Magnesium supplementation and deoxycorticosterone acetate – salt hypertension: effect on arterial mechanical properties and on activity of endothelin-1

2002 ◽  
Vol 80 (6) ◽  
pp. 553-561 ◽  
Author(s):  
Nathalie Berthon ◽  
Pascal Laurant ◽  
Daniel Hayoz ◽  
Dominique Fellmann ◽  
Hans R Brunner ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Vessels ◽  
Carotid Arteries ◽  
Peripheral Resistance ◽  
Mesenteric Arteries ◽  
Lumen Diameter ◽  
Magnesium Supplementation ◽  
Endothelin 1 ◽  
Acetate Salt ◽  
Salt Hypertension

The aim of this study was to show whether the decrease in blood pressure induced by Mg supplementation in deoxycorticosterone acetate – salt (DOCA–salt) hypertensive rats is associated with mechanical modifications of blood vessels and (or) changes in tissular production and (or) vasoconstrictor activity to endothelin-1. DOCA–salt treatment increased blood pressure, media thickness, cross-sectional area, and lumen diameter of carotid arteries. Distensibility and incremental elastic modulus versus stress were not altered in carotid arteries, suggesting that the DOCA–salt vessel wall adapts structurally to preserve its blood pressure buffering capacity. Magnesium supplementation attenuated DOCA–salt hypertension. In comparison with normotensive rats, systolic, mean, and pulse pressures were higher whereas diastolic pressure was not different in Mg-supplemented DOCA-salt rats. Magnesium supplementation did not significantly modify the elastic parameters of carotid arteries. In resistance mesenteric arteries, DOCA–salt hypertension induces an inward hypertrophic remodeling. Magnesium supplementation attenuates wall hypertrophy and increases lumen diameter to the normotensive diameter, suggesting a decrease in peripheral resistance. Magnesium supplementation normalizes the altered vasoconstrictor activity of endothelin-1 in mesenteric arteries and attenuates endothelin-1 overproduction in kidney, left ventricle, and aorta of DOCA-salt rats. These findings suggest that Mg supplementation prevents blood pressure elevation by attenuating peripheral resistance and by decreasing hypertrophic effect of endothelin-1 via inhibition of endothelin-1 production.Key words: hypertension, resistance, distensibility, blood vessels, magnesium.

Endothelin-1 expression in blood vessels of DOCA-salt hypertensive rats treated with the combined ETA/ETB endothelin receptor antagonist bosentan

1995 ◽  
Vol 73 (3) ◽  
pp. 390-398 ◽  
Author(s):  
Richard Larivière ◽  
Pavol Sventek ◽  
Gaétan Thibault ◽  
Ernesto L. Schiffrin
Keyword(s):  
Gene Expression ◽  
Blood Pressure ◽  
Receptor Antagonist ◽  
Blood Vessels ◽  
Thoracic Aorta ◽  
Mesenteric Arteries ◽  
Endothelin Receptor ◽  
Hypertensive Rats ◽  
Endothelin 1 ◽  
Wet Weight

In previous studies it has been shown that blood vessels of deoxycorticosterone acetate (DOCA) salt hypertensive rats present significantly higher immunoreactive ET-1 (ir-ET-1) content and increased ET-1 gene expression. DOCA-salt hypertensive rats respond to treatment with the combined ETA/ETB endotheiin receptor antagonist bosentan with lowering of blood pressure. In the present study, we investigated the ir-ET-1 levels and the expression of the ET-1 gene in blood vessels of DOCA-salt hypertensive rats treated or not treated with bosentan. Blood pressure was significantly lower in bosentan-treated rats (185 ± 6 mmHg; 1 mmHg = 133.3 Pa) compared with DOCA-salt hypertensive rats (203 ± 4 mmHg; p < 0.01). Plasma ir-ET-1 concentration was slightly but significantly elevated (p < 0.01) in DOCA-salt hypertensive rats compared with uninephrectomized control rats, and was further increased (p < 0.01) in bosentan-treated rats. The tissue wet weight and ir-ET-1 content of segments of thoracic aorta were significantly increased (p < 0.01) in DOCA-salt hypertensive rats in comparison with control rats, but were similar in bosentan-treated DOCA-salt rats. The abundance of ET-1 mRNA measured by Northern blot analysis in thoracic aorta and the ir-ET-1 content were attenuated by bosentan treatment. Tissue wet weight and ir-ET-1 content in the mesenteric vascular bed were similar in bosentan-treated and -untreated DOCA-salt rats, and were significantly higher in both groups than in control rats (p < 0.01). ET-1 mRNA levels were increased in mesenteric arteries of DOCA-salt hypertensive rats and were further enhanced by bosentan treatment. These data suggest that inhibition of ETA and ETB receptor mediated ET-1 responses by bosentan has a slight but beneficial effect on blood pressure of DOCA-salt hypertensive rats. Chronic blockade of both ET receptors results in increased circulating levels of ET-1 and attenuated ET-1 expression and vascular hypertrophy in aorta but not in the mesenteric vasculature. ET-1 may be involved in the maintenance of elevated blood pressure in DOCA-salt hypertension and perhaps other experimental models of hypertension in the rat in part through a vascular hypertrophic effect.Key words: endothelin-1, endothelin receptor antagonist, aorta, mesenteric arteries, immunoreactive ET-1, preproET-1 mRNA, gene expression.

