scholarly journals Leptin Increases Blood Pressure and Markers of Endothelial Activation during Pregnancy in Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Hisham Saleh Ibrahim ◽  
Effat Omar ◽  
Gabrielle Ruth Anisah Froemming ◽  
Harbindar Jeet Singh
Keyword(s):  
Blood Pressure ◽  
Underlying Mechanism ◽  
Endothelial Activation ◽  
Treated Group ◽  
Urinary Protein Excretion ◽  
Urinary Protein ◽  
Sprague Dawley ◽  
Protein Excretion ◽  
Sprague Dawley Rats ◽  
Group 1

Raised leptin levels have been reported in the placentae and serum of women with elevated blood pressure and proteinuria during pregnancy. The role of leptin in this however remains unknown. This study investigates the effect of leptin administration on systolic blood pressure (SBP) and proteinuria and serum markers of endothelial activation during pregnancy inSprague Dawley rats. From day 1 of pregnancy, 24 rats were randomised into those given either saline (group 1) or leptin at 60 or 120 μg/kg/body weight/day (groups 2 and 3 resp.). SBP was measured every 5 days and 24-h urinary protein was measured at days 0 and 20 of pregnancy. Animals were euthanised on day 20 of pregnancy, and serum was collected for estimation of E-selectin and ICAM-1. Compared to group 1, SBP during the latter part of the pregnancy was significantly higher in the leptin-treated group (P<0.01). Urinary protein excretion, serum E-selectin, and ICAM-1 were significantly higher in leptin-treated rats (P<0.05). It seems that leptin administration to normotensiveSprague Dawley ratsduring pregnancy significantly increases SBP, urinary protein excretion, and markers of endothelial activation. However, further studies are required to examine the underlying mechanism responsible for this and its relevance to preeclampsia in humans.

Office blood pressure is a predictor of aortic elastic properties and urinary protein excretion in subjects with white coat hypertension

2016 ◽  
Vol 203 ◽  
pp. 98-103 ◽  
Author(s):  
Konstantinos Aznaouridis ◽  
Charalambos Vlachopoulos ◽  
Konstantina Masoura ◽  
Panagiota Pietri ◽  
Gregory Vyssoulis ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Elastic Properties ◽  
Urinary Protein Excretion ◽  
Urinary Protein ◽  
Office Blood Pressure ◽  
White Coat ◽  
White Coat Hypertension ◽  
Protein Excretion ◽  
Aortic Elastic Properties

The effect of tumor-associated protein RCAS1 gene silencing on blood pressure and urinary protein excretion in pregnant mouse: a pilot study

2010 ◽  
Vol 203 (4) ◽  
pp. 364.e6-364.e12 ◽  
Author(s):  
Ekaterine Tskitishvili ◽  
Hitomi Nakamura ◽  
Yukiko Kinugasa-Taniguchi ◽  
Takeshi Kanagawa ◽  
Koichiro Shimoya ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Pilot Study ◽  
Gene Silencing ◽  
Pregnant Mouse ◽  
Urinary Protein Excretion ◽  
Urinary Protein ◽  
Protein Excretion

scholarly journals Evidence that an angiotensin-converting enzyme inhibitor has a different effect on glomerular injury according to the different phase of the disease at which the treatment is started.

1994 ◽  
Vol 5 (4) ◽  
pp. 1139-1146
Author(s):  
N Perico ◽  
S C Amuchastegui ◽  
V Colosio ◽  
G Sonzogni ◽  
T Bertani ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Converting Enzyme ◽  
Systolic Blood Pressure ◽  
Ace Inhibitor ◽  
Diabetic Rats ◽  
Urinary Protein Excretion ◽  
Urinary Protein ◽  
Converting Enzyme ◽  
Glomerular Injury ◽  
Protein Excretion

In rats with streptozotocin-induced diabetes, the effect of an angiotensin-converting enzyme (ACE) inhibitor on the evolution of glomerular injury according to the time at which the treatment is started with respect to the onset of the disease was studied. Three groups of animals were used, a control Group 1 and two groups of diabetic rats treated with insulin (Groups 2 and 3). The latter were monitored until urinary protein excretion reached 40 to 50 mg/24 h (on average, 23 wk after the induction of the diabetes). At this time, Group 2 continued to receive insulin alone, whereas Group 3 was also given the ACE inhibitor moexipril for 8 more wk. Untreated diabetic rats showed a moderate increase in systolic blood pressure that was normalized by moexipril administration. Urinary protein excretion progressively increased during the 8-wk follow-up in untreated diabetics that, at the end of the study, developed moderate glomerular sclerosis. Moexipril treatment lowered urinary protein excretion to a normal range and completely prevented glomerular injury. Three other groups of rats were similarly treated, except that moexipril treatment was started later on (when proteinuria reached 100 to 200 mg/24 h, on average, 32 wk after the induction of diabetes), and were monitored for another 8 wk. Untreated and treated diabetics had comparable blood glucose levels throughout. Systolic blood pressure, significantly increased in untreated diabetic rats, was effectively controlled by moexipril administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential evolution of blood pressure and renal lesions after RAS blockade in Lyon hypertensive rats

