Effects of Water Deprivation and Morphine Administration on Atrial Natriuretic Peptide mRNA Levels in Rat Auricles

Fukui, Kiyoshi; Itoh, Hiroshi; Takahashi, Toshiaki; Abe, Youichi

doi:10.1254/jjp.57.45

Cited by 4 publications

(4 citation statements)

References 24 publications

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“…The mechanisms by which morphine increases ANF and BNP have not yet been elucidated, but it appears that the regulation of ANF is mediated, at least in part, by opioid receptors, without a concomitant rise in blood pressure (Gutkowska, Strick, Pan & McCann, 1993). Therefore, based on the above reports, and on studies showing that acute morphine treatment enhances ANF synthesis in the atria of adult rats (Fukui, Iwao, Nakamura, Tamaki & Abe, 1991) we hypothesized that maternal exposure to morphine may directly alter the cardiac natriuretic peptides, ANF and BNP, during ontogeny. Consequently, studies were performed to characterize the maturation-induced changes in cardiac natriuretic peptides in rat offspring from birth to 3 weeks of age, and to assess the influences of prenatal treatment of the mother with morphine upon the changes of cardiac ANF and BNP at the protein and mRNA levels.…”

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confidence: 99%

Altered regulation of natriuretic peptides in the rat heart by prenatal exposure to morphine

Ernest

Jankowski

Mukaddam‐Daher

et al. 1998

The Journal of Physiology

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Both endogenous and exogenous opioids modulate blood pressure and cardiac function by stimulating cardiac synthesis of atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP). Since morphine crosses the placental barrier, it could alter the ANF‐BNP system in the fetal heart. The aim of this study was to characterize cardiac natriuretic peptides in normal rat development and in rats prenatally exposed to morphine. Female rats received either saline or morphine (10 or 20 mg kg−1 day−1) via osmotic minipumps during gestation. The effects of this treatment were investigated in offspring at 1, 4 and 22 days of age. During maturation, atrial ANF and ANF mRNA increased by 3‐fold from birth to 3 weeks of age, but BNP and BNP mRNA tended to decrease. In the ventricles, both ANF and BNP content decreased at 3 weeks after birth, from 25.11 ± 3.6 to 0.81 ± 0.1 ng (P < 0.001), and from 3.36 ± 0.33 to 0.19 ± 0.01 ng (P < 0.001), respectively. However, whereas ventricular ANF mRNA decreased, BNP mRNA levels did not change during maturation. Prenatal exposure to morphine significantly increased ANF content in the left atria of 22‐day‐old rats, and in the right atria of 1‐, 4‐ and 22‐day‐old rats compared with age‐matched saline controls. In contrast, prenatal exposure to 20 mg kg−1 day−1 morphine significantly inhibited BNP and BNP mRNA in the ventricles at all ages studied. These observations suggest that alterations in mRNA synthesis or stability and/or post‐translational processing of ANF and BNP occur in the heart during maturation, and that prenatal exposure to morphine alters cardiac production, and possibly release, of both peptides.

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confidence: 99%

Altered regulation of natriuretic peptides in the rat heart by prenatal exposure to morphine

Ernest

Jankowski

Mukaddam‐Daher

et al. 1998

The Journal of Physiology

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“…Cardiac ANP is largely restricted to secretory granules, secretion leading to membrane-receptor and cGMP-dependent protection. It is possible SLP enhances both ANP expression and subsequent secretion, since opioidergic stimuli (including morphine and μ and κ-OR agonists) increase cardiac ANP secretion [26]–[28], which can be temporally dissociated from Nppa expression [26]. Potential protection via SLP-dependent ANP/BNP expression is consistent with impaired I-R tolerance in mice lacking the natriuretic peptide receptor guanylyl cyclase-A [33].…”

Section: Discussionmentioning

confidence: 92%

“…There are no prior reports of OR-dependent control of cardiac ANP/BNP expression, though the secretion of ANP may be enhanced by ORs [26]–[28]. Surprisingly, ANP/BNP involvement in pre- or post-conditioning has not been tested, despite increased secretion with brief ischemia and reduced I-R injury with exogenously applied peptide [29]–[31].…”

