Effect of angiotensin II on uterine and systemic vasculature in pregnant sheep.

Naden, Raymond P.; Rosenfeld, Charles R.

doi:10.1172/jci110277

Cited by 102 publications

(81 citation statements)

References 17 publications

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“…Inasmuch as there were significant agedependent changes in MAP and HR, analysis of the absolute values might miss important changes in the responses to ANG II. Therefore, the data were further analyzed using the relative change from baseline (%⌬), which takes into account the changes in baseline values and permits a comparison across ages and between hemodynamic parameters (32). At each study period, systemic i.v.…”

Section: Resultsmentioning

confidence: 99%

“…In what may be an analogous situation, the adult uterine vascular bed predominantly expresses AT 2 in the VSM (21,23). It also demonstrates dose-dependent increases in vascular resistance during systemic ANG II infusions that are less than systemic responses (21,32). Furthermore, as seen in the neonatal hindlimb, it too is unresponsive to intra-arterial ANG II infusions until there is evidence that the peptide has spilled over into the systemic circulation (56).…”

Section: Peripheral Effects Of Ang II After Birthmentioning

confidence: 99%

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Differential Responses to Systemic and Local Angiotensin II Infusions in Conscious Postnatal Sheep

Velaphi

2002

Pediatric Research

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vascular smooth muscle until 2 wk postnatal when they are replaced by AT 1 . Thus, the mechanisms whereby ANG II increases MAP after birth are unclear. We examined the effects of ANG II on femoral vascular resistance (FmVR) and blood flow (FmBF) in serial studies of newborn sheep (n ϭ 7) at 7-14 d, 15-21 d, and 22-35 d. Animals had femoral catheters implanted for systemic ANG II infusions and cardiovascular monitoring, and a flow probe was implanted on the contralateral artery proximal to the superficial saphenous artery, which contained a catheter for intra-arterial ANG II infusions. Studies were performed using a range of systemic and intra-arterial ANG II doses. Systemic ANG II increased MAP dose-dependently at all ages (p Ͻ 0.001); however, responses were not age dependent. FmBF rose dose dependently at 7-14 d (p Ͻ 0.001) and was unchanged at older ages. The transition from fetal to newborn life is associated with numerous hemodynamic changes, including alterations in HR, blood pressure, PVR, and the distribution of cardiac output (1-4). The autonomic nervous system and the reninangiotensin system (RAS) are considered important modulators of the cardiovascular changes in the perinatal period. This is supported by evidence of increased circulating levels of catecholamines and ANG II during and after parturition (1, 4 -6). ANG II is the predominant vasoactive agent associated with the RAS and is believed to be an important regulator of blood pressure in fetal, neonatal, and adult sheep (7-9). The effects of ANG II on blood pressure may reflect its direct action on VSM through increases in PVR or on cardiac output by increasing venous return or HR (4, 10 -13). Indirect effects on VSM also may occur through activation of central autonomic nervous system activity or the release of other vasoactive mediators (11, 14 -16).ANG II mediates its actions by binding to specific AT. At least two AT subtypes have been identified, AT 1 and AT 2 , and their expression is developmentally regulated (17)(18)(19). In the adult, the AT 1 is the primary subtype expressed in most tissues, including VSM, and accounts for most biologic actions of ANG II (20,21). However, AT 2 are found in selective adult tissues, e.g. adrenal, myometrium, and uterine arteries from pregnant and nonpregnant women and sheep (9,(21)(22)(23)

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Section: Resultsmentioning

confidence: 99%

Section: Peripheral Effects Of Ang II After Birthmentioning

confidence: 99%

Differential Responses to Systemic and Local Angiotensin II Infusions in Conscious Postnatal Sheep

Velaphi

2002

Pediatric Research

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“…Experiments in primates have shown that the infusion of low-dose Ang II may actually increase uterine blood flow. 37 Rosenfeld et al 38 have shown that the low-dose infusion of Ang II has minimum effect on the uterine blood flow but that the pharmacological-dose (10 g/min) infusion decreases uterine blood flow in gravid ewes. For prorenin to participate in the regulation of blood flow, it must be available locally in a biologically active form.…”

Section: Discussionmentioning

confidence: 99%

Definitive Molecular Evidence of Renin-Angiotensin System in Human Uterine Decidual Cells

