Resistance artery vasodilation to magnesium sulfate during pregnancy and the postpartum state

2005 ◽  
Vol 288 (4) ◽  
pp. H1521-H1525 ◽  
Author(s):  
Anna G. Euser ◽  
Marilyn J. Cipolla
Keyword(s):  
Magnesium Sulfate ◽  
Systemic Blood Pressure ◽  
Mesenteric Arteries ◽  
Sprague Dawley ◽  
Resistance Arteries ◽  
Buffer Solution ◽  
Sprague Dawley Rats ◽  
Small Resistance ◽  
Vascular Beds ◽  
Hepes Buffer Solution

This study compared the vasodilatory responses to magnesium sulfate (MgSO4) of cerebral and mesenteric resistance arteries and determined whether the responses varied between different gestational groups. Third-order branches (<200 μm) of the posterior cerebral (PCA) and mesenteric arteries (MA) were dissected from nonpregnant (NP; n = 6), late pregnant (LP; day 19, n = 6), and postpartum (PP; day 3, n = 6) Sprague-Dawley rats. A concentration-response curve was performed by replacing the low-MgSO4 (1.2 mM) HEPES buffer solution with increasing concentrations of MgSO4 (4, 6, 8, 16, and 32 mM) and measuring lumen diameter at each concentration. All groups exhibited concentration-dependent dilation to MgSO4, decreasing the amount of tone in the vessels. However, MA were significantly more sensitive to MgSO4 than PCA. Whereas there was no difference in the response between different gestational groups in MA, the PCA from the LP and PP groups showed a significantly diminished response to MgSO4. The percent dilation at 32 mM MgSO4 for PCA versus MA in NP, LP, and PP animals was 36 ± 2 vs. 51 ± 7% ( P < 0.05), 19 ± 9 vs. 54 ± 6% ( P < 0.01 vs. PCA and NP), and 12 ± 5 vs. 52 ± 11% ( P < 0.01 vs. PCA and NP). These results demonstrate that MgSO4 is a vasodilator of small resistance arteries in the cerebral and mesenteric vascular beds. The refractory responses of the PCA in LP and PP groups demonstrate changes in the cerebrovascular vasodilatory mechanisms with gestation. The greater sensitivity of the MA to MgSO4-induced vasodilation suggests that the prophylactic effect of MgSO4 on eclamptic seizures may be more closely related to the lowering of systemic blood pressure than to an effect on cerebral blood flow.

Role of CO in attenuated vasoconstrictor reactivity of mesenteric resistance arteries after chronic hypoxia

2002 ◽  
Vol 282 (1) ◽  
pp. H30-H37 ◽  
Author(s):  
Rayna J. Gonzales ◽  
Benjimen R. Walker
Keyword(s):  
Chronic Hypoxia ◽  
Protoporphyrin Ix ◽  
Aortic Ring ◽  
Mesenteric Arteries ◽  
Zinc Protoporphyrin ◽  
Sprague Dawley ◽  
Resistance Arteries ◽  
Sprague Dawley Rats ◽  
Oxide Synthase

Chronic hypoxia (CH) is associated with a persistent reduction in systemic vasoconstrictor reactivity. Experiments on aortic ring segments isolated from CH rats suggest that enhanced vascular expression of heme oxygenase (HO) and resultant production of the vasodilator carbon monoxide (CO) may underlie this attenuated vasoreactivity after hypoxia. Similar to the aorta, small arteries from CH rats exhibit blunted reactivity; however, the regulatory role of CO in the resistance vasculature has not been established. Therefore, we examined the significance of HO activity on responsiveness to phenylephrine (PE) in the mesenteric circulation of control and CH rats. To document that the mesenteric bed demonstrates reduced reactivity after CH, we determined the vasoconstrictor responses of conscious, chronically instrumented male Sprague-Dawley rats to PE under control conditions and then immediately after exposure to 48 h CH (0.5 atm). All rats showed reduced mesenteric vasoconstriction to PE after CH. To examine the role of CO in reduced reactivity, small mesenteric arteries (100–200 μm intraluminal diameter) from control and 48-h CH rats were isolated and mounted on glass cannulas, pressurized to 60 mmHg and superfused with increasing concentrations of PE under normoxic conditions. Similar to the intact circulation, vessels from CH rats exhibited reduced vasoconstrictor sensitivity to PE compared with controls that persisted in the presence of nitric oxide synthase inhibition. The HO inhibitor, zinc protoporphyrin IX (5 μM) enhanced reactivity only in CH vessels. Additionally, a range of concentrations of the HO substrate heme-l-lysinate caused vasodilation in CH vessels but not in controls. Thus we conclude that CO contributes a significant vasodilator influence in resistance vessels after CH that may account for diminished vasoconstrictor responsiveness under these conditions.