Section: Discussionmentioning

confidence: 99%

Unique Transcriptional Profile of Sustained Ligand-Activated Preconditioning in Pre- and Post-Ischemic Myocardium

et al. 2013

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BackgroundOpioidergic SLP (sustained ligand-activated preconditioning) induced by 3–5 days of opioid receptor (OR) agonism induces persistent protection against ischemia-reperfusion (I-R) injury in young and aged hearts, and is mechanistically distinct from conventional preconditioning responses. We thus applied unbiased gene-array interrogation to identify molecular effects of SLP in pre- and post-ischemic myocardium.Methodology/Principal FindingsMale C57Bl/6 mice were implanted with 75 mg morphine or placebo pellets for 5 days. Resultant SLP did not modify cardiac function, and markedly reduced dysfunction and injury in perfused hearts subjected to 25 min ischemia/45 min reperfusion. Microarray analysis identified 14 up- and 86 down-regulated genes in normoxic hearts from SLP mice (≥1.3-fold change, FDR≤5%). Induced genes encoded sarcomeric/contractile proteins (Myh7, Mybpc3,Myom2,Des), natriuretic peptides (Nppa,Nppb) and stress-signaling elements (Csda,Ptgds). Highly repressed genes primarily encoded chemokines (Ccl2,Ccl4,Ccl7,Ccl9,Ccl13,Ccl3l3,Cxcl3), cytokines (Il1b,Il6,Tnf) and other proteins involved in inflammation/immunity (C3,Cd74,Cd83, Cd86,Hla-dbq1,Hla-drb1,Saa1,Selp,Serpina3), together with endoplasmic stress proteins (known: Dnajb1,Herpud1,Socs3; putative: Il6, Gadd45g,Rcan1) and transcriptional controllers (Egr2,Egr3, Fos,Hmox1,Nfkbid). Biological themes modified thus related to inflammation/immunity, together with cellular/cardiovascular movement and development. SLP also modified the transcriptional response to I-R (46 genes uniquely altered post-ischemia), which may influence later infarction/remodeling. This included up-regulated determinants of cellular resistance to oxidant (Mgst3,Gstm1,Gstm2) and other forms of stress (Xirp1,Ankrd1,Clu), and repression of stress-response genes (Hspa1a,Hspd1,Hsp90aa,Hsph1,Serpinh1) and Txnip.ConclusionsProtection via SLP is associated with transcriptional repression of inflammation/immunity, up-regulation of sarcomeric elements and natriuretic peptides, and modulation of cell stress, growth and development, while conventional protective molecules are unaltered.

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“…On the contrary, total sodium restriction for 3 weeks augmented granularity in the left atrium without changes in the right atrium. Furthermore, morphine treatment increased only right atrial ANP mRNA 4 hr after administration (21,22) whereas left ventricular ANP concentration rose with dexamethasone treatment by day 2 (23). These observations indicate that changes in the ANP cardiac system are induced differentially because of functional differences in the heart chambers.…”

Section: What Is the Mechanism By Which Crh Induces These Profound Renalmentioning

confidence: 99%

Corticotropin-releasing hormone causes antidiuresis and antinatriuresis by stimulating vasopressin and inhibiting atrial natriuretic peptide release in male rats

Gutkowska¹,

Jankowski²,

Mukaddam‐Daher³

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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In both normally hydrated and volume-expanded rats, there was a biphasic effect of corticotropin-releasing hormone (CRH) (1-10 g, i.v.) on renal function. Within the first hour, CRH caused antidiuresis, antinatriuresis, and antikaliuresis together with reduction in urinary cGMP output that, in the fourth hour, were replaced by diuresis, natriuresis, and kaliuresis accompanied by increased cGMP output. Plasma arginine vasopressin (AVP) concentrations increased significantly within 5 min, reached a peak at 15 min, and declined by 30 min to still-elevated values maintained for 180 min. Changes in plasma atrial natriuretic peptide (ANP) were the mirror image of those of AVP. Plasma ANP levels were correlated with decreased ANP in the left ventricle at 30 min and increased ANP mRNA in the right atrium at 180 min. All urinary changes were reversed by a potent AVP type 2 receptor (V 2R) antagonist. Control 0.9% NaCl injections evoked an immediate increase in blood pressure and heart rate measured by telemetry within 3-5 min. This elevation of blood pressure was markedly inhibited by CRH (5 g). We hypothesize that the effects are mediated by rapid, direct vasodilation induced by CRH that decreases baroreceptor input to the brain stem, leading to a rapid release of AVP that induces the antidiuresis by direct action on the V 2Rs in the kidney. Simultaneously, acting on V 2Rs in the heart, AVP inhibits ANP release and synthesis, resulting in a decrease in renal cGMP output that is responsible for the antinatriuretic and antikaliuretic effects.

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Effects of Water Deprivation and Morphine Administration on Atrial Natriuretic Peptide mRNA Levels in Rat Auricles

Cited by 4 publications

References 24 publications

Altered regulation of natriuretic peptides in the rat heart by prenatal exposure to morphine

Altered regulation of natriuretic peptides in the rat heart by prenatal exposure to morphine

Unique Transcriptional Profile of Sustained Ligand-Activated Preconditioning in Pre- and Post-Ischemic Myocardium

Corticotropin-releasing hormone causes antidiuresis and antinatriuresis by stimulating vasopressin and inhibiting atrial natriuretic peptide release in male rats

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