Key result
Genetic deletion of eNOS in mice resulted in ~15% higher systolic and diastolic blood pressure compared to wild-type mice, but did not alter circadian blood pressure patterns.
Endothelial nitric oxide is important for regulating vascular tone but is not involved in generating the circadian rhythm of blood pressure.
eNOS regulates mean BP independently of circadian rhythm in mice; leaves open its role in human dipping and requires clinical validation.
Endothelial nitric oxide synthase knock out mice (eNOS-/-) are mildly hypertensive in comparison to wild-type (WT) mice. Hypertension in eNOS-/- mice is partly the result of an increase in peripheral resistance due to the absence of the vasodilatory action of NO. No data are available for these animals regarding the 24 h blood pressure profile under the 12:12 h light-dark cycle (LD) and constant dark (DD) conditions. Therefore, this study aimed to investigate by radiotelemetry the circadian rhythms in systolic blood pressure (SBP) and diastolic blood pressure (DBP) of six eNOS-/- mice and five wild-type mice under LD and DD. Data were collected beginning 3 wks after operation (implantation of sensor) for 2 wks under LD and for another 2 wks thereafter under DD. Our results show that eNOS-/- mice were hypertensive under all experimental conditions. SBP and DBP were significantly higher by about 15% in eNOS-/- mice. No differences were found in the pattern of the circadian rhythms, rhythmicity, or period lengths during LD or DD. The genetic deletion of eNOS seems to lead to higher SBP and DBP, but the circadian blood pressure pattern is still preserved with higher values during the night (active phase) and lower values during the daytime (rest phase). Thus, endothelial-derived NO plays an important role in the regulation of vascular tone and haemodynamics, but it is not important for the circadian organization of SBP and DBP.
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Arraj et al. (2007) studied Hypertension (n=11). eNOS knock-out vs. Wild-type mice was evaluated on Circadian rhythms in systolic and diastolic blood pressure. Genetic deletion of eNOS in mice resulted in ~15% higher systolic and diastolic blood pressure compared to wild-type mice, but did not alter circadian blood pressure patterns.
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