Abstract P222: Venous Dilation Contributes to 5-HT-induced Hypotension

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Bridget M Seitz ◽  
Teresa Krieger-Burke ◽  
Stephanie W Watts
Keyword(s):  
Blood Pressure ◽  
Imaging System ◽  
Isometric Force ◽  
Peripheral Resistance ◽  
Vena Cava ◽  
Mesenteric Arteries ◽  
Conscious Rat ◽  
Cross Sectional ◽  
Induced Hypotension ◽  
Vascular Bed

Serotonin (5-hydroxytryptamine, 5-HT) infusion in a normal conscious rat decreases mean arterial pressure (MAP), in part by reduction in total peripheral resistance. Microsphere experiments have shown 5-HT increases blood flow within the splanchnic vascular bed, with the greatest being in the intestine and spleen. Interestingly, 5-HT does not cause a direct relaxation of resistant (small or large) mesenteric arteries. The present study addresses the possibility of the venous circulation contributing to the 5-HT induced fall in blood pressure. Our working hypothesis is venous dilation, specifically dilation of veins measurable within the splanchnic vascular bed, contributes to 5-HT-induced hypotension. Using an ultrasound imaging system (Vevo 2100 imaging system; 21 MHz probe,Visual Sonics Inc.), telemetry-implanted, anesthetized male Sprague Dawley rats underwent cross-sectional imaging which was controlled for respiration and cardiac cycles. The following vessels were imaged: abdominal aorta (AA); portal vein (PV); abdominal inferior vena cava (IVC); and superior mesenteric vein (SMV). Following the collection of baseline MAP and vessel diameter measurements, Alzet osmotic mini-pumps containing vehicle (saline; n=9) or 5-HT (25 ug/kg/min; n=9) were implanted for 1 week. After, 24 hours of infusion, 5-HT increased the vein diameter (SMV 17.48±2%; PV 17.67±2%; IVC 46.87±8%) and maintained the AA diameter ( AA 0.93±1%) from baseline while reducing MAP (vehicle 101.93±3; 5-HT 84.68±2 mm Hg; p<0.05).One-week post removal of all osmotic mini-pumps, there was no difference in the MAP or diameter of all noted vessels between the two treatment groups. To correlate with in vivo findings, the PV and IVC, when isolated in a tissue bath for measurement of isometric force and contracted with endothelin 1, relaxed in a concentration dependent fashion to 5-HT and 5-carboxamidotryptamine (5-HT 1/7 receptor agonist;1 nM-10 uM). Collectively, these findings highlight the contribution of splanchnic venous dilation in 5-HT-induced hypotension and propose a possible mechanism for 5-HT reduction in blood pressure.

scholarly journals Dependence of the efficiency of the initial state of fosinopril structure common carotid arteries, intravascular blood flow and central hemodynamics at patients with arterial hypertension

2015 ◽  
Vol 12 (3) ◽  
pp. 30-33
Author(s):  
L V Melnikova ◽  
L F Bartosh ◽  
O A Grechishkina
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Carotid Arteries ◽  
Peak Flow ◽  
Peripheral Resistance ◽  
Initial State ◽  
Central Hemodynamic ◽  
Functional Features ◽  
The Common ◽  
Common Carotid Arteries

Aim. To study changes in structural and functional features of the common carotid arteries and central hemodynamic parameters under the influence of fosinopril at hypertensive patients depending on achieving target blood pressure.Material and methods. The study included 116 patients with essential hypertension. All patients underwent a general clinical study, an ultrasound scan of the common carotid arteries (CCA ) with the assessment of the structure and intravascular blood flow, and echocardiography with the definition of the parameters of central hemodynamic and intravascular, ambulatory blood pressure monitoring (ABPM) before the study and after 24 weeks of antihypertensive therapy angiotensin - converting enzyme fosinopril. Two groups of patients: the first group consisted of 74 people with the achievement of the targets of blood pressure (BP), the second 42 people who have not been achieved target BP levels.Results. In the first group there was a statistically significant decrease in the proportion of peripheral resistance, increased systolic index, distensibility coefficient of the common carotid arteries peak flow velocity. In the second group specific peripheral resistance was significantly increased, the thickness of the intima-media increased, decreased peak flow velocity.Conclusion. Effectiveness depends on fosinopril initial state total peripheral resistance, cardiac output, structural and functional features elastic arteries.

