Differential modulation by estrogen of α2-adrenergic and I1-imidazoline receptor-mediated hypotension in female rats

2004 ◽  
Vol 97 (4) ◽  
pp. 1237-1244 ◽  
Author(s):  
Mahmoud M. El-Mas ◽  
Abdel A. Abdel-Rahman
Keyword(s):  
Blood Pressure ◽  
Standard Deviation ◽  
Mean Arterial Pressure ◽  
Locomotor Activity ◽  
Arterial Pressure ◽  
Autonomic Control ◽  
Female Rats ◽  
Estrogen Replacement ◽  
Sprague Dawley ◽  
Ovx Rats

We have recently shown that estrogen negatively modulates the hypotensive effect of clonidine (mixed α2-/I1-receptor agonist) in female rats and implicates the cardiovascular autonomic control in this interaction. The present study investigated whether this effect of estrogen involves interaction with α2- and/or I1-receptors. Changes evoked by a single intraperitoneal injection of rilmenidine (600 μg/kg) or α-methyldopa (100 mg/kg), selective I1- and α2-receptor agonists, respectively, in blood pressure, hemodynamic variability, and locomotor activity were assessed in radiotelemetered sham-operated and ovariectomized (Ovx) Sprague-Dawley female rats with or without 12-wk estrogen replacement. Three time domain indexes of hemodynamic variability were employed: the standard deviation of mean arterial pressure as a measure of blood pressure variability and the standard deviation of beat-to-beat intervals (SDRR) and the root mean square of successive differences in R-wave-to-R-wave intervals as measures of heart rate variability. In sham-operated rats, rilmenidine or α-methyldopa elicited similar hypotension that lasted at least 5 h and was associated with reductions in standard deviation of mean arterial pressure. SDRR was reduced only by α-methyldopa. Ovx significantly enhanced the hypotensive response to α-methyldopa, in contrast to no effect on rilmenidine hypotension. The enhanced α-methyldopa hypotension in Ovx rats was paralleled with further reduction in SDRR and a reduced locomotor activity. Estrogen replacement (17β-estradiol subcutaneous pellet, 14.2 μg/day, 12 wk) of Ovx rats restored the hemodynamic and locomotor effects of α-methyldopa to sham-operated levels. These findings suggest that estrogen downregulates α2- but not I1-receptor-mediated hypotension and highlight a role for the cardiac autonomic control in α-methyldopa-estrogen interaction.

Abstract P154: Ultrasound Imaging for Serial Measurements of Venous Diameters in Rats

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Teresa Krieger-Burke ◽  
Bridget M Seitz ◽  
Gregory D Fink ◽  
Stephanie W Watts
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Real Time ◽  
Ultrasound Imaging ◽  
Imaging System ◽  
Sprague Dawley ◽  
Reliable Technique ◽  
Venous Capacitance ◽  
Anesthetized Rats

The purpose of our study was to investigate serial ultrasound imaging in rats as a means to quantify the diameters of splanchnic veins in real time and the effect of drugs on venous capacitance. A 21 MHz probe ( Vevo 2100 imaging system,Visual Sonics Inc.) was used to collect images containing the portal vein (PV) and the superior mesenteric vein (SMV) in anesthetized male Sprague-Dawley rats maintained at 37°C. Stable landmarks were established and we were able to repeatedly locate specific cross-sections of PV and SMV. When controlled for respiratory and cardiac cycles during measurements, respective diameters of these vessels remained within 0.75±0.15% and 0.2±0.10% of baseline (PV: 2.02±0.15 mm; SMV: 1.67±0.05 mm) when located and measured every 5 minutes over 45 minutes (n=3 rats). PV and SMV remained within 1.0±0.6% and 0.38±0.9% from baseline, respectively, when measured on separate days over 10 weeks in a preliminary study using 2 rats. The consistency of raw vessel measurements allowed these vessels to serve as their own control during subchronic pharmacologic interventions. In a second study, the vasodilator sodium nitroprusside (2 mg/kg, i.v. bolus) was administered to anesthetized rats (n=3) following collection of baseline vessel measurements. PV and SMV diameters increased 37.23±2.4% and 29.77±8.8% from baseline by 30 minutes post drug administration while mean arterial pressure decreased 10.32±1.7 mmHg. Conversely, the administration of the venoconstrictor sarafotoxin (S6C) (5 ng/kg, i.v. bolus) to other anesthetized rats (n=3) decreased PV and SMV diameters 22.10±2.4% and 9.44±1.6% from baseline within 5 minutes, associated with an increase in mean arterial pressure of 12.85±3.2 mmHg. Together these results support serial ultrasound imaging as a reliable technique to accurately measure acute and subchronic changes in the diameter of splanchnic veins concurrent with blood pressure changes in intact rats. The ability to follow rat abdominal vein diameters in real time will assist in determining the role of the venous circulation in blood pressure regulation.

