Exposure to stimulatory CpG oligonucleotides during gestation induces maternal hypertension and excess vasoconstriction in pregnant rats

2016 ◽  
Vol 310 (8) ◽  
pp. H1015-H1025 ◽  
Author(s):  
Styliani Goulopoulou ◽  
Camilla F. Wenceslau ◽  
Cameron G. McCarthy ◽  
Takayuki Matsumoto ◽  
R. Clinton Webb
Keyword(s):  
Blood Pressure ◽  
Dna Sequences ◽  
Female Rats ◽  
Cpg Odn ◽  
Resistance Arteries ◽  
Pregnant Rats ◽  
Cpg Dna ◽  
Contractile Responses ◽  
Cpg Oligonucleotides ◽  
Maternal Hypertension

Bacterial infections increase risk for pregnancy complications, such as preeclampsia and preterm birth. Unmethylated CpG DNA sequences are present in bacterial DNA and have immunostimulatory effects. Maternal exposure to CpG DNA induces fetal demise and craniofacial malformations; however, the effects of CpG DNA on maternal cardiovascular health have not been examined. We tested the hypothesis that exposure to synthetic CpG oligonucleotides (ODNs) during gestation would increase blood pressure and cause vascular dysfunction in pregnant rats. Pregnant and nonpregnant female rats were treated with CpG ODN (ODN 2395) or saline (Veh) starting on gestational day 14 or corresponding day for the nonpregnant groups. Exposure to CpG ODN increased systolic blood pressure in pregnant (Veh: 121 ± 2 mmHg vs. ODN 2395: 134 ± 2 mmHg, P < 0.05) but not in nonpregnant rats (Veh: 111 ± 2 mmHg vs. ODN 2395: 108 ± 5 mmHg, P > 0.05). Mesenteric resistance arteries from pregnant CpG ODN-treated rats had increased contractile responses to U46619 [thromboxane A2 (TxA2) mimetic] compared with arteries from vehicle-treated rats [Emax (%KCl), Veh: 87 ± 4 vs. ODN 2395: 104 ± 4, P < 0.05]. Nitric oxide synthase (NOS) inhibition increased contractile responses to U46619, and CpG ODN treatment abolished this effect in arteries from pregnant ODN 2395-treated rats. CpG ODN potentiated the involvement of cyclooxygenase (COX) to U46619-induced contractions. In conclusion, exposure to CpG ODN during gestation induces maternal hypertension, augments resistance artery contraction, increases the involvement of COX-dependent mechanisms and reduces the contribution of NOS-dependent mechanisms to TxA2-induced contractions in mesenteric resistance arteries.

Abstract 030: Low-dose Aspirin During Pregnancy Does Not Prevent Augmentation of Arterial Contractions to Thromboxane A 2 in a Rat Model of Pregnancy-Induced Hypertension

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Oluwatobiloba Osikoya ◽  
Paresh A Jaini ◽  
An Nguyen ◽  
Melissa Valdes ◽  
Styliani Goulopoulou
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Low Dose ◽  
Daily Intake ◽  
Treated Group ◽  
Pregnant Rats ◽  
Contractile Responses ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Maternal Hypertension

Background: Daily intake of low dose aspirin after 12 weeks of gestation is currently recommended as a preventative intervention in pregnancies at high risk of developing preeclampsia. We previously showed that treating pregnant rats with a synthetic ligand of Toll-like receptor 9 (TLR9; ODN2395) activated the innate immune system causing preeclampsia-like characteristics such as maternal hypertension, vascular oxidative stress, and augmented vascular responses to thromboxane A 2 (TxA 2 ). Hypothesis: Low-dose aspirin treatment would ameliorate ODN2395-induced augmented responses to TxA 2 in maternal arteries. Methods: Pregnant rats were treated with ODN2395 (300 μg) or vehicle on gestational day (GD) 14, 16, 18. Daily low-dose aspirin treatment (1.5 mg/kgBW) started on GD10 and continued throughout gestation. Systolic blood pressure was measured using the tail-cuff method on GD19. On GD21, uterine (UTA) and mesenteric resistance artery (MES) responses to a TxA 2 mimetic (U46619, 10 -9 -10 -6 M) was measured with a wire myograph. Results: Uterine arteries from the ODN2395+Aspirin-treated group had greater contractile responses to U46619 compared to all other groups [Emax, %KCl: Control (n=6): 109.2±8.8; ODN2395 (n=5): 124.4±20.2; Aspirin (n=5): 76.08±11.2; ODN2395+Aspirin (n=5): 134.7±4.5, p<0.05]. Aspirin alone reduced MES responses to U46619 compared to control and MES from ODN2395 and ODN2395+Aspirin groups had greater contractile responses to U46619 compared to Aspirin alone [Emax, %KCl: Control (n=8): 109.8±5.2; ODN2395 (n=6): 111.1±4.3; Aspirin (n=7): 89.4±3.6; ODN2395+Aspirin (n=8): 121.7±6.3, p<0.05]. Rats treated with ODN2395 and ODN+Aspirin had greater systolic blood pressure compared to control rats [control (n=8): 97.3±3.2 mmHg, ODN2395 (n=6): 121.3±4.3 mmHg, Aspirin (n=8): 100.3±2.9 mmHg, ODN2395+Aspirin (n=7): 127.5 ±6.7 mmHg, p<0.05]. Conclusion: Exposure to a TLR9 agonist during pregnancy resulted in augmented contractile responses to a TxA 2 mimetic in maternal arteries when rats were in a regime of low-dose aspirin. This was shown in arteries from both reproductive and non-reproductive vascular beds.

