Effect of removal of adventitia on vascular smooth muscle contraction and relaxation

2001 ◽  
Vol 280 (6) ◽  
pp. H2876-H2881 ◽  
Author(s):  
M. C. González ◽  
S. M. Arribas ◽  
F. Molero ◽  
M. S. Fernández-Alfonso
Keyword(s):  
Vascular Function ◽  
Smooth Muscle Contraction ◽  
Isometric Tension ◽  
Organ Bath ◽  
Sprague Dawley ◽  
Iliac Arteries ◽  
Sprague Dawley Rats ◽  
The Media ◽  
Vascular Smooth Muscle Contraction ◽  
Contraction And Relaxation

The aim of the present study was to determine whether the adventitia of large arteries modulates vascular function. We developed a method to obtain functional vascular rings devoid of adventitia. Carotid and iliac arteries from 3-mo-old Sprague-Dawley rats were denuded from adventitia after treatment with collagenase followed by gentle peeling. Adventitia removal and integrity of the media was demonstrated by optical and confocal microscopy. Arterial rings with or without adventitia and with or without endothelium were mounted in an organ bath for isometric tension recording. Responses to 75 mM KCl or norepinephrine (0.1 nM–1 μM) were significantly reduced in segments without adventitia. Acetylcholine-induced relaxation (0.1 μM–0.1 mM) was enhanced in arteries without adventitia, whereas sodium nitroprusside-induced responses were not modified. These results demonstrate that the combination of stripping with a previous collagenase treatment allows us to obtain functional rings devoid of adventitia and that this layer plays a role in contractile capacity and in endothelium-modulated responses.

scholarly journals Optimal Wire Myography Normalization for the Rat Dorsal Penile, Internal Pudendal and Internal Iliac Arteries

2021 ◽  
pp. 931-937
Author(s):  
T.A. Azeez ◽  
M.R. Andrade ◽  
J.D. La Favor
Keyword(s):  
Force Production ◽  
Sprague Dawley ◽  
Internal Pudendal Artery ◽  
Initial Tension ◽  
Iliac Arteries ◽  
Penile Artery ◽  
Sprague Dawley Rats ◽  
Internal Iliac ◽  
Contraction And Relaxation ◽  
Internal Iliac Arteries

In functional arterial studies using wire myography, the determination of a vessel’s standardized normalization factor (factor k) is an essential step to ensure optimal contraction and relaxation by the arteries when stimulated with their respective vasoactive agents and to obtain reproducible results. The optimal factor k for several arteries have been determined; however, the optimal initial tension and factor k for the arteries involved in erection remains unknown. Hence, in the present study we set out to determine the optimal factor k for the internal iliac artery, proximal and distal internal pudendal artery (IPA), and dorsal penile artery. After isolating, harvesting, and mounting the arteries from male Sprague-Dawley rats on a multi wire myograph, we tested arterial responsivity to high K+-stimulation when the factor k was set at 0.7, 0.8, 0.85, 0.9, 0.95, 1.0, 1.1, and 1.2 to determine the factor k setting that results in the greatest K+-induced active force production for each vessel type. The data showed the optimal factor k is 0.90-0.95 for the dorsal penile, distal internal pudendal and internal iliac arteries while it is 0.85-0.90 for proximal internal pudendal artery. These optimal values corresponded to initial passive tension settings of 1.10±0.16 - 1.46±0.23, 1.28±0.20 - 1.69±0.34, 1.03±0.27 - 1.33±0.31, and 1.33±0.31 - 1.77±0.43 mN/mm for the dorsal penile, distal IP, proximal IP, and internal iliac arteries, respectively.