The arterial depressor response to chronic low-dose angiotensin II infusion in female rats is estrogen dependent

2012 ◽  
Vol 302 (1) ◽  
pp. R159-R165 ◽  
Author(s):  
Amanda K. Sampson ◽  
Lucinda M. Hilliard ◽  
Karen M. Moritz ◽  
Merlin C. Thomas ◽  
Chris Tikellis ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Low Dose ◽  
Renin Angiotensin System ◽  
Female Rats ◽  
Ang Ii ◽  
Pressure Regulation ◽  
Estrogen Replacement ◽  
Sprague Dawley ◽  
Arterial Pressure Regulation

The complex role of the renin-angiotensin-system (RAS) in arterial pressure regulation has been well documented. Recently, we demonstrated that chronic low-dose angiotensin II (ANG II) infusion decreases arterial pressure in female rats via an AT2R-mediated mechanism. Estrogen can differentially regulate components of the RAS and is known to influence arterial pressure regulation. We hypothesized that AT2R-mediated depressor effects evident in females were estrogen dependent and thus would be abolished by ovariectomy and restored by estrogen replacement. Female Sprague-Dawley rats underwent ovariectomy or sham surgery and were treated with 17β-estradiol or placebo. Mean arterial pressure (MAP) was measured via telemetry in response to a 2-wk infusion of ANG II (50 ng·kg−1·min−1 sc) or saline. MAP significantly decreased in females treated with ANG II (−10 ± 2 mmHg), a response that was abolished by ovariectomy (+4 ± 2 mmHg) and restored with estrogen replacement (−6 ± 2 mmHg). Cardiac and renal gene expression of components of the RAS was differentially regulated by estrogen, such that overall, estrogen shifted the balance of the RAS toward the vasodilatory axis. In conclusion, estrogen-dependent mechanisms offset the vasopressor actions of ANG II by enhancing RAS vasodilator pathways in females. This highlights the potential for these vasodilator pathways as therapeutic targets, particularly in women.

scholarly journals BLACK CUMIN (NIGELLA SATIVA) EFFECT ON BLOOD PRESSURE, MEAN ARTERIAL PRESSURE, PROTEINURIA IN PREECLAMPTIC MODEL RATS

2020 ◽  
pp. 127-133
Author(s):  
JOHNY MARPAUNG ◽  
M. F. G. SIREGAR ◽  
MAKMUR SITEPU ◽  
ADANG BACHTIAR
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Diastolic Blood Pressure ◽  
Nigella Sativa ◽  
Day Treatment ◽  
Female Rats ◽  
Control Group ◽  
Control Group Design ◽  
Black Cumin

Objective: This research aimed to show effect of black cumin (nigella sativa) on blood pressure, mean arterial pressure (MAP), proteinuria in preeclamptic model rats. Methods: This is analytical research with true experimental design in laboratory pregnant female rats (Rattus norvegicus), which get black cumin seed extract (Nigella sativa) at a dose of 500 mg/kg/day and 2000 mg/kg/day. Treatment of all samples was performed simultaneously and during the treatment was observed using Postest Only Control Group Design. The research was conducted at Biology Laboratory in July 2019. To assess the comparison of parameters (systolic and diastolic blood pressure, mean arterial pressure and proteinuria) between groups the ANOVA test was used if the data were normally distributed and Kruskal Wallis test was used if the data were abnormally distributed. Results: Systolic and diastolic blood pressure and MAP decreased in preeclampsia models rats by administering 500 mg (P1) and 2000 mg (cumin) black cumin extract (P2). However, a dose of 2000 mg black cumin extract had a more significant decrease in systolic blood pressure and MAP. The results of this research indicate that all treatment groups showed improvement after day 9 of the administration of nigella that no treatment group showed proteinuria. Conclusion: Black cumin is proven to reduce systolic and diastolic blood pressure, Mean Arterial Pressure and proteinuria.