Regional variation in resistance artery diameter responses to alpha-adrenergic stimulation during pregnancy

1993 ◽  
Vol 264 (1) ◽  
pp. H78-H85 ◽  
Author(s):  
G. D'Angelo ◽  
G. Osol
Keyword(s):  
Regional Variation ◽  
Mesenteric Arteries ◽  
Lumen Diameter ◽  
Sprague Dawley ◽  
Resistance Arteries ◽  
Adrenergic Stimulation ◽  
Uterine Arteries ◽  
Sprague Dawley Rats ◽  
Pressor Responses ◽  
Pregnant State

Whole animal pressor responses are blunted during pregnancy; yet, uterine arteries, paradoxically, become significantly more sensitive to the constrictor effects of phenylephrine (PE). The objectives herein were to investigate 1) the regional variation (uterine vs. mesenteric arteries) in dose-lumen diameter relationship to alpha-adrenergic stimulation during pregnancy, and 2) the selectivity of these sensitivity shifts for this pathway (PE vs. KCl). Lumen diameter was measured in isolated, pressurized (50 mmHg) arterial segments from age-matched virgin (nonpregnant; NP) and late pregnant (LP; days 19-20) Sprague-Dawley rats. Uterine arcuate vs. mesenteric arteries from NP rats were equally sensitive to either vasoconstrictor. Arcuate arteries from LP rats, however, were 4.5-fold more sensitive to PE (P < 0.01) compared with those from NP controls. Furthermore, diameter curves became superimposed at [PE] > or = 0.1 microM, even though initial diameter of arcuate arteries from LP rats was significantly larger (P < 0.001). Conversely, mesenteric arteries from LP rats were three-fold less sensitive to PE (P < 0.02), and the diameter curve displayed a corresponding parallel rightward shift. Pregnancy did not affect the sensitivity to KCl depolarization in either arcuate or mesenteric arteries. The percent reduction in lumen diameter to the maximum [KCl] was significantly decreased only in arcuate arteries from LP rats (P < 0.001). Thus, during pregnancy, divergent constrictor responses specific to alpha-adrenergic stimulation occur in resistance arteries from the uterine vs. splanchnic circulations. Consequently, concentrations of PE that are subthreshold in NP uterine arteries can elicit large changes in lumen diameter and thereby have a pronounced effect on uterine vascular resistance in the pregnant state.

Contribution of vasomotion to vascular resistance: a comparison of arteries from virgin and pregnant rats

1998 ◽  
Vol 85 (6) ◽  
pp. 2255-2260 ◽  
Author(s):  
Robert J. Gratton ◽  
Robin E. Gandley ◽  
John F. McCarthy ◽  
Walter K. Michaluk ◽  
Bryan K. Slinker ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Vessel Diameter ◽  
Mesenteric Arteries ◽  
Oscillatory Activity ◽  
Sprague Dawley ◽  
Resistance Arteries ◽  
Adrenergic Agonist ◽  
Pregnant Rats ◽  
Sprague Dawley Rats ◽  
Vasomotor Activity