Abstract P214: The Non-canonical Stress Tolerance Cascade for Toll-like Receptor 9 in the Vasculature Signals Through Liver Kinase B1

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Cameron G McCarthy ◽  
Camilla F Wenceslau ◽  
Safia Ogbi ◽  
Theodora Szasz ◽  
R.Clinton Webb
Keyword(s):  
Protein Kinase ◽  
Stress Tolerance ◽  
Vascular Function ◽  
Cytosolic Calcium ◽  
Toll Like Receptor ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Liver Kinase B1 ◽  
Tlr9 Activation

Toll-like receptor (TLR)9 is a pattern recognition receptor of the innate immune system. Recently, a non-canonical stress tolerance pathway has been reported for TLR9 in non-immune cells (cardiomyocytes and neurons), independent of inflammatory signaling. It was observed that TLR9 inhibited sarco/endoplasmic reticulum Ca 2+ -ATPase (SERCA)2, increasing cytosolic calcium, and resulting in 5’ AMP-activated protein kinase (AMPK)α activation. In our laboratory, we have reported that TLR9 treatment in vivo causes arterial dysfunction that contributes to the pathogenesis of hypertension and that these phenotypes occurred in conjunction with vascular AMPKα phosphorylation (Thr172). However, whether a dysregulation in calcium homeostasis via the non-canonical stress tolerance cascade underlies the impaired vascular function after TLR9 stimulation needs to be clarified. We hypothesized that TLR9 activation would inhibit SERCA2 activity in the vasculature. SERCA2 activity was assessed using a luciferase-based ATP quantification kit. Microsomes were isolated from pooled aortae of Sprague-Dawley rats and subjected to treatment with either Vehicle (Veh) or ODN2395 (2 μM), with or without a SERCA2 inhibitor (thapsigargin; 1 μM). The presence of thapsigargin increased ATP concentrations similarly in both Veh and ODN2395 [ATP (μM), Veh: 19±3 vs. Veh+thapsigargin: 140±35; ODN2395: 22±9 vs. ODN2395+thapsigargin: 129±12, both p<0.05], suggesting TLR9 activation did not inhibit SERCA2 activity. Next, MRA from Sprague-Dawley rats were divided into three sections for Western blot analysis of AMPKα-activating kinases, specifically calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2) and liver kinase B1 (LKB1). ODN2395 alone did not increase protein expression of phospho-CaMKK2 Ser511 (p>0.05), again suggesting calcium-independent activation of AMPKα. However, ODN2395 did increase phospho-LKB1 Ser428 (3.8 fold vs. Veh, p<0.05), and this increase in expression was inhibited by pre-incubation with TLR9 antagonist ODN2088 (20 μM) (p>0.05). These results suggest that the TLR9 non-canonical stress tolerance pathway in the vasculature is mediated by LKB1, and not SERCA2 inhibition.

SYNTHESIS OF DNA AND LECITHIN IN TISSUE CULTURE AND OESTROGEN RECEPTOR ACTIVITY IN RAT MAMMARY TUMOURS DEPENDENT ON AND INDEPENDENT OF THE OVARY

1979 ◽  
Vol 81 (2) ◽  
pp. 183-198 ◽  
Author(s):  
ANNE-MARIE SCOTT ◽  
SUSAN MURPHY ◽  
R. A. HAWKINS
Keyword(s):  
Tissue Culture ◽  
Dna Synthesis ◽  
Oestrogen Receptor ◽  
Receptor Activity ◽  
Sprague Dawley ◽  
Mammary Tumours ◽  
Sprague Dawley Rats ◽  
The Media

Dimethylbenz(a)anthracene (DMBA)-induced and transplanted rat mammary tumours (2 lines) were examined for oestrogen receptor activity, and for sensitivity to hormones in vivo (by ovariectomy) and in vitro (by tissue culture). In vivo, the growth of all tumours induced by the administration of DMBA in random-bred Sprague–Dawley rats was found to be dependent on the ovary, whilst in all transplanted tumours (12 TG-3 and six TG-5 lines), maintained in an inbred strain of Sprague–Dawley rats, growth was found to be independent of the ovary. In vitro, the capacity for DNA synthesis in DMBA-induced tumours was better maintained after 24 h when insulin (10 μg/ml) and corticosterone (5 μg/ml) or insulin, corticosterone and prolactin (each 5 μg/ml) were present in the medium (five out of 12 and eight out of 11 tumours respectively); no effect of hormones in the media was detected after 48 h. In the transplanted tumours, no effect of hormones on DNA synthesis was detected after either 24 or 48 h of culture. Synthesis of lecithin was not detectably influenced by the presence of hormones in either DMBA-induced or transplanted tumours. Oestrogen receptor concentrations were, on average, significantly higher in the DMBA-induced tumours than in either line of transplanted tumour. For 22 DMBA-induced tumours and 15 transplanted tumours, the effect of hormones in vitro (`response') was directly correlated with receptor concentration at time 0 (Spearman's ρ = + 0·59) and inversely correlated with the rate of DNA synthesis (`basal') at time 0 (Spearman's ρ = −0·62). No single parameter or pair of parameters permitted accurate distinction between the tumour types.

