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 Nicorandil as a novel therapy for advanced diabetic nephropathy in the eNOS-deficient mouse

2012 ◽  
Vol 302 (9) ◽  
pp. F1151-F1160 ◽  
Author(s):  
Katsuyuki Tanabe ◽  
Miguel A. Lanaspa ◽  
Wataru Kitagawa ◽  
Christopher J. Rivard ◽  
Makoto Miyazaki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Diabetic Nephropathy ◽  
Oxidant Stress ◽  
Nitric Oxide Donor ◽  
K Channel ◽  
Glomerular Injury ◽  
Novel Therapy ◽  
Glucose Levels ◽  
Stress Studies

Nicorandil is an orally available drug that can act as a nitric oxide donor, an antioxidant, and an ATP-dependent K channel activator. We hypothesized that it may have a beneficial role in treating diabetic nephropathy. We administered nicorandil to a model of advanced diabetic nephropathy (the streptozotocin-induced diabetes in mice lacking endothelial nitric oxide synthase, eNOSKO); controls included diabetic eNOS KO mice without nicorandil and nondiabetic eNOS KO mice treated with either nicorandil or vehicle. Mice were treated for 8 wk. Histology, blood pressure, and renal function were determined. Additional studies involved examining the effects of nicorandil on cultured human podocytes. Here, we found that nicorandil did not affect blood glucose levels, blood pressure, or systemic endothelial function, but significantly reduced proteinuria and glomerular injury (mesangiolysis and glomerulosclerosis). Nicorandil protected against podocyte loss and podocyte oxidative stress. Studies in cultured podocytes showed that nicorandil likely protects against glucose-mediated oxidant stress via the ATP-dependent K channel as opposed to its NO-stimulating effects. In conclusion, nicorandil may be beneficial in diabetic nephropathy by preserving podocyte function. We recommend clinical trials to determine whether nicorandil may benefit diabetic nephropathy or other conditions associated with podocyte dysfunction.

Abstract 037: Exaggerated Placental Ischemia-induced Hypertension in Endothelin Receptor Type B (ETB)-deficient Pregnant Rats s Independent of Increased sFlt-1 or ROS Levels

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Frank T Spradley
Keyword(s):  
Blood Pressure ◽  
Acute Hypoxia ◽  
Pressure Control ◽  
Normal Pregnancy ◽  
Endothelin Receptor ◽  
Maternal Circulation ◽  
Pregnant Rats ◽  
Uterine Perfusion ◽  
Placental Ischemia ◽  
In Pregnancy

While the pathogenesis of preeclampsia is not fully understood, studies implicate placental ischemia. Reduced uterine perfusion pressure (RUPP)-induced placental ischemia/hypoxia in animal models stimulates release of factors like antiangiogenic sFlt-1 into the maternal circulation increasing vascular-renal ET-1. ET-1 promotes hypertension via reactive oxygen species (ROS). Blockade of vasoconstrictive ETA abolishes RUPP hypertension. Deficiency of vasodilatory ETB in rats leads to increased blood pressure in pregnancy. While ETB deficiency markedly enhances RUPP hypertension, it is unknown if there is exaggerated RUPP-induced sFlt-1, ET-1 or ROS levels in ETB-def rats. The hypothesis was tested that placental ischemia/hypoxia-induced release of sFlt-1 and circulating ET-1 and ROS are greater in ETB-def rats. Eighteen-week-old ETB-def and transgenic (Tg) control pregnant rats were generated with Wistar Hannover males. RUPP or Sham surgeries were on gestational day 14 and assessment of plasmas and placentas at day 19. RUPP increased placental sFlt-1 (pg/mg) similarly in RUPP ETB-def (781±113, N=5) vs Sham ETB-def (573±54, N=12) and RUPP Tg (631±62, N=5) vs Sham Tg (547±31, N=12) (P<0.05). In placental explant cultures, acute hypoxia (48 h 1% O2 vs normoxia 6% O2) stimulated a comparable release of sFlt-1 (pg/mg) in Sham ETB-def (2577±135 vs 2070±78) and Sham Tg (3208±318 vs 2553±107) (P<0.05). Unexpectedly, plasma sFlt-1 (pg/mL) was lower in RUPP ETB-def (153±48) vs Sham ETB-def (476±125) and RUPP Tg (238±32) vs Sham Tg (463±102) (P<0.05). Plasma ET-1 (fmol/L) was exaggerated in RUPP ETB-def (954±70) and greater in Sham ETB-def (735±43) vs RUPP Tg (122±14) or Sham Tg (142±41) (P<0.05). Plasma H2O2 (umol/L) was not exaggerated in RUPP ETB-def (5.4±1.2) or RUPP Tg (4.0±0.5) but was greater (P<0.05) in Sham ETB-def (6.2±0.3) vs Sham Tg (3.6±0.3). In conclusion, these data suggest in 1) normal pregnancy, ETB is crucial for blood pressure control by regulating bioavailable ET-1 to prevent ROS production and 2) placental ischemia, ETB reduces excess ET-1 to buffer hypertension independently of sFlt-1 or ROS. These data support ETB physiology as important in controlling blood pressure in pregnancy and its loss in mediating hypertension in preeclampsia.

