Postnatal development of blood pressure and baroreflex in mice

Ishii, Tôru; Kuwaki, Tomoyuki; Masuda, Yoshiaki; Fukuda, Yasuichiro

doi:10.1016/s1566-0702(01)00339-3

Cited by 51 publications

(55 citation statements)

References 31 publications

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“…These results reveal that both the sensitivity to pressure and the magnitude of intrinsic tone were significantly greater in neonatal than in adult mouse cerebral arteries. From a teleological perspective, these results reflect a matching between the pressure range over which intrinsic tone is developed and mean arterial pressures that average 80 mmHg in adults but only 30 mmHg in neonates (18,19). From a mechanistic perspective, the observed age-related differences in pressure sensitivity could be explained by corresponding differences in the contributions of either myogenic tone or endothelial factors to the development of intrinsic tone.…”

Section: Intrinsic Tone In the Immature Cerebral Microcirculationmentioning

confidence: 67%

Maturation depresses mouse cerebrovascular tone through endothelium-dependent mechanisms

Geary

Buchholz

Pearce

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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Pearce. Maturation depresses mouse cerebrovascular tone through endothelium-dependent mechanisms. Am J Physiol Regul Integr Comp Physiol 284: R734-R741, 2003. First published December 5, 2002 10.1152/ajpregu.00510.2002In light of previous observations that the range of arterial pressures over which cerebral blood flow is autoregulated differs dramatically in neonates and adults, the present experiments explored the hypothesis that pressure-induced intrinsic arterial tone is regulated differently in neonatal and adult cerebral arteries. In cannulated and pressurized endothelium-intact mouse cerebral arteries Ͻ150 m in diameter, active intrinsic tone was evident at intraluminal pressures as low as 10 mmHg in neonatal arteries, but only at pressures of 60 mmHg or greater in adult arteries. Administration of 10 M indomethacin produced no significant effect on tone at any pressure in either neonatal or adult arteries, but subsequent addition of 100 M nitroarginine methyl ester (NAME) significantly vasoconstricted both neonatal and adult arteries at all pressures. Conversely, administration of 100 M NAME alone significantly vasoconstricted adult arteries only, and subsequent addition of 10 M indomethacin produced a significant additional vasoconstriction in adult arteries only, indicating an important interaction between the nitric oxide synthase and cyclooxygenase pathways, at least in adult arteries. In the presence of both indomethacin and NAME, intrinsic tone was significantly greater in neonatal than adult arteries, but when the endothelium was removed, tone was similar in neonatal and adult arteries at all pressures. Together, these results suggest that pressure-induced myogenic tone is regulated similarly in neonatal and adult mouse cerebral arteries but that the contribution of endothelial vasoactive factors to intrinsic tone is highly age dependent. neonatal mouse; myogenic tone; pressure; cerebral artery NOT LONG AFTER the establishment of the nitrous oxide method for measurement of human cerebral blood flow in the late 1950s, it was widely recognized that cerebral perfusion was regulated independent of arterial pressure between pressures of Ϸ60 and Ϸ160 mmHg (22,25,37). This pattern of regulation, termed "cerebral autoregulation," has since been the focus of more than 2,600 studies that together indicate involvement of multiple different mechanisms in this response.Most important among these are the myogenic mechanisms that transduce changes in intraluminal hydraulic pressure and/or vascular wall stresses into changes in vascular smooth muscle contractility (10, 16). Release of vasoactive substances from the vascular endothelium in response to changes in shear stress also undoubtedly contributes to cerebrovascular autoregulatory adjustments (13). In addition, autonomic neurovascular mechanisms can potently influence the arterial pressure range over which cerebral autoregulation is effective (6).Owing to the central role of cerebral autoregulation for maintenance of cerebrovascular homeostasis, insults tha...