2002 ◽  
Vol 283 (5) ◽  
pp. R1041-R1045 ◽  
Author(s):  
Delphine Bertram ◽  
Nelly Blanc-Brunat ◽  
Jean Sassard ◽  
Ming Lo
Keyword(s):  
Blood Pressure ◽  
Antihypertensive Effect ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Urinary Protein Excretion ◽  
Urinary Protein ◽  
Histological Changes ◽  
Angiotensin System ◽  
Renal Lesions ◽  
Protein Excretion

The present work aimed to assess, in Lyon hypertensive (LH) rats, whether an early and prolonged inhibition of the renin-angiotensin system (RAS) could result in a blood pressure (BP) lowering and nephroprotection that persist after its withdrawal. Male LH rats received orally from 3 to 12 wk of age either an angiotensin-converting enzyme inhibitor perindopril at the doses of 0.4 and 3 mg · kg−1· day−1or an AT1receptor antagonist losartan at the dose of 10 mg · kg−1· day−1. BP, histological changes in the kidney, and urinary protein excretion were examined during and 10 wk after cessation of the treatments. Both perindopril and losartan decreased BP, prevented renal lesions, and limited urinary protein excretion. After cessation of the treatment, BP returned to the level of never-treated LH rats in rats having received 3 mg · kg−1· day−1of perindopril while it remained slightly lower in those treated with 0.4 mg · kg−1· day−1of perindopril or with losartan. This lack of marked persistent antihypertensive effect contrasted with a durable decrease in urinary protein excretion and improvement of the renal histological lesions. In conclusion, it is possible to separate the BP-lowering effects of RAS blockade from those on glomerulosclerosis and urinary protein excretion.

Interleukin-10 reduces inflammation, endothelial dysfunction, and blood pressure in hypertensive pregnant rats

2010 ◽  
Vol 298 (3) ◽  
pp. R713-R719 ◽  
Author(s):  
John H. Tinsley ◽  
Sanique South ◽  
Valorie L. Chiasson ◽  
Brett M. Mitchell
Keyword(s):  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Systolic Blood Pressure ◽  
Interleukin 10 ◽  
Urinary Protein Excretion ◽  
Urinary Protein ◽  
Hypertensive Disorders Of Pregnancy ◽  
Endothelin 1 ◽  
Protein Excretion ◽  
Hypertensive Disorders

Hypertensive disorders of pregnancy are characterized by systemic and placental inflammation; however, treatment for these conditions has remained elusive. We tested whether administration of the anti-inflammatory cytokine interleukin-10 (IL-10) during pregnancy would attenuate the hypertension, endothelial dysfunction, proteinuria, and inflammation seen in pregnant DOCA/saline-treated (PDS) rats. Normal pregnant (NP) rats and PDS were given daily intraperitoneal injections of recombinant IL-10 from gestational day 13 until death on day 20. Systolic blood pressure, aortic endothelium-dependent relaxation responses, and urinary protein excretion were measured on days 13 and 20 of gestation. Fetal number and development, plasma endothelin-1 levels, serum and placental levels of IFNγ and IL-10, and aortic and placental levels of platelet endothelial cell adhesion molecule (PECAM) were assessed on gestational day 20. Systolic blood pressure, aortic endothelial dysfunction, and urinary protein excretion were significantly increased at gestational day 13 in PDS rats. However, all of these were restored to NP levels following IL-10 treatment in PDS rats. IL-10 treatment also significantly increased the number of pups per litter in PDS rats and did not further affect fetal development. The beneficial effects of IL-10 in PDS rats were likely mediated by the decreased plasma levels of endothelin-1, decreased levels of circulating and placental IFNγ, as well as decreased aortic and placental expression of PECAM. These data demonstrate that exogenous IL-10 can normalize blood pressure and endothelial function in pregnancy-induced hypertensive rats and may be beneficial in women with hypertensive disorders of pregnancy.

Leptin-induced increase in blood pressure and markers of endothelial activation during pregnancy in Sprague Dawley rats is prevented by resibufogenin, a marinobufagenin antagonist

2020 ◽  
Vol 20 (2) ◽  
pp. 184-190 ◽  
Author(s):  
Maryam Jameelah Md Hassan ◽  
Nor Salmah Bakar ◽  
Mardiana Abdul Aziz ◽  
Norizan Kamal Basah ◽  
Harbindar Jeet Singh
Keyword(s):  
Blood Pressure ◽  
Endothelial Activation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

scholarly journals Improvements of renal lesions and function by angiotensin and endothelin receptor antagonism in nitric oxide-deficient rats