Regulation of renal CYP4A expression and 20-HETE synthesis by nitric oxide in pregnant rats

2003 ◽  
Vol 285 (2) ◽  
pp. F295-F302 ◽  
Author(s):  
Mong-Heng Wang ◽  
Jishi Wang ◽  
Hsin-Hsin Chang ◽  
Barbara A. Zand ◽  
Miao Jiang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Rat Kidney ◽  
Late Pregnancy ◽  
Inhibitory Effect ◽  
Female Rats ◽  
Male Rats ◽  
Pregnant Rats ◽  
Renal Vasoconstriction ◽  
Dependent Inhibition

20-Hydroxyeicosatetraenoic acid (20-HETE), which promotes renal vasoconstriction, is formed in the rat kidney primarily by cytochrome P-450 (CYP) 4A isoforms (4A1, 4A2, 4A3, 4A8). Nitric oxide (NO) has been shown to bind to the heme moiety of the CYP4A2 protein and to inhibit 20-HETE synthesis in renal arterioles of male rats. However, it is not known whether NO interacts with and affects the activity of CYP4A1 and CYP4A3, the major renal CYP4A isoforms in female rats. Incubation of recombinant CYP4A1 and 4A3 proteins with sodium nitroprusside (SNP) shifted the absorbance at 440 nm, indicating the formation of a ferric-nitrosyl-CYP4A complex. The absorbance for CYP4A3 was about twofold higher than that of CYP4A1. Incubation of SNP or peroxynitrite (PN; 0.01–1 mM) with CYP4A recombinant membranes caused a concentration-dependent inhibition of 20-HETE synthesis, with both chemicals having a greater inhibitory effect on CYP4A3-catalyzed activity. Moreover, incubation of CYP4A1 and 4A3 proteins with PN (1 mM) resulted in nitration of tyrosine residues in both proteins. In addition, PN and SNP inhibited 20-HETE synthesis in renal microvessels from female rats by 65 and 59%, respectively. We previously showed that microvessel CYP4A1/CYP4A3 expression and 20-HETE synthesis are decreased in late pregnancy. Therefore, we investigated whether such a decrease is dependent on NO, the synthesis of which has been shown to increase in late pregnancy. Administration of NG-nitro-l-arginine methyl ester (l-NAME) to pregnant rats for 6 days ( days 15- 20 of pregnancy) caused a significant increase in systolic blood pressure, which was prevented by concurrent treatment with the CYP4A inhibitor 1-aminobenzotriazole (ABT). Urinary NO2/NO3 excretion decreased by 40 and 52% in l-NAME- and l-NAME + ABT-treated groups, respectively. Interestingly, renal microvessel 20-HETE synthesis showed a marked increase following l-NAME treatment, and this increase was diminished with coadministration of ABT. These results demonstrate that NO interacts with CYP4A proteins in a distinct manner and it interferes with renal microvessel 20-HETE synthesis, which may play an important role in the regulation of blood pressure and renal function during pregnancy.