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Section: Intrinsic Tone In the Immature Cerebral Microcirculationmentioning

confidence: 67%

Maturation depresses mouse cerebrovascular tone through endothelium-dependent mechanisms

Geary

Buchholz

Pearce

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The procedure described in our previous study was used (21). In brief, recordings of AP were scanned by a computer program developed at our institution to identify the spontaneous sequences of three or more consecutive beats in which systolic AP (SAP) progressively increased or decreased by more than 1 mmHg per beat.…”

Section: Experiments 3: Conscious Animalsmentioning

confidence: 99%

Orexin neuron-mediated skeletal muscle vasodilation and shift of baroreflex during defense response in mice

Zhang

Sakurai²,

Fukuda³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Zhang, Wei, Takeshi Sakurai, Yasuichiro Fukuda, and Tomoyuki Kuwaki. Orexin neuron-mediated skeletal muscle vasodilation and shift of baroreflex during defense response in mice. Am J Physiol Regul Integr Comp Physiol 290: R1654 -R1663, 2006. First published January 12, 2006 doi:10.1152/ajpregu.00704.2005We have previously shown that some features of the defense response, such as increases in arterial blood pressure (AP), heart rate (HR), and ventilation were attenuated in prepro-orexin knockout (ORX-KO) mice. Here, we examined whether the same was true in orexin neuron-ablated [orexin/ataxin-3 transgenic mice (ORX/ATX-Tg)] mice. In addition, we examined other features of the defense response: skeletal muscular vasodilation and shift of baroreceptor reflex. In both anesthetized and conscious conditions, basal AP in ORX/ATX-Tg mice was significantly lower by ϳ20 mmHg than in wild-type (WT) controls, as was the case in ORX-KO mice. The difference in AP disappeared after treatment with an ␣-blocker but not with a ␤-blocker, indicating lower sympathetic vasoconstrictor outflow. Stimulation of the perifornical area (PFA) in urethane-anesthetized ORX/ATX-Tg mice elicited smaller and shorter-lasting increases in AP, HR, and ventilation, and skeletal muscle vasodilation than in WT controls. In addition, air jet stress-induced elevations of AP and HR were attenuated in conscious ORX/ATX-Tg mice. After pretreatment with a ␤-blocker, atenolol, stimulation of PFA suppressed phenylephrine (50 g/kg iv)-induced bradycardia (⌬HR ϭ Ϫ360 Ϯ 29 beats/ min without PFA stimulation vs. Ϫ166 Ϯ 26 during stimulation) in WT. This demonstrated the resetting of the baroreflex. In ORX/ ATX-Tg mice, however, no significant suppression was observed (Ϫ355 Ϯ 16 without stimulation vs. Ϫ300 Ϯ 30 during stimulation). The present study provided further support for our hypothesis that orexin-containing neurons in PFA play a role as a master switch to activate multiple efferent pathways of the defense response and also operate as a regulator of basal AP.hypothalamus; stress; blood pressure; respiration OREXIN A AND B, also known as hypocretin 1 and 2, respectively, are hypothalamic neuropeptides. They are cleaved from a common precursor molecule, prepro-orexin, undergoing proteolytic processing (33,41). Although the localization of orexin-containing cell bodies is restricted to the hypothalamus, the orexin-containing fibers and terminals are widely distributed in the hypothalamus, thalamus, cerebral cortex, circumventricular organs, brain stem, and spinal cord (13,28). This anatomic feature establishes the basis that orexin contributes to multiple physiological functions, including feeding behavior, energy homeostasis, sleep-wake cycle, and regulation of the autonomic and neuroendocrine systems (25,36,41).At present, there are two genetically engineered mice models of orexin deficiency to study possible roles of intrinsic orexin in physiological functions mentioned above. One is the prepro-orexin knockout (ORX-KO) mouse that was developed by a conv...

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“…Mean arterial blood pressure also increased in parallel from 86 to 110 mm Hg and remained constant thereafter. Baroreflex heart rate control matures at around 2 weeks after birth in the mouse (Ishii, 2001) Cardiac output fractions to the kidneys and intestines are markedly lower in newborn rabbits, when compared to adults (Boda et al, 1971).…”

Section: Comparative Speciesmentioning

confidence: 99%

Postnatal anatomical and functional development of the heart: A species comparison

Hew

Keller²

2003

Birth Defects Research Pt B

121

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Postnatal development of blood pressure and baroreflex in mice

Cited by 51 publications

References 31 publications

Maturation depresses mouse cerebrovascular tone through endothelium-dependent mechanisms

Maturation depresses mouse cerebrovascular tone through endothelium-dependent mechanisms

Orexin neuron-mediated skeletal muscle vasodilation and shift of baroreflex during defense response in mice

Postnatal anatomical and functional development of the heart: A species comparison

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