hypertensive and Healthy Adolescents

Abstract

Background and Purpose: Nitric oxide (NO)/endothelin imbalance may play a role in the regulation of cerebral blood flow. The aim of the present study was to assess whether these endothelial factors influence middle cerebral artery blood flow velocities (MCAV) and cerebrovascular reactivity (CVR) in healthy and hypertensive adolescents. Subjects and Methods: 106 adolescents (61 hypertensive and 45 normotensive) underwent transcranial Doppler measurements of the middle cerebral artery at rest and after 30 s of breath-holding (BH) and 60 s of hyperventilation (HV). Additionally, NO and endothelin-1 (ET-1) concentrations of the serum were assessed. The correlation between NO and ET-1 levels as well as MCAV and CVR values was analyzed. Results: Resting MCAVs were higher among hypertensive teenagers (76.5 ± 24 vs. 62.8 ± 15.6 cm/s, respectively, p < 0.001). CVR values did not differ between hypertensive and healthy adolescents after the BH and HV procedure. A significant negative correlation was found between absolute MCAV values and NO concentrations. ET-1 was positively related to MCAV. Conclusions: Cerebral blood flow velocities, but not CVR values, are associated with serum NO and ET-1 concentrations in adolescents.

Impaired cerebral vasoreactivity in white coat hypertensive adolescents

“…The role of the imbalance between the NO and endothelin has been proven to be crucial in the development of the arterial/ arteriolar changes observed in hypertension. Whilst in the territory of the middle-sized arteries, the increase in the endothelin concentration seems to be a determining factor of target-organ damages [31], cerebral arteriolar reactivity is mainly determined by nitric oxide [33]. In the present study, we have also demonstrated that nitric oxide concentration of the plasma was lower in both white coat and sustained hypertensive patients compared to healthy teenagers.…”

Mechanisms involved in the cerebrovascular dilator effects of cortical spreading depression

“…Findings, based upon available information, showed that responses of the human cerebral circulation to stimuli such as arterial blood hypercapnia, changes in arterial blood pressure, and changes in metabolism are similar in direction and magnitude to those determined in a variety of commonly used experimental animals (Katona et al ., 2006; Meadows et al ., 2005; Zhang et al ., 2004; Drake and Iadecola, 2007). More specific to this discussion, the previously identified dilator agents released by other species during CSD, including CGRP, NO, and acetylcholine, apparently have similar dilator effects on human cerebral arteries (Edvinsson et al ., 1987; Jansen-Olesen et al ., 1996; Hansen et al ., 2007; Sams et al ., 2000; Zvan et al ., 2002).…”

Retinal Arteriolar and Middle Cerebral Artery Responses to Combined Hypercarbic/Hyperoxic Stimuli

“…In both vascular beds, the primary involvement of endotheliumderived nitric oxide and endothelin (ET)-1 has been demonstrated. 19,[25][26][27] Endothelin-1 is a potent vasoconstrictor with lasting effect, 28,29 whereas nitric oxide has a much shorter half life, 30 which may explain why hyperoxia causes a concentration-dependent cumulative response in the retinal circulation. Moderate hyperoxia (P ET O 2 300 mm Hg) combined with hypercarbia induced mild vasoconstriction in the retina relative to the preceding normocarbic/normoxic II condition; however, there was no change in calculated RA blood flow be-tween the hypercarbia/hyperoxia-300 stimulus and baseline.…”