Abstract P215: Hyperglycemic Rats Have Increased Fetal Demise But Not Hypertension During Pregnancy

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Frank T Spradley ◽  
Barbara Wilson ◽  
Christopher Anderson
Keyword(s):  
Blood Pressure ◽  
Epidemiological Studies ◽  
Adverse Outcomes ◽  
Nitric Oxide Donor ◽  
Gk Rat ◽  
Pregnant Rats ◽  
Fetal Demise ◽  
Glucose Levels ◽  
Maternal Hypertension ◽  
Placental Ischemia

While obesity is a major cause for pregnancy complications including preeclampsia and fetal demise, it is not exactly clear the precise obesity-related metabolic factors that promote these adverse outcomes. Epidemiological studies have pointed toward hyperglycemia as one such factor. Therefore, we tested the hypothesis that hyperglycemic rats have hypertension and fetal demise during pregnancy. For this purpose, we utilized the type II diabetic model, the Goto-Kakizaki (GK) rat (N=16), compared to normoglycemic Wistar Hannover (WH) rats (N=9), which were maintained on Envigo 8640 standard chow. The GK rat allows for assessment of hyperglycemia on pregnancy without confounding obesity. Maternal fasting glucose levels were significantly greater (P<0.05) in GK (97±8 mg/dL) vs. WH (72±9 mg/dL) rats by gestational day 19. Body weight was lower (P<0.05) in GK (248±4 g) versus WH (289±4 g) pregnant rats, whereas perirenal fat (1.56±0.07 g vs. 1.38±0.07 g, P>0.05) and circulating levels of the adipokine, leptin (1.6±0.2 ng/mL vs. 2.2±0.3 ng/mL, P>0.05) were similar between GK and WH pregnant groups, respectively. Endothelial-dependent relaxation to acetylcholine (sensitivity as logEC50: -5.2±0.3 M vs -5.2±0.4 M) and endothelial-independent relaxation to the nitric oxide-donor sodium nitroprusside (logEC50: -7.2±0.2 M vs. -7.5±0.1 M) were similar (P>0.05) in uterine arteries isolated from GK and WH rats, respectively. It was then determined if reduced uterine perfusion pressure (RUPP)-induced placental ischemia, a significant contributor to the development of preeclampsia, promoted greater maternal hypertension in GK rats. RUPP was conducted on gestational day 14 and blood pressure assessed on day 19. RUPP produced hypertension to a similar extent (P>0.05) in GK (116±5 mmHg vs. Sham 102±5 mmHg) and WH (124±4 mmHg vs. Sham 100±2 mmHg) groups. Blood pressure was similar under Sham conditions. Fetal demise was already greater in Sham GK vs. Sham WH pregnant rats (% absorptions: 13±2 vs. 2±2, P<0.05) but increased similarly following RUPP in GK (61±11 %) and WH (65±5 %) pregnant rats. In conclusion, these data suggest that high glucose levels promote fetal demise during pregnancy but do not exaggerate the outcomes of placental ischemia-induced hypertension.

scholarly journals Renal epoxyeicosatrienoic acid synthesis during pregnancy

2005 ◽  
Vol 288 (1) ◽  
pp. F221-F226 ◽  
Author(s):  
Yiqiang Zhou ◽  
Hsin-Hsin Chang ◽  
Juan Du ◽  
Cong-Yi Wang ◽  
Zheng Dong ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Immunohistochemical Analysis ◽  
Acid Synthesis ◽  
The Body ◽  
Female Rats ◽  
Epoxyeicosatrienoic Acid ◽  
Pregnant Rats ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Renal Tubular

Epoxyeicosatrienoic acids (EETs), which belong to cytochrome P-450 (CYP)-derived eicosanoids, have been implicated to vasodilate renal arterioles, inhibit sodium transport in the nephron, and regulate blood pressure in several animal models. Because pregnancy is associated with changes of blood pressure, the aim of this study was to examine whether renal EET synthesis is altered and whether EETs are involved in blood pressure regulation during pregnancy in rats. Renal microsomal epoxygenase activity increased by 47, 97, and 63% on days 6, 12, and 19 of gestation, respectively. The elevation of epoxygenase activity during pregnancy was associated with an increase in CYP2C11, CYP2C23, and CYP2J2 protein expression on days 6, 12, and 19 of gestation. Moreover, immunohistochemical analysis showed that renal tubular CYP2C11, CYP2C23, and CYP2J2 expression was significantly increased in pregnant rats on days 6, 12, and 19 of gestation. Administration of 6-(2-propargyloxyphenyl)hexanoic acid (PPOH), a selective epoxygenase inhibitor, caused a dose-dependent inhibition of microsomal expoxygenase activity without a significant effect on ω-hydroxylase activity in female rats. Interestingly, administration of PPOH (20 mg·kg−1·day−1 for 4 days starting on day 15 of pregnancy) increased blood pressure by 21 mmHg and caused a significant decrease in the body weight of fetal pups (1.3 ± 0.08 g in control vs. 1.1 ± 0.06 g in PPOH). Moreover, PPOH treatment significantly decreased renal microsomal epoxygenase activity and the expression of CYP2C11, CYP2C23, and CYP2J in pregnant rats. This study demonstrates that EET synthesis in the kidney is elevated during pregnancy, and CYP2C11, 2C23, and CYP2J2 are responsible for the change of renal EET synthesis. The inhibition results demonstrate that the downregulation of renal epoxygenase activity by PPOH causes hypertension in pregnant rats. This study suggests that EETs may contribute to the control of blood pressure during pregnancy.