Inhibitory effect of interleukin-6 on vascular smooth muscle contraction

1994 ◽  
Vol 266 (3) ◽  
pp. H898-H902 ◽  
Author(s):  
F. Ohkawa ◽  
U. Ikeda ◽  
K. Kawasaki ◽  
E. Kusano ◽  
M. Igarashi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Contraction ◽  
Interleukin 6 ◽  
Smooth Muscle Contraction ◽  
Inhibitory Effect ◽  
Sprague Dawley ◽  
Intracellular Cgmp ◽  
Dependent Relationship ◽  
Vascular Smooth Muscle Contraction

Our objective was to investigate the direct effect of interleukin-6 (IL-6) on the vascular smooth muscle contraction. We measured the contraction of endothelium-denuded aortic rings isolated from Sprague-Dawley rats. We also investigated the involvement of vasodilator prostaglandin and guanosine 3',5'-cyclic monophosphate (cGMP) productions in the effect of IL-6 using cultured rat vascular smooth muscle cells (VSMC). Exposing the aortic rings to recombinant murine IL-6 (50 U/ml) for 180 min significantly suppressed the phenylephrine (10(-9)-10(-5) M)-induced contraction. This inhibitory effect of IL-6 on the contraction tended to exhibit a dose-dependent relationship (0.5-50 U/ml). The effect of IL-6 was totally eliminated in the presence of indomethacin (10(-5) M). The release of immunoreactive 6-ketoprostaglandin F1 alpha from cultured rat VSMC was significantly increased by exposure to IL-6. Intracellular cGMP concentration in VSMC was not affected by IL-6. In conclusion, IL-6 is a potent inhibitor of the alpha-adrenergic-stimulated contraction of vascular smooth muscle. Its action is endothelium independent and mediated by the increased synthesis of prostacyclin in VSMC.

Sexual dimorphism in vasopressin-induced contraction of rat aorta

1991 ◽  
Vol 260 (2) ◽  
pp. H453-H458 ◽  
Author(s):  
J. N. Stallone ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Estrous Cycle ◽  
Vascular Reactivity ◽  
Rat Aorta ◽  
Isometric Tension ◽  
Female Rats ◽  
Male Rats ◽  
Maximal Response ◽  
Sprague Dawley ◽  
Tension Development ◽  
Sprague Dawley Rats

Previously, we reported that, in the rat, pressor responsiveness to vasopressin (VP) is higher in males than in females during most phases of the estrous cycle. To explore the role of the vasculature in this phenomenon, we examined vascular reactivity to VP in thoracic aortas of male rats and female rats during each phase of the estrous cycle. Aortic rings were prepared from age-matched male and female Sprague-Dawley rats and mounted for isometric tension recording. Maximal response of female aortas to VP (4,246 +/- 163 mg/mg ring dry wt) was more than twice (P less than 0.001) that of male aortas (1,877 +/- 215 mg/mg ring wt). Sensitivity of female aortas to VP was substantially higher (P less than 0.001) than that of male aortas (EC50: 10.9 +/- 0.7 vs. 19.0 +/- 1.6 nM, respectively). Maximal rate of tension development (dT/dtmax) during contraction with VP was nearly twofold higher (P less than 0.01) in female aortas (536 +/- 23 mg/min) than in male aortas (300 +/- 19 mg/min). Maximal response, sensitivity, and dT/dtmax of female aortas did not vary significantly during the estrous cycle. Maximal response of female aortas to phenylephrine (PE; 1,251 +/- 93 mg/mg ring wt) was half that (P less than 0.001) of male aortas (2,546 +/- 194 mg/mg ring wt); sensitivity to PE did not differ significantly (EC50: 0.33 +/- 0.02 vs. 0.38 +/- 0.06 microM, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Chronic Ingestion of High Dosed Phikud Navakot Extraction Induces Mesangiolysis in Rats with Alteration of AQP1 and Hsp60 Expressions