Activation of Two Inward Chloride Transport Systems in Rat Femoral Arterial Smooth Muscle in Deoxycorticosterone Acetate/Salt Hypertension

1997 ◽  
Vol 93 (4) ◽  
pp. 295-298 ◽  
Author(s):  
Alexander A. Harper ◽  
Julian P. L. Davis ◽  
Alan R. Chipperfield
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Membrane Potential ◽  
Systolic Blood Pressure ◽  
Chloride Transport ◽  
Transport Systems ◽  
Arterial Smooth Muscle ◽  
Deoxycorticosterone Acetate ◽  
Acetate Salt ◽  
Salt Hypertension

1. Intracellular [Cl−] ([Cl−]i) was measured with ion-selective microelectrodes in rat femoral arterial smooth muscle in normotensive controls and after the induction of deoxycorticosterone acetate/salt hypertension. 2. Linear regression of [Cl−]i and time after the induction of hypertension showed good correlation (r = 0.96) for 5–6 weeks, as [Cl−]i increased from 30 ± 1 mmol/l (mean ± SD, n = 16), to 49 ± 2 mmol/l (n = 9, P < 0.0001). 3. Arterial systolic blood pressure also increased linearly (r = 0.97) for 5–6 weeks as hypertension developed from 122 ± 1 mmHg (n = 20) to 187 ± 7 mmHg (n = 14): there was consequently a linear relationship between [Cl−]i and arterial systolic blood pressure (r = 0.96). 4. The increase in [Cl−]i was partly because Na+−K+−Cl− co-transport activity, estimated from the fall in [Cl−]i caused by bumetanide, was greater in hypertension (18 mmol/l) than in normotension (10 mmol/l). This finding, and the depolarization of the membrane potential in hypertension (−56 ± 3 mV compared with −64 ± 4 mV in normotension; P < 0.0001), confirms previous studies. 5. The increase in [Cl−]i was also partly due to greater activity of an Na+- and HCO3−-independent, acetazolamide-sensitive inward Cl− transport system; thus acetazolamide reduced [Cl−]i by 7 mmol/l in normotension and by 16 mmol/l in hypertension. 6. In Cl−-free media, the membrane potential in normotension (−59 ± 5 mV) was not significantly different from that in hypertension (−60 ± 4 mV). 7. The role of [Cl−]i in the depolarization of the membrane potential in hypertension is discussed.

scholarly journals Integrative mechanisms of blood pressure regulation in humans and rats: cross-species similarities

2010 ◽  
Vol 298 (3) ◽  
pp. R755-R759 ◽  
Author(s):  
N. Charkoudian ◽  
E. Gusman ◽  
M. J. Joyner ◽  
B. G. Wallin ◽  
J. Osborn
Keyword(s):  
Interindividual Variability ◽  
Individualized Medicine ◽  
Peripheral Resistance ◽  
Baseline Period ◽  
Sprague Dawley ◽  
Deoxycorticosterone Acetate ◽  
Hemodynamic Variables ◽  
Acetate Salt ◽  
Sprague Dawley Rats ◽  
Salt Hypertension

As our understanding of the importance of individualized medicine continues to grow, the clinical relevance of interindividual variability in hemodynamic variables is receiving increasing attention. However, it is not known whether the rat, which is often used for studies of cardiovascular regulation, exhibits similar interindividual variability. In the present study, we evaluated whether the magnitude of interindividual variability in cardiac output (CO) and total peripheral resistance (TPR) was similar in humans and in rats. We assessed interindividual variability of mean arterial pressure (MAP), CO, and TPR during control conditions in normotensive humans ( n = 40) and during normotension and deoxycorticosterone acetate-salt hypertension in Sprague-Dawley rats ( n = 16). Humans and rats showed marked interindividual variability in CO and TPR but low variability in MAP. During deoxycorticosterone acetate-salt hypertension, CO was maintained, but TPR was elevated compared with the baseline period. We conclude that the magnitudes of interindividual variability of MAP, CO, and TPR are quantitatively similar in humans and rats, providing support for the relevance of this variability in both species and suggesting that studies in rats could be designed to address questions specific to individualized medicine in hypertension.

scholarly journals Chronic V2 Vasopressin Receptor Stimulation Increases Basal Blood Pressure and Exacerbates Deoxycorticosterone Acetate-Salt Hypertension

Endocrinology ◽  
2002 ◽  
Vol 143 (7) ◽  
pp. 2759-2766 ◽  
Author(s):  
Sandrine Fernandes ◽  
Patrick Bruneval ◽  
Albert Hagege ◽  
Didier Heudes ◽  
Saïd Ghostine ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vasopressin Receptor ◽  
Receptor Stimulation ◽  
Deoxycorticosterone Acetate ◽  
Acetate Salt ◽  
Salt Hypertension ◽  
Basal Blood Pressure ◽  
V2 Vasopressin Receptor
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