scholarly journals Altered vascular contractility in adult female rats with hypertension programmed by prenatal glucocorticoid exposure

2006 ◽  
Vol 188 (3) ◽  
pp. 435-442 ◽  
Author(s):  
P W F Hadoke ◽  
R S Lindsay ◽  
J R Seckl ◽  
B R Walker ◽  
C J Kenyon
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Adult Female ◽  
Vascular Function ◽  
Mesenteric Arteries ◽  
Female Rats ◽  
Control Group ◽  
Pregnant Rats ◽  
Vascular Contractility

Excessive exposure to glucocorticoids during gestation reduces birth weight and induces permanent hypertension in adulthood. The mechanisms underlying this programmed elevation of blood pressure have not been established. We hypothesised that prenatal glucocorticoid exposure may lead to vascular dysfunction in adulthood. Pregnant rats received dexamethasone (Dex) (100 μg/kg, s.c.) or vehicle (control) daily throughout pregnancy. Blood pressure was elevated (students t-test, unpaired; P < 0.05) in adult female offspring (aged 12–16 weeks) of Dex-treated mothers (148.0 ± 3.6 mmHg, n=10) compared with the control group (138.0 ± 2.5 mmHg, n=8). Vascular responsiveness in aortae and mesenteric arteries was differentially affected by prenatal Dex: aortae were less responsive to angiotensin II, whereas mesenteric arteries were more responsive to norepinephrine, vasopressin and potassium (mesenteric arteries respond poorly to angiotensin II in vitro). Acetylcholine-mediated, endothelium-dependent relaxation was similar in both groups. Prenatal exposure to Dex had no effect on blood pressure or aldosterone response to acute (15 min, i.v.) infusion of angiotensin II (75 ng/kg per min). In contrast, chronic (2-week, s.c.) infusion of angiotensin II (100 ng/kg per min) produced a greater elevation (P < 0.05) of blood pressure in Dex-treated rats (150.0 ± 3.6 mmHg) than in controls (135.3 ± 5.4 mmHg), and aldosterone levels were higher in Dex-treated animals. There was no angiotensin II-induced medial hypertrophy/hyperplasia in mesenteric arteries from Dex-treated rats. These results indicate that vascular function is altered in a region-specific manner in rats with glucocorticoid-programmed hypertension. Despite a striking increase in mesenteric artery contraction in Dex-treated rats, in vivo studies suggest that abnormalities of the renin-angiotensin-aldosterone system, rather than enhanced vascular contractility, may be responsible for the elevation of blood pressure in these animals.

scholarly journals Ameliorative effect of apelin-13 against renal complications in L-NAME-induced preeclampsia in rats

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11110
Author(s):  
Reham Z. Hamza ◽  
Abdel Aziz A. Diab ◽  
Mansour H. Zahra ◽  
Ali K. Asalah ◽  
Mai S. Attia ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Histopathological Examination ◽  
Female Rats ◽  
Serum Urea ◽  
Pregnant Rats ◽  
Arterial Blood ◽  
Total Urine