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Kanchana Kengkoom ◽  
Sumate Ampawong
Keyword(s):  
Vascular Function ◽  
Cell Damage ◽  
Protective Role ◽  
Histopathological Study ◽  
High Dose ◽  
Sprague Dawley ◽  
Endothelial Lining ◽  
Sprague Dawley Rats ◽  
Aqp1 Expression ◽  
Chronic Ingestion

Phikud Navakot (PN) is commonly used in Thai traditional medicine for alleviation of cardiovascular and cerebrovascular symptoms; however little is known about the chronic toxicity effects of the extracts from the herbs in PN. Repeated extraction doses of 10, 100, and 1,000 mg/kg/day were randomly administered to both male and female Sprague Dawley rats for 12 months. Histopathological study revealed that mesangiolysis was predominately found at the highest dose. Aquaporin 1 (AQP1) expression in the mesangiolytic glomeruli was significantly lower than in the intact glomeruli. This may be relevant to an imbalance of vascular function manifested by AQP1 alteration. In the mesangiolytic glomeruli, 60 kDa heat shock protein (Hsp60) was significantly upregulated on the endothelial lining cells of aneurysm and vascular cyst. Hsp60 increase may be related to endothelial cell damage due to its intracellular protective role. Blood urea nitrogen and creatinine levels remained within their normal range indicating well-functioning renal reserve function. In conclusion, high dosed PN may affect the endothelium leading to inability of vascular permeability and consequence to mesangiolysis. Our results suggest that only a high dose of chronic oral administration of PN is relatively toxic in association with mesangiolysis. The NOAEL was determined to be 100 mg/kg/day.

Endothelial vasoconstrictor prostanoids modulate contractions to acetylcholine and ANG II in Ren-2 rats

1997 ◽  
Vol 272 (1) ◽  
pp. H493-H500 ◽  
Author(s):  
G. Noll ◽  
M. G. Lang ◽  
M. R. Tschudi ◽  
D. Ganten ◽  
T. F. Luscher
Keyword(s):  
Angiotensin Ii ◽  
Vascular Function ◽  
Tissue Perfusion ◽  
Isometric Tension ◽  
Sprague Dawley ◽  
Resistance Arteries ◽  
Angiotensin I ◽  
Transgenic Rats ◽  
Endothelin 1 ◽  
Thromboxane Receptor Antagonist

We investigated vascular function in mouse Ren-2 transgenic rats with hypertension. Mesenteric resistance arteries of transgenic and Sprague-Dawley rats (controls) were isolated at ages 6 and 12 wk and suspended in myographs for isometric tension recording. Systolic blood pressure was higher in transgenic than control rats (P < 0.05). Contractions to norepinephrine and endothelin-1 were comparable in transgenic and control rats, but the sensitivity decreased with age in both strains (P < 0.05). Contractions to angiotensin I were comparable in 6-wk-old transgenic rats and controls, but the response to angiotensin I was more pronounced in transgenic rats at 12 wk of age. Contractions to angiotensin II were higher in transgenic rats and decreased with age in both strains. Preincubation with the cyclooxygenase inhibitor meclofenamate or the thromboxane receptor antagonist SQ-30741 blunted the response only in 6-wk-old transgenic rats. In quiescent vascular rings, acetylcholine evoked endothelium-dependent contractions after inhibition of nitric oxide formation by N omega-nitro-L-arginine methyl ester only in transgenic rats. These contractions were inhibited by SQ-30741 (P < 0.05) but not by the thromboxane synthase inhibitor CGS-13080. Contractions to the thromboxane analogue U-46619 were comparable in both strains at the age of 6 wk; sensitivity was increased in transgenic rats at 12 wk (P < 0.05). In conclusion, in mesenteric resistance arteries of Ren-2 transgenic rats I) contractions to angiotensin I and II but not to norepinephrine and endothelin-1 are increased, and 2) acetylcholine as well as angiotensin II modulate endothelium-dependent contractions mediated by prostaglandin H2. These alterations together with increased sensitivity to thromboxane could contribute to maintenance as well as to impaired tissue perfusion of this form of hypertension.

