Increased concentrations of plasma neuropeptide Y in patients with eclampsia and preeclampsia

Khatun, Selina; Kanayama, Naohiro; Belayet, Hossain Md; Bhuiyan, A.B.; Jahan, Sultana; Begum, Anowara; Kobayashi, Takao; Terao, Toshihiko

doi:10.1016/s0002-9378(00)70342-5

Cited by 32 publications

(25 citation statements)

References 19 publications

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“…NPY levels increase during pregnancy [30] and during the menopause [9]. These findings suggest that NPY is unrelated to serum progesterone concentrations, although correlations between progesterone and NPY levels were not evaluated.…”

Section: Discussionmentioning

confidence: 91%

Effect of medroxyprogesterone on arterial blood gases, leptin and neuropeptide Y in postmenopausal females

Saaresranta¹,

Irjala²,

Polo³

2002

Eur Respir J

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Natural progesterone, a potent respiratory stimulant, stimulates leptin production in premenopausal females. Leptin and its counterpart neuropeptide Y (NPY) have recently been linked with respiration. The effect of medroxyprogesterone acetate (MPA) on arterial blood gases, serum leptin and NPY was evaluated in this study.Fourteen postmenopausal females with respiratory impairment, due mostly to chronic obstructive pulmonary disease, were recruited for a randomised, double-blind, placebocontrolled crossover trial. Arterial blood gases, serum leptin and NPY concentrations were measured at baseline and after 14 days of treatment with placebo and MPA, separated by a 6-week washout period.Thirteen patients completed the trial. The mean ¡ SD carbon dioxide tension in arterial blood (Pa,CO 2 ) was 5.4 ¡ 0.6 kPa at baseline, and decreased by 0.8 ¡ 0.3 kPa during treatment with MPA. The oxygen tension in arterial blood (Pa,O 2 ) and pH did not change. At baseline, the mean base excess was 0.6¡1. Medroxyprogesterone acetate effectively decreased the carbon dioxide tension in postmenopausal females with chronic respiratory impairment. The results suggest that a decrease in the carbon dioxide tension of o0.9 kPa is necessary for a reduction in serum leptin concentration.

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Section: Discussionmentioning

confidence: 91%

Effect of medroxyprogesterone on arterial blood gases, leptin and neuropeptide Y in postmenopausal females

Saaresranta¹,

Irjala²,

Polo³

2002

Eur Respir J

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“…However, the intermediary mechanisms linking placental ischemia and the increased BP in PE are unclear. Recent studies in a pregnant rat model of RUPP, produced by occlusion of the lower abdominal aorta and the main uterine branches of the ovarian arteries, have suggested significant changes in renal functions as a possible cause of the increased BP (Alexander, 2001a; Sibai, 2005bHibbard, 2005Hibbard, 2005Silver, 1998Hibbard, 2005Moran, 2003Greenwood, 2001Sibai, 2005bKazerooni, 2003Xiang, 2005Khatun, 2000Brosnihan, 2004Brosnihan, 2004Minegishi, 1999Resnik, 2005Shaarawy, 2005Elsheikh, 2001Hayashi, 2005 AngII, angiotensin II; Ang-(1-7), angiotensin (1-7); ANP, atrial natriuretic peptide; BNP, brain natriuretic peptide; BP, blood pressure; NPY, neuropeptide-Y; TNF-α, tumor necrosis factor-α; VEGF, vascular endothelial growth factor. .…”

Section: Uteroplacental Circulation During Normal Pregnancy and Pementioning

confidence: 99%

“…Plasma NPY is further increased in PE-eclampsia (Khatun, 2000). NPY is found in noradrenergic neurons that act on arteries, including the uterine artery, and thereby functions as an important regulator of uterine blood flow.…”