Pre-eclampsia (PE) accompanying acute liver and kidney injury has remained a master cause of both fetal and maternal mortality and morbidity. Vasoactive mediators, oxidative stress and inflammatory imbalanceshave an important role in PE pathogenesis. Apelin is an adipokine that improves endothelial dysfunction; has anti-inflammatory and antioxidant effects; moreover, its level reduced during PE. This study aimed to explore the effects of apelin-13 administration on preeclampsia-associated renal dysfunction and proteinuria. Thirty-three pregnant female rats were divided into three groups; group: 1 (normal pregnant rats), group: 2 (preeclamptic rats); where rats were injected subcutaneously with 75 mg L-NAME/ kg body weight/day beginning from 9th to 20th day of pregnancy andgroup 3 (apelin-13 treated preeclamptic rats); In which L-NAME-induced preeclamptic rats were subcutaneously injected with 6 × 10−8 mol apelin-13/kg body weight/twice daily starting from 6th to 20th day of pregnancy. In all groups, mean arterial blood pressure, total urine protein, serum urea, creatinine, nitric oxide (NO), endothelin-1 (ET-1), interleukin–6 (IL-6) and malondialdhyde (MDA) were measured. Histopathological examination of kidney tissues was also done. preeclamptic rats showed significantly increased mean arterial blood pressure, total urine proteins, serum urea, creatinine, ET-1, IL-6, and MDA, but revealed a significantly decreased serum NO level. On the other hand, apelin treatment significantly improved these parameters together with amelioration of kidney histoarchitecture in the treated group. In conclusion, apelin may be a potentially curative candidate for prohibiting kidney damage and have a therapeutic benefit in PE rat models.

Renal 20-HETE inhibition attenuates changes in renal hemodynamics induced by l-NAME treatment in pregnant rats

2005 ◽  
Vol 289 (5) ◽  
pp. F1116-F1122 ◽  
Author(s):  
Hui Huang ◽  
Yiqiang Zhou ◽  
Venugopal T. Raju ◽  
Juan Du ◽  
Hsin-Hsin Chang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Combined Treatment ◽  
Renal Hemodynamics ◽  
Female Rats ◽  
Control Group ◽  
Pregnant Rats ◽  
Functional Changes ◽  
No Inhibition ◽  
Renal Vascular

We previously reported that inhibition of nitric oxide (NO) synthesis by N-nitro-l-arginine methyl ester (l-NAME) during late pregnancy leads to increased production of renal vascular 20-hydroxyeicosatetraenoic acid (20-HETE), a cytochrome P-450 (CYP) 4A-derived vasoconstrictor, in pregnant rats. However, the effect of upregulation of vascular 20-HETE production on renal function after NO inhibition is not known. To test the hypothesis that increased gestational vascular 20-HETE synthesis after NO inhibition is involved in mediating blood pressure and renal functional changes, we first determined the IC50 value of the effect of nitroprusside (SNP), a NO donor, on renal 20-HETE production in cortical microsomes. We then divided pregnant rats and age-matched virgin rats into a vehicle control group, an l-NAME treatment group (0.25 mg/ml in drinking water), and a group treated with l-NAME plus N-methylsulfonyl-12,12-dibromododec-11-enamide (DDMS; CYP4A-selective inhibitor, 10 mg·kg−1·day−1 iv). After 4 days of treatment, we measured blood pressure, renal blood flow (RBF), renal vascular resistance (RVR), and glomerular filtration rate (GFR) in each group. The addition of SNP (IC50 = 22 μM) decreased renal cortical 20-HETE production. In pregnant rats, l-NAME treatment led to significantly higher mean arterial pressure (MAP) and RVR, and lower RBF and GFR. Combined treatment with DDMS and l-NAME significantly attenuated the increases in MAP and RVR and the decrease in GFR, but not the reduction in RBF induced by l-NAME treatment. l-NAME and l-NAME plus DDMS had no significant impact on renal hemodynamics in virgin rats. In addition, chronic treatment with DDMS selectively inhibited cortical 20-HETE production without a significant effect on CYP4A expression in l-NAME-treated pregnant rats. In conclusion, NO effectively inhibits renal cortical microsomal 20-HETE production in female rats. In pregnant rats, the augmentation of renal 20-HETE production after NO inhibition is associated with increased MAP and RVR, whereas decreased GFR is negated by treatment of a selective and competitive CYP4A inhibitor. These results demonstrate that the interaction between renal 20-HETE and NO is important in the regulation of renal function and blood pressure in pregnant rats.

scholarly journals Glomerular hemodynamic effects of late pregnancy in rats with experimental membranous glomerulonephropathy.