scholarly journals Melanocortin-4 Receptor Deficiency Attenuates Placental Ischemia-Induced Hypertension in Pregnant Rats

Hypertension ◽  
2019 ◽  
Vol 73 (1) ◽  
pp. 162-170 ◽  
Author(s):  
Frank T. Spradley ◽  
Ana C. Palei ◽  
Christopher D. Anderson ◽  
Joey P. Granger
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Perfusion Pressure ◽  
Wild Type ◽  
Pregnant Rats ◽  
Melanocortin 4 Receptor ◽  
Induced Hypertension ◽  
Sympathetic Nervous ◽  
Uterine Perfusion ◽  
Placental Ischemia

Preeclampsia is a pregnancy-specific disorder of new-onset hypertension linked to placental ischemia. While obesity is a major risk factor for preeclampsia, not all obese pregnant women develop pregnancy-induced hypertension or preeclampsia. Previously, we reported that placental ischemia-induced hypertension is dependent upon intact signaling of the sympathetic nervous system. Moreover, in various models of obesity, blockade of MC4R (melanocortin-4 receptor) signaling protects against the development of hypertension via suppression of the sympathetic nervous system. Less is known about this pathway during obese pregnancy. Although blockade of MC4R may lead to increased body weight during pregnancy, we tested the hypothesis that placental ischemia-induced hypertension is attenuated in obese MC4R-deficient pregnant rats. On gestational day 14, MC4R wild-type or heterozygous-deficient (MC4R-def) rats were subjected to chronic placental ischemia via the reduced uterine perfusion pressure procedure or Sham surgery then examined on gestational day 19. In Sham MC4R-def versus Sham wild-type pregnant rats, there was increased body weight, fat mass, and circulating leptin levels but they had similar fetus weights. Reduced uterine perfusion pressure reduced fetus weights in both strains. Reduced uterine perfusion pressure increased blood pressure in wild-type rats but this response was significantly attenuated in MC4R-def rats, although blood pressure was elevated in Sham MC4R-def over Sham wild-type. These data indicate that while obese MC4R-def pregnant rats have higher blood pressure during pregnancy, placental ischemia-induced hypertension is attenuated in obese MC4R-def pregnant rats. Thus, obese women with abnormal MC4R signaling may be less susceptible to the development of placental ischemia-induced hypertension.

Abstract 206: Hyperleptinemia Increases Blood Pressure and Decreases Pup Weight in Pregnant Rats

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Ana C Palei ◽  
Eric M George ◽  
Marietta Arany ◽  
Kathy Cockrell ◽  
Joey P Granger
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Normal Pregnancy ◽  
Developed Countries ◽  
Late Gestation ◽  
Sprague Dawley ◽  
Pregnant Rats ◽  
Glucose Levels ◽  
Sprague Dawley Rats ◽  
Relationship Of

While the relationship of obesity to cardiovascular disease is well recognized, it also has important implications for pregnancy outcomes. Indeed, there is compelling evidence that obesity increases the risk of preeclampsia (PE). The risk of severe and mild PE and PE occurring in early and late gestation are greater in obese and overweight women. Despite the fact that obesity is the leading attributable risk for PE in developed countries, the pathophysiological mechanisms whereby obesity and metabolic factors such as leptin increases the risk for developing PE are unclear. Hyperleptinemia over the levels seen in normal pregnancy has been associated with preeclampsia. Thus the aim of this study was to investigate whether chronic hyperleptinemia causes changes in cardiovascular, metabolic and reproductive systems of pregnant rats. On gestational day (GD) 14, Sprague Dawley rats were assigned to normal pregnant (NP, n=8) group or to NP plus Leptin group (NP+Lep, n=8), in which miniosmotic pump with leptin (0.5 μg/kg/min) was placed intraperitoneally. On GD 19, mean arterial pressure (MAP) was recorded, rats were sacrificed, and blood, placentas and pups were collected. Body weight (BW) and food intake (FI) were measured on GD 16-18. Serum leptin concentration was elevated in NP+Lep compared with NP (0.82 ± 0.05 vs 17.98 ± 2.75 ng/mL, P<0.05). Circulating insulin and glucose levels were similar in NP and NP+Lep groups (both P>0.05). MAP was higher in NP+Lep compared with NP (102.40 ± 2.38 vs 121.30 ± 8.13 mmHg, P<0.05). BW was decreased in NP+Lep compared with NP at GD 19 (330.90 ± 9.08 vs 284.10 ± 8.58 g, P<0.05), probably due to the reduced FI of the NP+Ins group compared with NP during GD 16-18 (23.45 ± 0.61 vs 8.61 ± 0.83 g/day, P<0.05). Although the number of viable fetuses per rat was similar between groups (P>0.05), fetuses and placentas of the NP+Lep group were lighter than those of the NP group (2.29 ± 0.06 vs 2.11 ± 0.06 g and 0.58 ± 0.01 vs 0.50 ± 0.02 g, respectively, both P<0.05). In conclusion, leptin increases blood pressure, despite its effect of reducing body weight during pregnancy, representing a possible mechanism to induce hypertension in preeclampsia. In addition, leptin decreases pup and placental weights, which could lead to abnormal fetal outcomes.