Effect of pioglitazone on vascular reactivity in vivo and in vitro

1996 ◽  
Vol 270 (3) ◽  
pp. R660-R666 ◽  
Author(s):  
T. A. Kotchen ◽  
H. Y. Zhang ◽  
S. Reddy ◽  
R. G. Hoffmann
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
Vascular Function ◽  
Vascular Reactivity ◽  
Sprague Dawley ◽  
Vasoactive Agents ◽  
Sprague Dawley Rats ◽  
Pressor Responses

Pioglitazone (a thiazolidinedione derivative) increases insulin sensitivity and prevents hypertension in the Dahl-salt-sensitive (S) rat. The present study was undertaken to determine if pioglitazone modulates pressor responsiveness to vasoactive agents, both in vivo and in vitro. In vivo, pretreatment with pioglitazone inhibited (P < 0.02) pressor responses to both norepinephrine and angiotensin II in conscious Dahl-S, but not in Sprague-Dawley rats. In vitro, pioglitazone augmented the capacity of insulin to inhibit pressor responses of strips of thoracic aortas to norepinephrine, but not to angiotensin. Additionally, in vitro, incubation with insulin plus pioglitazone augmented acetylcholine-induced, but not nitroprusside-induced vasodilation. Pioglitazone pretreatment increased (P < 0.001) in vitro insulin-stimulated glucose uptake in adipose tissue, but not in thoracic aortas of Dahl-S. We hypothesize that pioglitazone attenuates hypertension by modulating the effects of insulin on vascular function, resulting in both blunted vasoconstriction and augmented acetylcholine-induced vasodilation. These alterations are not accounted for by an effect of pioglitazone on glucose uptake by vascular smooth muscle.

scholarly journals Clinically relevant concentrations of dexmedetomidine may reduce oxytocin-induced myometrium contractions in pregnant rats

2020 ◽  
Vol 15 (4) ◽  
pp. 451-458
Author(s):  
Dong Joon Kim ◽  
Young Joon Ki ◽  
Bo Hyun Jang ◽  
Seongcheol Kim ◽  
Sang Hun Kim ◽  
...  
Keyword(s):  
Complete Loss ◽  
Organ Bath ◽  
Dependent Manner ◽  
Active Tension ◽  
Sprague Dawley ◽  
Concentration Dependent Manner ◽  
Pregnant Rats ◽  
Uterine Contractions ◽  
Sprague Dawley Rats ◽  
High Doses

Background: Recently, there have been some trials to use dexmedetomidine in the obstetric field but concerns regarding the drug include changes in uterine contractions after labor. We aimed to evaluate the effects of dexmedetomidine on the myometrial contractions of pregnant rats.Methods: In a pilot study, the contraction of the myometrial strips of pregnant Sprague-Dawley rats in an organ bath with oxytocin at 1 mU/ml was assessed by adding dexmedetomidine from 10-6 to 10-2 M accumulatively every 20 min, and active tension and the number of contractions were evaluated. Then, changes in myometrial contractions were evaluated from high doses of dexmedetomidine (1.0 × 10−4 to 1.2 × 10−3 M). The effective concentrations (EC) for changes in uterine contractions were calculated using a probit model.Results: Active tension and the number of contractions were significantly decreased at 10-3 M and 10-4 M dexmedetomidine, respectively (P < 0.05). A complete loss of contractions was seen at 10-2 M. Dexmedetomidine (1.0 × 10−4 to 1.2 × 10−3 M) decreased active tension and the number of contractions in a concentration-dependent manner. The EC95 of dexmedetomidine for inhibiting active tension and the number of contractions was 5.16 × 10-2 M and 2.55 × 10-5 M, respectively.Conclusions: Active tension of the myometrium showed a significant decrease at concentrations of dexmedetomidine higher than 10-3 M. Thus, clinical concentrations of dexmedetomidine may inhibit uterine contractions. Further research is needed for the safe use of dexmedetomidine in the obstetrics field.

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