NO mediates effects of estrogen on central regulation of blood pressure in restrained, ovariectomized rats

2003 ◽  
Vol 285 (4) ◽  
pp. R842-R849 ◽  
Author(s):  
Anton Cherney ◽  
Heather Edgell ◽  
Teresa L. Krukoff
Keyword(s):  
Arterial Pressure ◽  
Psychological Stress ◽  
Cardiovascular Responses ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
No Production ◽  
Estrogen Replacement ◽  
Ovx Rats ◽  
Intracerebroventricular Injections ◽  
The Brain

We tested the hypotheses that estrogen replacement in ovariectomized (OVX) rats attenuates cardiovascular responses to psychological stress and that nitric oxide (NO) in the brain mediates these effects. Female rats were OVX; one group received 17β-estradiol (OVX-E) for 11-12 days and the other received vehicle (OVX-V). Seven days after OVX, OVX-E and OVX-V rats were chronically instrumented for arterial pressure measurements and intracerebroventricular injections. Later (4-5 days), OVX-E and OVX-V rats received intracerebroventricular injections of NG-nitro-l-arginine (88 μg/kg), an inhibitor of constitutive NO production, or vehicle. Mean arterial pressure (MAP) and heart rate responses were then measured in conscious rats exposed to two cycles of 1-h restraint/1-h rest. We show that MAP responses in restrained OVX-E rats were attenuated both during restraint and during rest. Although inhibition of NO production in the brain had no effect on MAP responses to restraint in OVX-V rats, it augmented responses in restrained OVX-E rats, especially during periods of rest, so that MAPs in restrained OVX-E and OVX-V rats were indistinguishable. Finally, NO levels in hypothalami and brain stems were elevated in restrained OVX-E, but not OVX-V, rats compared with their respective unrestrained controls. These results show that estrogen replacement in OVX rats reduces arterial pressure responses to psychological stress and that these effects are mediated, at least in part, by NO.

scholarly journals l-Arginine supplementation abolishes the blood pressure and endothelin response to chronic increases in plasma sFlt-1 in pregnant rats

2012 ◽  
Vol 302 (2) ◽  
pp. R259-R263 ◽  
Author(s):  
Sydney R. Murphy ◽  
Babbette LaMarca ◽  
Kathy Cockrell ◽  
Marietta Arany ◽  
Joey P. Granger
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Blood Pressure Response ◽  
No Synthase ◽  
Pressure Response ◽  
No Production ◽  
Sprague Dawley ◽  
Pregnant Rats ◽  
Synthase Inhibitor

While soluble fms-like tyrosine kinase-1 (sFlt-1) and endothelin-1 (ET-1) have been implicated in the pathogenesis of preeclampsia (PE), the mechanisms whereby increased sFlt-1 leads to enhanced ET-1 production and hypertension remain unclear. It is well documented that nitric oxide (NO) production is reduced in PE; however, whether a reduction in NO synthesis plays a role in increasing ET-1 and blood pressure in response to chronic increases in plasma sFlt-1 remains unclear. The purpose of this study was to determine the role of reduced NO synthesis in the increase in blood pressure and ET-1 in response to sFlt-1 in pregnant rats. sFlt-1 was infused into normal pregnant (NP) Sprague-Dawley rats (3.7 μg·kg−1·day−1 for 6 days beginning on day 13 of gestation) treated with the NO synthase inhibitor NG-nitro-l-arginine methyl ester (100 mg/l for 4 days) or supplemented with 2% l-Arg (in drinking water for 6 days beginning on day 15 of gestation). Infusion of sFlt-1 into NP rats significantly elevated mean arterial pressure compared with control NP rats: 116 ± 2 vs. 103 ± 1 mmHg ( P < 0.05). NO synthase inhibition had no effect on the blood pressure response in sFlt-1 hypertensive pregnant rats (121 ± 3 vs. 116 ± 2 mmHg), while it significantly increased mean arterial pressure in NP rats (128 ± 4 mmHg, P < 0.05). In addition, NO production was reduced ∼70% in isolated glomeruli from sFlt-1 hypertensive pregnant rats compared with NP rats ( P < 0.05). Furthermore, prepro-ET-1 in the renal cortex was increased ∼3.5-fold in sFlt-1 hypertensive pregnant rats compared with NP rats. Supplementation with l-Arg decreased the sFlt-1 hypertension (109 ± 3 mmHg, P < 0.05) but had no effect on the blood pressure response in NP rats (109 ± 3 mmHg) and abolished the enhanced sFlt-1-induced renal cortical prepro-ET expression. In conclusion, a reduction in NO synthesis may play an important role in the enhanced ET-1 production in response to sFlt-1 hypertension in pregnant rats.