Section: Vasoactive Neurohumoral Factors In Normal Pregnancy and Pementioning

confidence: 99%

Neurovascular Mechanisms of Hypertension in Pregnancy

Stennett

Khalil²

2006

CNR

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Normal pregnancy is associated with significant changes in the neuronal and vascular control mechanisms of blood pressure (BP). Preeclampsia (PE) is a major complication of pregnancy characterized by proteinuria, and increased vascular resistance and BP. If untreated, PE leads to eclampsia with serious seizures and severe hypertension. However, the neurovascular mechanisms of hypertension in pregnancy and PE are unclear. Studies in animal models of hypertension in pregnancy suggest that inadequate cytotrophoblast invasion of uterine spiral arteries causes reduction in uteroplacental perfusion pressure leading to placental ischemia/hypoxia. Placental ischemia may promote the release of biologically active factors such as cytokines and reactive oxygen species. These circulating factors may increase the vascular permeability, cross the blood-brain barrier, and affect the sympathetic tone and the neuronal control mechanisms of BP. Placental factors could also cause endothelial cell dysfunction and inhibit nitric oxide (NO)-cyclic guanosine monophosphate (cGMP), prostacyclin (PGI(2))-cyclic adenosine monophosphate (cAMP), and hyperpolarizing factor vascular relaxation pathways. Additionally, placental factors may induce endothelium-derived contracting factors such as endothelin, thromboxane and angiotensin II, which stimulate Ca(2+)-dependent vascular smooth muscle (VSM) contraction or increase protein kinase C activity and enhance myofilament sensitivity to intracellular free calcium concentration ([Ca(2+)](i)). The increased sympathetic tone combined with systemic decrease in endothelium-dependent vascular relaxation and enhanced VSM contraction may contribute to the increased vascular resistance and BP associated with PE. The hypertensive state in severe PE may weaken the blood-brain barrier and precipitate convulsions and cerebral hemorrhage. Careful monitoring of maternal neuronal, endothelial, and VSM function during pregnancy should circumvent the life-threatening neurovascular complications of PE-eclampsia.

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“…Preliminary data on a small number of subjects indicated increased plasma concentrations of NPY in women with eclampsia and PE, as compared to normotensive pregnant women (Khatun et al , 2000). Moreover, systemic NPY concentrations in PE women have been shown to correlate with mean arterial pressure (MAP) before delivery (Kokot et al , 1999).…”

Section: Introductionmentioning

confidence: 96%

Elevated levels of neuropeptide Y in preeclampsia: A pilot study implicating a role for stress in pathogenesis of the disease

et al. 2016

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Objective To determine if preeclampsia (PE) is associated with dysregulation of the neuropeptide Y (NPY) system. Methods The study enrolled 114 subjects either with normal pregnancy (NP) or with PE. Systolic blood pressure (SBP) was collected from patients using a standard sphygmomanometer. The PE patients were divided into two groups based on the gestational age (GA) at delivery – placental PE (PLPE, GA <34 weeks) or maternal PE (MTPE, GA ≥ 34 weeks). NPY was measured in platelet rich plasma (PRP), platelet poor plasma (PPP) and in the serum of NP and PE patients utilizing radioimmunoassay. Serum levels of soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF) were measured in NP and PE subjects by ELISA. Results SBP was higher in PE compared to NP. Circulating NPY in serum and PRP, as well as NPY content per 100,000 platelets, but not its concentrations in PPP, were elevated in PE, as compared to NP. The highest NPY concentrations were observed in sera and PRP of patients with MTPE. PE patients had also elevated levels of sFlt-1, as compared to NP, although no difference between PLPE and MTPL groups were observed. There was no increase in P1GF in PE patients. Conclusion Systemic NPY is elevated in PE patients, as compared to NP. This increase is observed in blood fractions containing platelets, suggesting accumulation of the peptide in these cells. NPY concentrations are particularly high in patients with MTPE, underlying differences in etiology between PLPE and MTPE. Our study implicates NPY as a potential target in antihypertensive therapies for PE patients.

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Increased concentrations of plasma neuropeptide Y in patients with eclampsia and preeclampsia

Cited by 32 publications

References 19 publications

Effect of medroxyprogesterone on arterial blood gases, leptin and neuropeptide Y in postmenopausal females

Effect of medroxyprogesterone on arterial blood gases, leptin and neuropeptide Y in postmenopausal females

Neurovascular Mechanisms of Hypertension in Pregnancy

Elevated levels of neuropeptide Y in preeclampsia: A pilot study implicating a role for stress in pathogenesis of the disease

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