Intrinsic oscillatory activity, or vasomotion, within the microcirculation has many potential functions, including modulation of vascular resistance. Alterations in oscillatory activity during pregnancy may contribute to the marked reduction in vascular resistance. The purpose of this study was 1) to mathematically model the oscillatory changes in vessel diameter and determine the effect on vascular resistance and 2) to characterize the vasomotion in resistance arteries of pregnant and nonpregnant (virgin) rats. Mesenteric arteries were isolated from Sprague-Dawley rats and studied in a pressurized arteriograph. Mathematical modeling demonstrated that the resistance in a vessel with vasomotion was greater than that in a static vessel with the same mean radius. During constriction with the α1-adrenergic agonist phenylephrine, the amplitude of oscillation was less in the arteries from pregnant rats. We conclude that vasomotor activity may provide a mechanism to regulate vascular resistance and blood flow independent of static changes in arterial diameter. During pregnancy the decrease in vasomotor activity in resistance arteries may contribute to the reduction in peripheral vascular resistance.

Abstract 637: Hydrogen Sulfide Acts on Endothelial Cells to Elicit Dilation.

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Nancy L Kanagy ◽  
Jessica M Osmond ◽  
Olan Jackson-Weaver ◽  
Benjimen R Walker
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Mesenteric Arteries ◽  
Direct Effects ◽  
Sprague Dawley ◽  
Imaging Studies ◽  
Knock Out ◽  
Event Frequency ◽  
Sprague Dawley Rats

Hydrogen sulfide (H 2 S), produced by the enzyme cystathionine-γ lyase (CSE), dilates arteries by hyperpolarizing and relaxing vascular smooth muscle cells (VSMC) and CSE knock-out causes hypertension and endothelial dysfunction showing the importance of this system. However, it is not clear if H 2 S-induced VSMC depolarization and relaxation is mediated by direct effects on VSMC or indirectly through actions on endothelial cells (EC). We reported previously that disrupting EC prevents H 2 S-induced vasodilation suggesting H 2 S might act directly on EC. Because inhibiting large-conductance Ca 2+ -activated K + (BK Ca ) channels also inhibits H 2 S-induced dilation, we hypothesized that H 2 S activates EC BK Ca channels to hyperpolarize EC and increase EC Ca 2+ which stimulates release of a secondary hyperpolarizing factor. Small mesenteric arteries from male Sprague-Dawley rats were used for all experiments. We found that EC disruption prevented H 2 S-induced VSMC membrane potential ( E m ) hyperpolarization. Blocking EC BK Ca channels with luminal application of the BK Ca inhibitor, iberiotoxin (IbTx, 100 nM), also prevented NaHS-induced dilation and VSMC hyperpolarization but did not affect resting VSMC E m showing EC specific actions. Sharp electrode recordings in arteries cut open to expose EC demonstrated H 2 S-induced hyperpolarization of EC while Ca 2+ imaging studies in fluor-4 loaded EC showed that H 2 S increases EC Ca 2+ event frequency. Thus H 2 S can act directly on EC. Inhibiting the EC enzyme cytochrome P 450 2C (Cyp2C) with sulfaphenazole also prevented VSMC depolarization and vasodilation. Finally, inhibiting TRPV4 channels to block the target of the Cyp2C product 11,12-EET inhibited NaHS-induced dilation. Combined with our previous report that CSE inhibition decreases BK Ca currents in EC, these results suggest that H 2 S stimulates EC BK Ca channels and activates Cyp2C upstream of VSMC hyperpolarization and vasodilation.