Interferon Gamma Neutralization Reduces Blood Pressure, Uterine Artery Resistance Index, and Placental Oxidative Stress in Placental Ischemic Rats

2021 ◽  
Author(s):  
Olivia K Travis ◽  
Geilda A Tardo ◽  
Chelsea Giachelli ◽  
Shani Siddiq ◽  
Henry T Nguyen ◽  
...  
Keyword(s):  
Interferon Gamma ◽  
Vascular Function ◽  
Uterine Artery ◽  
Resistance Index ◽  
Pregnant Rats ◽  
Maternal Hypertension ◽  
Uterine Perfusion ◽  
Placental Ischemia ◽  
Precise Role

Preeclampsia (PE) is characterized by maternal hypertension, intrauterine growth restriction, increased cytolytic natural killer cells (cNKs), which secrete interferon gamma (IFNγ). However, the precise role of IFNγ in contributing to PE pathophysiology remains unclear. Using the Reduced Uterine Perfusion Pressure (RUPP) rat model of placental ischemia, we tested the hypothesis that neutralization of IFNγ in RUPPs will decrease placental reactive oxygen species (ROS) and improve vascular function resulting in decreased MAP and improved fetal growth. On Gestation Day (GD) 14, the RUPP procedure was performed and on GDs 15 and 18, a subset of normal pregnant rats (NP) and RUPP rats were injected with 10μg/kg of an anti rat-IFNγ monoclonal antibody. On GD18, Uterine Artery Resistance Index (UARI) was measured via Doppler Ultrasound and on GD19, mean arterial pressure (MAP) was measured, animals were sacrificed, and blood and tissues were collected for analysis. Increased MAP was observed in RUPP rats compared to NP and was reduced in RUPP+anti-IFNγ. Placental ROS was also increased in RUPP rats compared to NP and was normalized in RUPP+anti-IFNγ. Fetal and placental weights were reduced in RUPP rats, but were not improved following anti-IFNγ treatment. However, UARI was elevated in RUPP compared to NP and was reduced in RUPP+anti-IFNγ. In conclusion, we observed that IFNγ neutralization reduced MAP, UARI, and placental ROS in RUPP recipients. These data suggest that IFNγ is a potential mechanism by which cNKs in contribute to PE pathophysiology and may represent a therapeutic target to improve maternal outcomes in PE.

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.

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.

scholarly journals Elastin-Like Polypeptide: VEGF-B Fusion Protein for Treatment of Preeclampsia

Hypertension ◽  
2021 ◽  
Author(s):  
Jamarius P. Waller ◽  
John Aaron Howell ◽  
Hali Peterson ◽  
Eric M. George ◽  
Gene L. Bidwell
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Reduction ◽  
Subcutaneous Administration ◽  
Growth Factor Receptor ◽  
Endothelial Cell Proliferation ◽  
Tyrosine Kinase Receptor ◽  
Pregnant Rats ◽  
Uterine Perfusion ◽  
Placental Ischemia

Preeclampsia is characterized by the development of elevated blood pressure during the second and third trimesters of pregnancy that is accompanied by end organ dysfunction. The pathogenesis of preeclampsia is multifactorial but is commonly characterized by endothelial dysfunction and the overproduction of antiangiogenic factors, including the soluble VEGF (vascular endothelial growth factor) receptor sFlt-1 (soluble Fms-like tyrosine kinase receptor 1). Previously, administration of exogenous VEGF-A, bound to a carrier protein called ELP (elastin-like polypeptide), significantly reduced free sFlt-1 levels and attenuated the hypertensive response in a rodent model of preeclampsia. However, VEGF-A administration induces multifactorial effects mediated through its direct activation of the Flk-1 receptor. In response to this, we developed a therapeutic chimera using ELP bound to VEGF-B, a VEGF isoform that binds to sFlt-1 but not to Flk-1. The purpose of this study was to evaluate the in vitro activity and pharmacological properties of ELP-VEGF-B and to test its efficacy in the reduced uterine perfusion pressure rat model of placental ischemia. ELP-VEGF-B was less potent than ELP-VEGF-A in stimulation of endothelial cell proliferation and matrix invasion, indicating that it is a weaker angiogenic driver. However, after repeated subcutaneous administration in pregnant rats, ELP-VEGF-B was maternally sequestered and reduced blood pressure when compared with saline treated animals following induction of placental ischemia (123.38±11.4 versus 139.98±10.56 mm Hg, P =0.0129). Blood pressure reduction was associated with a restoration of the angiogenic capacity of plasma from rats treated with ELP-VEGF-B. ELP-VEGF-B is a nonangiogenic, maternally sequestered protein with potential efficacy for treatment of preeclampsia.

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.

Sign in / Sign up

Export Citation Format

Share Document