2001 ◽  
Vol 2 (1_suppl) ◽  
pp. S211-S216
Author(s):  
Jean-Jacques Boffa ◽  
Ying Lu ◽  
Jean-Claude Dussaule ◽  
Christos Chatziantoniou
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Urinary Protein Excretion ◽  
Urinary Protein ◽  
Plasma Creatinine ◽  
Endothelin Receptor ◽  
Receptor Antagonists ◽  
Protein Excretion ◽  
Sclerotic Lesions ◽  
Renal Vascular

In previous studies, we have observed that antagonism of angiotensin or endothelin receptors prevented the development of nephroangio- and glomerulo-sclerosis during hypertension by inhibiting collagen I gene synthesis, through a mechanism independent of systemic haemodynamics. The present study investigated whether treatment with angiotensin or endothelin receptor antagonists, given at doses that did not reduce blood pressure, could produce regression of renal sclerotic lesions and improve renal function during hypertension. Hypertension and renal vascular fibrosis were induced in rats by chronic inhibition of NO synthesis using NGnitro-L-arginine methyl ester (L-NAME). Systolic blood pressure gradually increased following L-NAME administration, reaching a plateau of 170 mmHg after four weeks of treatment. At the same time, urinary protein excretion and plasma creatinine concentration were increased ten- and three-fold compared with controls, respectively (p<0.001). This increase was accompanied by the appearance of sclerotic lesions within renal vessels and glomeruli, as evidenced by Masson's trichromic staining (sclerotic index 2.34±0.29 vs. 0.10±0.01 in L-NAME four weeks and control, respectively, p<0.001). Thereafter, the L-NAME treatment was combined with either losartan (an AT1receptor antagonist), bosentan (an ETA/B antagonist), co-treatment with both agents, or vehicle for an additional period of four weeks. Blockade of AT1and/or ETA/B-receptors significantly reduced urinary protein excretion and plasma creatinine levels (p<0.01) and substantially improved renal vascular histology (sclerotic index 1.78±0.13, 1.57±0.22 and 1.85±0.15 respectively, p<0.01, vs. L-NAME eight week) without altering the L-NAME-induced increase of systolic pressure. These data indicate that angiotensin II and endothelin-1 participate in the mechanism(s) of renal vascular fibrosis by increasing extracellular matrix formation. Treatment with their respective receptor antagonists leads to the regression of renal vascular fibrosis and to the improvement of renal function by a common antifibrogenic mechanism that is independent of systemic haemodynamics.

scholarly journals Biphasic Vasodilator Action of Troglitazone on the Renal Microcirculation

2002 ◽  
Vol 13 (2) ◽  
pp. 342-349 ◽  
Author(s):  
Shuji Arima ◽  
Kentaro Kohagura ◽  
Kazuhisa Takeuchi ◽  
Yoshihiro Taniyama ◽  
Akira Sugawara ◽  
...  
Keyword(s):  
Constant Pressure ◽  
Calcium Influx ◽  
Late Phase ◽  
Underlying Mechanism ◽  
Urinary Protein Excretion ◽  
Urinary Protein ◽  
Protein Excretion ◽  
Glomerular Hemodynamics ◽  
Vasodilator Action ◽  
Dose Dependent

ABSTRACT. Recent studies have demonstrated that thiazolidinediones, novel antidiabetic compounds that improve the insulin sensitivity, lower BP and decrease urinary protein excretion. However, neither the target vasculature nor the underlying mechanism for their actions is well understood. In this study, the action of troglitazone (Tro), a thiazolidinedione compound, on the glomerular afferent (Af-Arts) and efferent (Ef-Arts) arterioles, crucial vascular segments to the control of glomerular hemodynamics, were directly examined. Rabbit Af-Arts or Ef-Arts were microdissected from the superficial cortex and perfused at constant pressure. Increasing doses of Tro (10−8 to 10−5 M) were added to both the bath and lumen of preconstricted arterioles. In Af-Arts, Tro caused dose-dependent and biphasic dilation. Tro at 10−5 M increased the diameter by 28 ± 6% (n = 8, P < 0.01) until 20 min, with the diameter remaining at this level for 60 min, and then Tro began to dilate Af-Arts again. At 120 min, Tro at 10−5 M further increased the diameter by 23 ± 4% (n = 6). Disrupting the endothelium had no effect on either dilation (n = 7 or n = 5). Pretreatment with SKF 96365 (50 μM), which inhibits both voltage- and receptor-operated calcium channels, abolished the early-phase dilation without affecting the late-phase dilation; 20 or 120 min after adding Tro at 10−5 M, the diameter increased by 4 ± 2% (n = 7) or 28 ± 3% (n = 6), respectively. In contrast to Af-Arts, Tro caused monophasic dilation in Ef-Arts; Tro at 10−5 M did not cause significant dilation until 80 min, and at 120 min the diameter increased by 37 ± 4% (n = 5). These results suggest that in the Af-Art Tro has biphasic endothelium-independent vasodilator action, which is partly mediated by an inhibition of calcium influx. This vasodilator action may play a role in the BP-lowering effect of Tro. In addition, by dilating the postglomerular Ef-Art, Tro may decrease the glomerular capillary pressure and hence the excretion of urinary protein.

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