Dietary carbohydrates modify cardiac myosin isoenzyme profiles of semistarved rats

1989 ◽  
Vol 256 (4) ◽  
pp. R976-R981
Author(s):  
G. S. Morris ◽  
R. E. Herrick ◽  
K. M. Baldwin
Keyword(s):  
Food Restriction ◽  
Systemic Blood Pressure ◽  
Left Ventricular ◽  
Cardiac Myosin ◽  
Dietary Carbohydrates ◽  
Sprague Dawley ◽  
Myosin Isoenzyme ◽  
Sprague Dawley Rats ◽  
Serum T3

Although food restriction reduces the relative expression of the rodent cardiac myosin isoenzyme V1, the contribution of accompanying metabolic changes to the induction and maintenance of this isoenzyme shift remains unknown. Hence, this study was undertaken to determine the role of carbohydrate (CHO) utilization in the regulation of cardiac myosin isoenzyme distribution in food-restricted rats. Female Sprague-Dawley rats received either a mixed diet (55% of calories as CHO, M) or a high-carbohydrate diet (75% of calories as CHO, HC). Additional animals in each dietary group received daily injections of triiodothyronine (T3; 0.075 microgram/100 microM + T3, HC + T3). Three weeks of food restriction reduced left ventricular Ca2+-activated myofibrillar adenosinetriphosphatase activity by 24% and the relative amount of the myosin V1 isoenzyme by 57% in the M group relative to free-eating controls (P less than 0.05). In contrast, these measures were reduced by only 9 and 21%, respectively, in the HC group. Administration of T3 exerted no apparent effect on V1 expression, regardless of diet. Furthermore, the increased expression of V1 in both HC and HC + T3 groups occurred independently of changes in several measures of thyroid status including serum T3 levels, O2 consumption, heart rate, and systemic blood pressure. These results further suggest that metabolic factors, specifically those associated with CHO utilization, can influence cardiac myosin isoenzyme expression.

Chronic intermittent hypoxia alters NE reactivity and mechanics of skeletal muscle resistance arteries

2006 ◽  
Vol 100 (4) ◽  
pp. 1117-1123 ◽  
Author(s):  
Shane A. Phillips ◽  
E. B. Olson ◽  
Julian H. Lombard ◽  
Barbara J. Morgan
Keyword(s):  
Skeletal Muscle ◽  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia ◽  
Physiological Salt Solution ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Resistance Arteries ◽  
Sprague Dawley Rats ◽  
Resting Tone ◽  
Wall Distensibility

Although arterial dilator reactivity is severely impaired during exposure of animals to chronic intermittent hypoxia (CIH), few studies have characterized vasoconstrictor responsiveness in resistance arteries of this model of sleep-disordered breathing. Sprague-Dawley rats were exposed to CIH (10% inspired O2 fraction for 1 min at 4-min intervals; 12 h/day) for 14 days. Control rats were housed under normoxic conditions. Diameters of isolated gracilis muscle resistance arteries (GA; 120–150 μm) were measured by television microscopy before and during exposure to norepinephrine (NE) and angiotensin II (ANG II) and at various intraluminal pressures between 20 and 140 mmHg in normal and Ca2+-free physiological salt solution. There was no difference in the ability of GA to constrict in response to ANG II ( P = 0.42; not significant; 10−10–10−7 M). However, resting tone, myogenic activation, and vasoconstrictor responses to NE ( P < 0.001; 10−9–10−6 M) were reduced in CIH vs. controls. Treatment of rats with the superoxide scavenger 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (tempol; 1 mM) in the drinking water restored myogenic responses and NE-induced constrictions of CIH rats, suggesting that elevated superoxide production during exposure to CIH attenuates vasoconstrictor responsiveness to NE and myogenic activation in skeletal muscle resistance arteries. CIH also leads to an increased stiffness and reduced vessel wall distensibility that were not correctable with oral tempol treatment.

Hindlimb unweighting alters endothelium-dependent vasodilation and ecNOS expression in soleus arterioles

2000 ◽  
Vol 89 (4) ◽  
pp. 1483-1490 ◽  
Author(s):  
William G. Schrage ◽  
Christopher R. Woodman ◽  
M. Harold Laughlin
Keyword(s):  
Sodium Nitroprusside ◽  
Group Treatment ◽  
Day Treatment ◽  
Weight Bearing ◽  
Immunoblot Analysis ◽  
Sprague Dawley ◽  
Resistance Arteries ◽  
Protein Levels ◽  
Sprague Dawley Rats ◽  
Mrna And Protein Expression