Chronic Lability of Arterial Pressure in the Rat Does Not Evolve into Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 405s-407s ◽  
Author(s):  
W. T. Talman ◽  
D. R. Alonso ◽  
D. J. Reis
Keyword(s):  
Heart Rate ◽  
Standard Deviation ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Histopathological Changes ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Electrolytic Lesions ◽  
The Mean ◽  
Catecholamine Neurons

1. In rats, electrolytic lesions of the A2 group of catecholamine neurons result in lability of arterial pressure without hypertension. 2. To establish whether labile arterial pressure, when chronic, will lead to fixed hypertension, we placed lesions in the A2 area of adult male Sprague-Dawley rats and measured mean arterial pressure, heart rate and their variability (expressed as the standard deviation) 11 months later. Controls were age-matched, unoperated or sham-operated rats. 3. In rats with A2 lesions: (a) the mean arterial pressure was lower (103 ± 7.5 mmHg; n = 6; P&lt;0.05) than in sham-operated (123 ± 4.7 mmHg; n = 4) or unoperated (120 ± 3.1 mmHg; n = 9) controls; (b) the standard deviation of mean arterial pressure was higher (16 ± 1.8 mmHg; P&lt;0.001) than in sham-operated (5 ± 0.7 mmHg) or unoperated controls (7 ± 0.6 mmHg); (c) the mean and standard deviation of heart rate did not differ between groups. No histopathological changes were detected in the A2 group. 4. Chronic lability of arterial pressure does not evolve into sustained hypertension nor does it induce systemic lesions.

Physiological elevation in plasma angiotensinogen increases blood pressure

2001 ◽  
Vol 281 (5) ◽  
pp. R1437-R1441 ◽  
Author(s):  
Christoph P. R. Klett ◽  
Joey P. Granger
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Femoral Vein ◽  
Formation Rate ◽  
Plasma Concentrations ◽  
Sprague Dawley ◽  
Arterial Blood

Hepatic angiotensinogen secretion is controlled by a complex pattern of physiological or pathophysiological mediators. Because plasma concentrations of angiotensinogen are close to the Michaelis-Menten constant, it was hypothesized that changes in circulating angiotensinogen affect the formation rate of ANG I and ANG II and, therefore, blood pressure. To further test this hypothesis, we injected purified rat angiotensinogen intravenously in Sprague-Dawley rats via the femoral vein and measured mean arterial blood pressure after arterial catheterization. In controls, mean arterial pressure was 131 ± 2 mmHg before and after the injection of vehicle (sterile saline). The injection of 0.8, 1.2, and 2.9 mg/kg angiotensinogen caused a dose-dependent increase in mean arterial blood pressure of 8 ± 0.4, 19.3 ± 2.1, and 32 ± 2.4 mmHg, respectively. In contrast, the injection of a purified rabbit anti-rat angiotensinogen antibody (1.4 mg/kg) resulted in a significant decrease in mean arterial pressure (−33 ± 3.2 mmHg). Plasma angiotensinogen increased to 769 ± 32, 953 ± 42, and 1,289 ± 79 pmol/ml, respectively, after substrate and decreased by 361 ± 28 pmol/ml after antibody administration. Alterations in plasma angiotensinogen correlated well with changes in plasma renin activity. In summary, variations in circulating angiotensinogen can result in changes in blood pressure. In contrast to renin, which is known as a tonic regulator for the generation of ANG I, angiotensinogen may be a factor rather important for long-term control of the basal activity of the renin-angiotensin system.

Abstract P170: Visit-to-visit Blood Pressure Variability Is Associated With Functional Decline In Older Adults: The S.ages Cohort

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Laure Rouch ◽  
Jean-Sébastien Vidal ◽  
Olivier Hanon
Keyword(s):  
Blood Pressure ◽  
Older Adults ◽  
Standard Deviation ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pulse Pressure ◽  
Daily Living ◽  
Blood Pressure Variability ◽  
Functional Decline ◽  
Over Time