1995 ◽  
Vol 6 (4) ◽  
pp. 1197-1201
Author(s):  
C Baylis ◽  
A Deng ◽  
W G Couser
Keyword(s):  
Blood Pressure ◽  
Late Pregnancy ◽  
Systemic Blood Pressure ◽  
Female Rats ◽  
Pregnant Rats ◽  
Renal Vasoconstriction ◽  
Heymann Nephritis ◽  
Single Nephron ◽  
Glomerular Capillary Hypertension ◽  
Membranous Glomerulonephropathy

In these studies, the Fx1A model of accelerated, passive Heymann nephritis was used to produce membranous glomerulonephropathy. Female rats were studied at 7 wk after the administration of the Fx1A antibody either in the virgin state or in late pregnancy. The goals of these experiments were to determine whether preexisting membranous glomerulonephropathy compromises the pregnancy and whether the pregnancy acutely worsens the renal function. Virgin rats with membranous glomerulonephropathy developed massive proteinuria and exhibited glomerular capillary hypertension but without declines in GFR. In late pregnancy, there was no worsening of the proteinuria and glomerular blood pressure fell to normal values. Both afferent and efferent arteriolar resistances increased in pregnant rats with membranous glomerulonephropathy compared with virgins, leading to falls in glomerular plasma flow and single-nephron GFR. There were no histologic abnormalities in the glomeruli of either virgin or late pregnant rats with membranous glomerulonephropathy, and both groups exhibited similar immunoglobulin G and complement deposits. Up to Day 19 (term is 22 days), the pregnancy in rats with membranous glomerulonephropathy appeared uneventful. Thus, this study indicates that the Fx1A model of membranous glomerulonephropathy does not compromise the course of the pregnancy, at least until close to term. Pregnancy lowers glomerular blood pressure in rats with membranous glomerulonephropathy because of both a fall in systemic blood pressure and the atypical renal vasoconstriction, which leads to declines in single-nephron GFR.

Modification of Pineal Ultrastructure by Exogenous Hormones

1967 ◽  
Vol 25 ◽  
pp. 170-171
Author(s):  
R. A. Turner ◽  
A. E. Rodin ◽  
D. K. Roberts
Keyword(s):  
Electron Microscopy ◽  
Endoplasmic Reticulum ◽  
Rough Endoplasmic Reticulum ◽  
Estradiol Benzoate ◽  
Female Rats ◽  
List Type ◽  
Type Number ◽  
Pregnant Rats ◽  
Gonadal Atrophy ◽  
Pineal Ultrastructure

There have been many reports which establish a relationship between the pineal and sexual structures, including gonadal hypertrophy after pinealectomy, and gonadal atrophy after injection of pineal homogenates or of melatonin. In order to further delineate this relationship the pineals from 5 groups of female rats were studied by electron microscopy:ControlsPregnant ratsAfter 4 weekly injections of 0.1 mg. estradiol benzoate.After 8 daily injections of 150 mcgm. melatonin (pineal hormone).After 8 daily injections of 3 mg. serotonin (melatonin precursor).No ultrastructural differences were evident between the control, and the pregnancy and melatonin groups. However, the estradiol injected animals exhibited a marked increase in the amount and size of rough endoplasmic reticulum within the pineal cells.

THE FALL OF BLOOD PRESSURE FOLLOWING INDUCTION OF DECIDUOMATA IN STEROID HYPERTENSIVE RATS RECEIVING PROGESTERONE

1968 ◽  
Vol 59 (2) ◽  
pp. 227-234 ◽  
Author(s):  
H. C. Moore ◽  
I. Cserhati ◽  
F. P. Biliczki
Keyword(s):  
Blood Pressure ◽  
Hypotensive Effect ◽  
Hypertensive Rats ◽  
Pregnant Rats ◽  
Hypertensive Rat ◽  
Equivalent Time ◽  
Metrial Gland ◽  
Blood Pressure Responses ◽  
A Minor ◽  
Maternal Decidua

ABSTRACT Experimental deciduomata and progesterone together lower the blood pressure in the steroid hypertensive rat from the 5th to 10th day of decidual growth i. e. from the 10th to 15th day of pseudopregnancy. This would suggest that the fall of blood pressure at an equivalent time of gestation in hypertensive pregnant rats could be due to the maternal decidua under the influence of progesterone. It is further considered that the metrial gland of the deciduoma is more likely to be responsible for the hypotensive effect and by comparison that the metrial gland is implicated in the hypotensive effect of pregnancy. Progesterone alone also exerts a minor hypotensive effect in those animals in which a nephrectomy forms part of the hypertension regimen and indicates one way in which a maternal renal factor could influence blood pressure responses in hypertensive pregnant rats.

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