The purpose of this study was to test the hypothesis that endothelium-dependent dilation is impaired in soleus resistance arteries from hindlimb-unweighted (HLU) rats. Male Sprague-Dawley rats (300–350 g) were exposed to HLU ( n = 14) or weight-bearing control (Con, n = 14) conditions for 14 days. After the 14-day treatment period, soleus first-order (1A) arterioles were isolated and cannulated with micropipettes to assess vasodilator responses to an endothelium-dependent dilator, ACh (10−9–10−4 M), and an endothelium-independent dilator, sodium nitroprusside (SNP, 10−9–10−4 M). Arterioles from HLU rats were smaller than Con arterioles (maximal passive diameter = 140 ± 4 and 121 ± 4 μm in Con and HLU, respectively) but developed similar spontaneous myogenic tone (43 ± 3 and 45 ± 3% in Con and HLU, respectively). Arteries from Con and HLU rats dilated in response to increasing doses of ACh, but dilation was impaired in arterioles from HLU rats ( P = 0.03), as was maximal dilation to ACh (85 ± 4 and 65 ± 4% possible dilation in Con and HLU, respectively). Inhibition of nitric oxide (NO) synthase (NOS) with N ω-nitro-l-arginine (300 μM) reduced ACh dilation by ∼40% in arterioles from Con rats and eliminated dilation in arterioles from HLU rats. The cyclooxygenase inhibitor indomethacin (50 μM) did not significantly alter dilation to ACh in either group. Treatment with N ω-nitro-l-arginine + indomethacin eliminated all ACh dilation in Con and HLU rats. Dilation to sodium nitroprusside was not different between groups ( P = 0.98). To determine whether HLU decreased expression of endothelial cell NOS (ecNOS), mRNA and protein levels were measured in single arterioles with RT-PCR and immunoblot analysis. The ecNOS mRNA and protein expression was significantly lower in arterioles from HLU rats than in Con arterioles (20 and 65%, respectively). Collectively, these data indicate that HLU impairs ACh dilation in soleus 1A arterioles, in part because of alterations in the NO pathway.

scholarly journals Vascular function in rats with adenine-induced chronic renal failure

2012 ◽  
Vol 302 (12) ◽  
pp. R1426-R1435 ◽  
Author(s):  
Lisa Nguy ◽  
Holger Nilsson ◽  
Jaana Lundgren ◽  
Maria E. Johansson ◽  
Tom Teerlink ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Vascular Function ◽  
Ex Vivo ◽  
Mesenteric Arteries ◽  
Maximal Response ◽  
Sprague Dawley ◽  
Resistance Arteries ◽  
Severe Renal Failure ◽  
Stress Markers

The aim of the present study was to characterize the function of resistance arteries, and the aorta, in rats with adenine-induced chronic renal failure (A-CRF). Sprague-Dawley rats were randomized to chow with or without adenine supplementation. After 6–10 wk, mesenteric arteries and thoracic aortas were analyzed ex vivo by wire myography. Plasma creatinine concentrations were elevated twofold at 2 wk, and eight-fold at the time of death in A-CRF animals. Ambulatory systolic and diastolic blood pressures measured by radiotelemetry were significantly elevated in A-CRF animals from week 3 and onward. At death, A-CRF animals had anemia, hyperphosphatemia, hyperparathyroidism, and elevated plasma levels of asymmetric dimethylarginine and oxidative stress markers. There were no significant differences between groups in the sensitivity, or maximal response, to ACh, sodium nitroprusside (SNP), norepinephrine, or phenylephrine in either mesenteric arteries or aortas. However, in A-CRF animals, the rate of aortic relaxation was significantly reduced following washout of KCl (both in intact and endothelium-denuded aorta) and in response to ACh and SNP. Also the rate of contraction in response to KCl was significantly reduced in A-CRF animals both in mesenteric arteries and aortas. The media of A-CRF aortas was thickened and showed focal areas of fragmented elastic lamellae and disorganized smooth muscle cells. No vascular calcifications could be detected. These results indicate that severe renal failure for a duration of less than 10 wk in this model primarily affects the aorta and mainly slows the rate of relaxation.