Objective: To investigate the impact of visit-to-visit systolic, diastolic, mean arterial pressure and pulse pressure variability on functional decline in non-institutionalized patients aged ≥ 65 years. Methods: 3042 subjects from the S.AGES (elderly subjects) cohort underwent clinical examinations every 6 months during 3 years. Systolic, diastolic, mean arterial pressure and pulse pressure variability were evaluated using standard deviation, coefficient of variation, average real variability, successive variation, variation independent of mean and residual standard deviation. Functional decline was assessed using the Activities of Daily Living (ADL) and Instrumental Activities of Daily Living (IADL) scales and defined over time as any help required to perform at least one task. Cox proportional hazards models were used for the analyses. Results: Among the 3042 subjects, 527 (17.3%) had functional decline (ADL) over time. After adjustment for demographics, systolic blood pressure, antihypertensive drugs, coronary artery disease, diabetes mellitus, chronic heart failure, atrial fibrillation, transient ischemic attack or stroke, smoking, dyslipidemia and Mini Mental State Examination at baseline, higher systolic blood pressure variability was associated with greater risk of functional decline (ADL) (adjusted HR per 1-SD increase of coefficient of variation = 1.12, 95% CI [1.03-1.22], p<0.01). Similar results were observed for diastolic blood pressure variability (adjusted HR = 1.11, 95% CI [1.01-1.22], p=0.03) and mean arterial pressure variability (adjusted HR = 1.15, 95% CI 1.05-1.25, p<0.01). Higher pulse pressure variability was no longer significantly associated with functional decline after adjustment for age (p=0.6). Similar patterns were found with all indicators of variability and loss of autonomy defined using IADL. Conclusion: Higher blood pressure variability could be a novel risk factor for functional decline and controlling blood pressure instability a promising interventional target in preserving autonomy in older adults.

scholarly journals Influence of testosterone on mean arterial pressure: A physiological study in male and female normotensive WKY and hypertensive SHR rats

2017 ◽  
Vol 104 (1) ◽  
pp. 25-34 ◽  
Author(s):  
SY Loh ◽  
N Salleh
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Testosterone Level ◽  
Female Rats ◽  
Plasma Testosterone ◽  
Shr Rats ◽  
Intact Female ◽  
Plasma Testosterone Level ◽  
Male And Female

Introduction Testosterone plays an important role in the blood pressure regulation. However, information with regard to the effect of this hormone on blood pressure in normotensive and hypertensive conditions is limited. Therefore, in this study, the relationship between plasma testosterone level and mean arterial pressure (MAP) was investigated under these conditions. Methods Normotensive Wistar-Kyoto (WKY) and hypertensive Spontaneous Hypertensive (SHR) male and female rats were gonadectomized with female rats treated with testosterone. Estrous cycle stages of intact female rats of both strains were identified by vaginal smear. Pressure in the carotid artery of anesthetized rats was measured via direct cannulation technique. The blood was withdrawn for plasma testosterone level measurement by enzyme-linked immunosorbent assay. Results Treatment of ovariectomized female WKY and SHR rats with testosterone for 6-week duration has resulted in MAP to increase (P < 0.05). In male WKY and SHR rats, MAP and plasma testosterone levels decreased by orchidectomy (P < 0.05). No significant differences in MAP and plasma testosterone levels were observed in intact female WKY and SHR rats between stages of the estrous cycle. Conclusions The effects seen in testosterone-treated ovariectomized female rats and in orchidectomized male rats suggested that testosterone could play an important role in causing the blood pressure to increase.

Blood Pressure Variability in Man: Its Relation to High Blood Pressure, Age and Baroreflex Sensitivity

1980 ◽  
Vol 59 (s6) ◽  
pp. 401s-404s ◽  
Author(s):  
G. Mancia ◽  
A. Ferrari ◽  
L. Gregorini ◽  
G. Parati ◽  
G. Pomidossi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Standard Deviation ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Blood Pressure Variability ◽  
Baroreflex Sensitivity ◽  
Variation Coefficient ◽  
Arterial Blood ◽  
Normotensive Subjects

1. Intra-arterial blood pressure and heart rate were recorded for 24 h in ambulant hospitalized patients of variable age who had normal blood pressure or essential hypertension. Mean 24 h values, standard deviations and variation coefficient were obtained as the averages of values separately analysed for 48 consecutive half-hour periods. 2. In older subjects standard deviation and variation coefficient for mean arterial pressure were greater than in younger subjects with similar pressure values, whereas standard deviation and variation coefficient for heart rate were smaller. 3. In hypertensive subjects standard deviation for mean arterial pressure was greater than in normotensive subjects of similar ages, but this was not the case for variation coefficient, which was slightly smaller in the former than in the latter group. Normotensive and hypertensive subjects showed no difference in standard deviation and variation coefficient for heart rate. 4. In both normotensive and hypertensive subjects standard deviation and even more so variation coefficient were slightly or not related to arterial baroreflex sensitivity as measured by various methods (phenylephrine, neck suction etc.). 5. It is concluded that blood pressure variability increases and heart rate variability decreases with age, but that changes in variability are not so obvious in hypertension. Also, differences in variability among subjects are only marginally explained by differences in baroreflex function.

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