The role of carotid chemoreceptors in the effects of hypoxia on renal blood flow in the late gestation sheep fetus

Green, Lucy; Robson, SC; Hanson, Mark A.

doi:10.1113/expphysiol.1997.sp004007

Cited by 7 publications

(5 citation statements)

References 31 publications

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“…As reported previously mean arterial pressure (MAP) was elevated after 45 min L-NAME infusion during normoxia and MAP rose during hypoxia in vehicle and L-NAME groups (Green et al 1995…”

supporting

confidence: 75%

Placental & Perinatal Physiology

1996

The Journal of Physiology

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It is known that hypoxia in the mammalian fetus stimulates peripheral chemoreceptors producing cardiovascular changes, like bradycardia, systemic hypertension and redistribution of cardiac output. We were interested to study the hypoxia response in the chick embryo, because in this model it is easy to induce blood gas changes and it is independent of the maternal changes. For this the chorioallantoic artery blood flow (CABF), heart rate (HR) and the cardiac output changes in response to 5 min of anoxia (100%) were measured in chick embryos from stage 34 (day 9) (Hamburger & Hamilton, 1951) until stage 43 (day 17).The eggs were opened at the air cell and placed in a small plexiglass box with a continuous flow of a N2/02 mixture (5 1 min-'). In 100 chick embryos, ten at each stage, the CABF was measured by placing the chorioallantoic artery in the lumen of a transonic flow-probe. The heart rate was derived from the blood flow signal. The CABF and HR were measured during normoxia, anoxia and recovery. In another group of chick embryos (n = 30), a small chorioallantoic vein was catheterized for injections of different labels of fluorescent microspheres (15 ,um) during normoxia and at the Journal of Physiology (1996) 494.P Ca2" sensitivity of volume regulatory 86Rb (K+) efflux from human term placental cytotrophoblast cells in culture

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“…As reported previously mean arterial pressure (MAP) was elevated after 45 min L-NAME infusion during normoxia and MAP rose during hypoxia in vehicle and L-NAME groups (Green et al 1995…”

supporting

confidence: 75%

Placental & Perinatal Physiology

1996

The Journal of Physiology

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“…Second, in hypoxic fetal sheep there is a rapid drop in fetal heart rate and a rise in mean arterial blood pressure that redistributes blood flow to the heart and brain at the expense of the renal circulation. Hypoxia therefore reduces renal blood flow, resulting in renal hypoperfusion (Robillard et al, 1986 ; Green et al, 1997 ). Third, the unique fetal circulation system allows oxygen-rich blood from the aorta to mix with oxygen-poor blood before reaching renal circulation (Nakamura et al, 1987 ).…”

Section: Discussionmentioning

confidence: 99%

Chronic Hypobaric Hypoxia Modulates Primary Cilia Differently in Adult and Fetal Ovine Kidneys

et al. 2017

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Hypoxic environments at high altitude have significant effects on kidney injury. Following injury, renal primary cilia display length alterations. Primary cilia are mechanosensory organelles that regulate tubular architecture. The effect of hypoxia on cilia length is still controversial in cultured cells, and no corresponding in vivo study exists. Using fetal and adult sheep, we here study the effect of chronic hypobaric hypoxia on the renal injury, intracellular calcium signaling and the relationship between cilia length and cilia function. Our results show that although long-term hypoxia induces renal fibrosis in both fetal and adult kidneys, fetal kidneys are more susceptible to hypoxia-induced renal injury. Unlike hypoxic adult kidneys, hypoxic fetal kidneys are characterized by interstitial edema, tubular disparition and atrophy. We also noted that there is an increase in the cilia length as well as an increase in the cilia function in the hypoxic fetal proximal and distal collecting epithelia. Hypoxia, however, has no significant effect on primary cilia in the adult kidneys. Increased cilia length is also associated with greater flow-induced intracellular calcium signaling in renal epithelial cells from hypoxic fetuses. Our studies suggest that while hypoxia causes renal fibrosis in both adult and fetal kidneys, hypoxia-induced alteration in cilia length and function are specific to more severe renal injuries in fetal hypoxic kidneys.

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“…) and prevents the initial fall in renal (Green et al . ) and pulmonary arterial (Moore & Hanson, ) blood flow in response to acute hypoxia in the late gestation fetus. This highlights the greater contribution of the carotid chemoreceptors over the aortic chemoreceptors in mediating the redistribution of blood flow away from the periphery and towards the brain during periods of oxygen deprivation in the fetus.…”

Section: Causes and Consequences Of Fetal Hypoxiamentioning

confidence: 99%

The fetal brain sparing response to hypoxia: physiological mechanisms

Giussani

2016

The Journal of Physiology

277

342

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figure legend. The fetal brain sparing response to hypoxia. The fetal brain sparing response to acute hypoxia is triggered by a carotid chemoreflex which leads to bradycardia and an increase in peripheral vasoconstriction. The bradycardia is mediated by a dominant vagal influence on the fetal heart. The neurally triggered peripheral vasoconstriction is maintained by the release of constrictor hormones into the fetal circulation as well as a local vascular oxidant tone, determined by the interaction between NO and ROS, such as the superoxide anion (·O 2 − ). Abstract How the fetus withstands an environment of reduced oxygenation during life in the womb has been a vibrant area of research since this field was introduced by Joseph Barcroft, a century ago. Studies spanning five decades have since used the chronically instrumented fetal sheep preparation to investigate the fetal compensatory responses to hypoxia. This defence is contingent on the fetal cardiovascular system, which in late gestation adopts strategies to decrease oxygen consumption and redistribute the cardiac output away from peripheral vascular beds and towards essential circulations, such as those perfusing the brain. The introduction of simultaneous measurement of blood flow in the fetal carotid and femoral circulations by ultrasonic transducers has permitted investigation of the dynamics of the fetal brain sparing response for the first time. Now we know that major components of fetal brain sparing during acute hypoxia are triggered exclusively by a carotid chemoreflex and that they are modified by endocrine agents and the recently discovered vascular oxidant tone. The latter is determined by the interaction between nitric oxide and reactive oxygen species. The fetal brain sparing response matures as the fetus approaches term, in association with the prepartum increase in fetal plasma cortisol, and treatment of the preterm fetus with clinically relevant doses of synthetic steroids mimics this maturation. Despite intense interest into how the fetal brain sparing response may be affected by adverse intrauterine conditions, this area of research has been comparatively scant, but it is likely to take centre stage in the near future. Dino Giussani is Professor of Cardiovascular

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The role of carotid chemoreceptors in the effects of hypoxia on renal blood flow in the late gestation sheep fetus

Cited by 7 publications

References 31 publications

Placental & Perinatal Physiology

Placental & Perinatal Physiology

Chronic Hypobaric Hypoxia Modulates Primary Cilia Differently in Adult and Fetal Ovine Kidneys

The fetal brain sparing response to hypoxia: physiological mechanisms

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