Effects of potassium on expression of renal sodium transporters in salt-sensitive hypertensive rats induced by uninephrectomy

2011 ◽  
Vol 300 (6) ◽  
pp. F1422-F1430 ◽  
Author(s):  
Ji Yong Jung ◽  
Sejoong Kim ◽  
Jay Wook Lee ◽  
Eun Sook Jung ◽  
Nam Ju Heo ◽  
...  
Keyword(s):  
Experimental Period ◽  
Urinary Sodium Excretion ◽  
Systemic Blood Pressure ◽  
Mixed Solution ◽  
Sprague Dawley ◽  
Sodium Transporters ◽  
Sprague Dawley Rats ◽  
Dietary Potassium ◽  
Wnk Kinases ◽  
Type 3

Dietary potassium is an important modulator of systemic blood pressure (BP). The purpose of this study was to determine whether dietary potassium is associated with an altered abundance of major renal sodium transporters that may contribute to the modulation of systemic BP. A unilateral nephrectomy (uNx) was performed in male Sprague-Dawley rats, and the rats were fed a normal-salt diet (0.3% NaCl) for 4 wk. Thereafter, the rats were fed a high-salt (HS) diet (3% NaCl) for the entire experimental period. The potassium-repleted (HS+KCl) group was given a mixed solution of 1% KCl as a substitute for drinking water. We examined the changes in the abundance of major renal sodium transporters and the expression of mRNA of With-No-Lysine (WNK) kinases sequentially at 1 and 3 wk. The systolic BP of the HS+KCl group was decreased compared with the HS group (140.3 ± 2.97 vs. 150.9 ± 4.04 mmHg at 1 wk; 180.3 ± 1.76 vs. 207.7 ± 6.21 mmHg at 3 wk). The protein abundances of type 3 Na+/H+ exchanger (NHE3) and Na+-Cl− cotransporter (NCC) in the HS+KCl group were significantly decreased (53 and 45% of the HS group at 1 wk, respectively; 19 and 8% of HS group at 3 wk). WNK4 mRNA expression was significantly increased in the HS+KCl group (1.4-fold of control at 1 wk and 1.9-fold of control at 3 wk). The downregulation of NHE3 and NCC may contribute to the BP-attenuating effect of dietary potassium associated with increased urinary sodium excretion.

scholarly journals Effects of probiotics on loperamide-induced constipation in rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takio Inatomi ◽  
Mihoko Honma
Keyword(s):  
Phosphate Buffer ◽  
Phosphate Buffer Solution ◽  
Sprague Dawley ◽  
Buffer Solution ◽  
Intestinal Transit Time ◽  
Treatment Groups ◽  
Sprague Dawley Rats ◽  
Gut Immunity ◽  
Group 3 ◽  
Group 2

AbstractThe role of probiotics in mitigating constipation, gut immunity, and gut microbiota has not been well studied. We aimed to evaluate the effects of probiotics on loperamide (LP)-induced constipation in Sprague–Dawley rats. Altogether, 150 male Sprague–Dawley rats (age 8 weeks) were used in the experiments following a 12-day acclimatisation period and were randomly divided into three treatment groups (groups 1, 2, and 3). Spastic constipation was induced via oral LP administration (3 mg/kg) for 6 days, 1 h before administering each test compound in groups 1 and 2. A probiotic solution (4 mL/kg body weight) was orally administered once a day for 6 days in group 2. In group 1, a phosphate buffer solution was orally administered once a day for 6 days, 1 h after each LP administration. In group 3, a phosphate buffer solution was orally administered once a day for 6 days. In the probiotic group, faecal parameters improved; faecal n-butyric acid, acetic acid, and IgA concentrations were increased; intestinal transit time was shortened; and disturbance of intestinal microbiota was inhibited. Our findings suggest that this probiotic was useful in improving various symptoms caused by constipation.

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