Ansari

et al. 2000

Hypertension

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Abstract-The tissue renin-angiotensin system (RAS) has been suggested to be present in human gestational tissues, but uncertainty exists about the authenticity of this RAS, and the cellular origin of this RAS has not been defined. In the present study, we confirmed the presence of authentic renin and angiotensinogen in the prolactin-producing decidual tissue by sequencing the cDNAs generated through reverse transcription-polymerase chain reaction, confirming cDNA product sizes, and by performing Northern blot analysis of the RNA. Our comparative data demonstrate that prolactin has the highest expression in the decidual tissue, followed by renin, and that angiotensinogen has the least expression. We demonstrated with fluorescent in situ hybridization that prolactin-expressing endocrine decidual cells are the same cells that express both renin and angiotensinogen.

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“…1A). Since there were age-dependent changes in basal hemodynamic parameters, the data were analyzed using the relative change from baseline (%⌬), which permits a comparison across ages and between hemodynamic variables (21,29). Although there were age-dependent differences in basal MAP and HR, there were no differences in baseline measurements obtained immediately before each dose of PE (p Ͼ 0.05, ANOVA) at each age.…”

Section: Resultsmentioning

confidence: 99%

“…To compare responses by hemodynamic parameters with different units, e.g. MAP, FmBF, and FmVR, and changes across postnatal age, data are presented as the relative or percentage change (%⌬) from baseline (21,29). One-way ANOVA for repeated measures was used to analyze the changes in hemodynamic parameters across postnatal ages and across doses within each age group.…”

Section: Methodsmentioning

confidence: 99%

Effects of Systemic and Local Phenylephrine and Arginine Vasopressin Infusions in Conscious Postnatal Sheep

et al. 2005

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Mean arterial pressure (MAP) increases after birth, however, the mechanisms remain unclear. Systemic angiotensin II (ANG II) infusions increase MAP in newborn sheep, but the direct effects of ANG II on peripheral vascular resistance (PVR) are minimal. Thus, its systemic pressor effects may reflect release of other pressor agents, e.g. ␣-agonists and/or AVP, suggesting they contribute to postnatal regulation of MAP and PVR. To address this, we performed studies in conscious sheep at 7-14, 15-21, and 22-35 d postnatal, infusing phenylephrine (PE) or AVP systemically or intra-arterially into the hindlimb while measuring MAP, heart rate (HR), and femoral blood flow (FmBF The transition at birth is accompanied by increases in MAP that occur in at least two phases. There is an initial rapid rise soon after birth, likely due to the removal of the low-resistance placental vascular bed and closure of several fetal vascular shunts. Simultaneous with this is an elevation in circulating levels of catecholamines, ANG II, and AVP (1-4). The second phase is characterized by a gradual rise in MAP that occurs over several days and appears to be developmentally regulated (1,5-9). The mechanisms regulating these changes in MAP are poorly understood and could include the postnatal clearance of placentally derived vasodilators, e.g. prostacyclin, nitric oxide, and estrogen (10,11), increases in central sympathetic outflow (12), age-dependent changes in VSM receptor expression or function (13), maturational and/or function changes in VSM (14), or increases in cardiac output (15). Although cardiac output increases in absolute terms, values (measured in milliliter per minute per kilogram) are reported to fall in the first month after birth (15).Alternatively, changes in either the availability or vascular responsiveness to circulating vasoactive substances may contribute to the regulation of postnatal MAP. For example, ANG II, catecholamines, and AVP modulate MAP in the fetus and adult (1,16 -19) and might also contribute to postnatal regulation of MAP. This could occur through an increase in their direct effects on PVR, which might be due to decreases in the synthesis of local vasodilators (10,11) or increases in VSM sensitivity.Indeed, the responses to norepinephrine and AVP in the isolated ear artery of the developing sheep increase with increasing postnatal age (20

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Effect of angiotensin II on uterine and systemic vasculature in pregnant sheep.

Abstract: A B S T R A C

Cited by 102 publications

References 17 publications

Differential Responses to Systemic and Local Angiotensin II Infusions in Conscious Postnatal Sheep

Differential Responses to Systemic and Local Angiotensin II Infusions in Conscious Postnatal Sheep

Definitive Molecular Evidence of Renin-Angiotensin System in Human Uterine Decidual Cells

Effects of Systemic and Local Phenylephrine and Arginine Vasopressin Infusions in Conscious Postnatal Sheep

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