Vasorelaxant effect of 5,7,4′- Trihydroxyflavanone (Naringenin) via endothelium dependent, potassium and calcium channels in Sprague Dawley rats: Aortic ring model

2021 ◽  
pp. 109620
Author(s):  
Chu Shan Tan ◽  
Wan Yin Tew ◽  
Chen Jingying ◽  
Mun Fei Yam
Keyword(s):  
Calcium Channels ◽  
Aortic Ring ◽  
Sprague Dawley ◽  
Vasorelaxant Effect ◽  
Ring Model ◽  
Sprague Dawley Rats

scholarly journals Endothelium-Independent Relaxation of Vascular Smooth Muscle Induced by Persimmon-Derived Polyphenol Phytocomplex in Rats

Nutrients ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 89
Author(s):  
Risa Kudo ◽  
Katsuya Yuui ◽  
Shogo Kasuda
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Mesenteric Arteries ◽  
Inositol Triphosphate ◽  
Sprague Dawley ◽  
Vasorelaxant Effect ◽  
Sprague Dawley Rats ◽  
The Mean ◽  
Artery Disease ◽  
Nitric Oxide Pathway

The vasorelaxant effect of polyphenols is well known, and the mortality rate due to coronary artery disease is low in people who consume polyphenol-containing foods. We aimed to elucidate the mechanism by which polyphenols derived from persimmon juice (PJ) and persimmon leaves (PLs) induce vasorelaxation and suppress vasocontraction in the superior mesenteric arteries isolated from male Sprague Dawley rats. Vasocontraction was induced with 1 µM phenylephrine, and polyphenol-induced vasorelaxation was expressed as a percentage of the previous tone induced by phenylephrine. PJ powder (100 mg/L) induced higher levels of vasorelaxation (mean ± standard error of the mean, 88.6% ± 4.4%) than PLs powder (1 g/L; 72.0% ± 10.8%). Nitric oxide pathway inhibitors (NG-nitro-L-arginine methyl ester + carboxy-PTIO) did not affect persimmon-derived polyphenol-induced vasorelaxation, whereas potassium chloride, tetraethylammonium, and potassium-channel inhibitors did. Vasorelaxation was endothelium independent with both extracts. Phenylephrine-induced vasocontraction was suppressed by pretreatment with PJ and PLs powder, even when inositol triphosphate-mediated Ca2+ release and extracellular Ca2+ influx were inhibited. These results suggest that persimmon-derived polyphenol phytocomplex cause vasorelaxation and inhibit vasocontraction through hyperpolarization of smooth muscle cells. Persimmon-derived polyphenols may be able to prevent cardiovascular diseases caused by abnormal contraction of blood vessels.

Relaxation response of abdominal aorta to androgens in orchidectomised Sprague–Dawley rats fed a high-salt diet

2012 ◽  
Vol 90 (12) ◽  
pp. 1647-1651 ◽  
Author(s):  
Ahmed Kolade Oloyo ◽  
Renuka R. Nair ◽  
Chikodi N. Anigbogu ◽  
Olusoga A. Sofola
Keyword(s):  
Abdominal Aorta ◽  
High Salt ◽  
Relaxation Response ◽  
Sprague Dawley ◽  
High Salt Diet ◽  
Salt Diet ◽  
Vasorelaxant Effect ◽  
Sprague Dawley Rats ◽  
The Status ◽  
Gonadal Status

Previous studies have demonstrated the acute relaxant effects of androgens on normal arterial beds, but not on any with underlying or induced pathologies. This study investigated whether the status of the gonads affects the direct actions of androgens on isolated abdominal aorta from male Sprague–Dawley rats fed a high-salt diet. A high-salt diet reduced the relaxation response to exogenous testosterone, but not to dehydroepiandrosterone (DHEA). Orchidectomy reduced the relaxation response to both testosterone and DHEA, while testosterone replacement restored the acute vasorelaxant effect of testosterone and DHEA in both normal and high-salt diet fed rats. Gonadal status appears to be important in the acute vasorelaxant effect of androgens.

Vasorelaxant Action of the Chloroform Fraction of Orthosiphon stamineus via NO/cGMP Pathway, Potassium and Calcium Channels

2016 ◽  
Vol 44 (07) ◽  
pp. 1413-1439 ◽  
Author(s):  
Mun Fei Yam ◽  
Chu Shan Tan ◽  
Mariam Ahmad ◽  
Shibao Ruan
Keyword(s):  
Calcium Channels ◽  
Channel Blocker ◽  
Soluble Guanylate Cyclase ◽  
Aortic Ring ◽  
Guanosine Monophosphate ◽  
Receptor Blocker ◽  
Chloroform Fraction ◽  
Orthosiphon Stamineus ◽  
Vasorelaxant Effect ◽  
Vasorelaxant Activity

Orthosiphon stamineus Benth. (Lamiaceae) is an important plant in traditional folk medicine that is used to treat hypertension and kidney stones. In humans, this plant has been tested as an addition regiment for antihypertensive treatment. Among the treatments for hypertension, O. stamineus had been to have diuretic and vasorelaxant effects in animal models. There is still very little information regarding the vasorelaxant effect of O. stamineus. Therefore, the present study was designed to investigate the vasorelaxant activity and mechanism of action of the fractions of O. stamineus. The vasorelaxant activity and the underlying mechanisms of the chloroform fraction of the 50% methanolic extract of O. stamineus (CF) was evaluated on thoracic aortic rings isolated from Sprague Dawley rats. CF caused relaxation of the aortic ring pre-contracted with phenylephrine in the presence and absence of endothelium, and pre-contracted with potassium chloride in endothelium-intact aortic ring. In the presence of endothelium, both indomethacin (a nonselective cyclooxygenase inhibitor) and [Formula: see text]-[1,2,4]Oxadiazolo[4,3-[Formula: see text]]quinoxalin-1-one (ODQ, selective soluble guanylate cyclase inhibitor) had a small effect on the vasorelaxation response. On the other hand, in the presence of Nω-nitro-L-arginine methyl ester (L-NAME, nitric oxide synthase inhibitor), methylene blue (cyclic guanosine monophosphate lowering agent), tetraethylammonium ([Formula: see text], nonselective calcium activator [Formula: see text] channel blocker), 4-aminopyridine (4-AP, voltage-dependent [Formula: see text] channel blocker), barium chloride ([Formula: see text], inwardly rectifying [Formula: see text] channel blocker), glibenclamide (nonspecific ATP-sensitive [Formula: see text] channel blocker), atropine (muscarinic receptor blocker) and propranolol (β-adrenergic receptor blocker), the vasorelaxant effect significantly reduced the relaxation stimulated by CF. CF was also found to be active in reducing [Formula: see text] release from the sarcoplasmic reticulum and blocking calcium channels.

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.

Abstract 484: The Vasorelaxing / No Release Effect Of Angiotensin-(1-9) Is Independent Of At2, Mas Or Mrgd Receptors

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Gabriel S Resende ◽  
Neyva Silva ◽  
Daniel C Villela ◽  
Robson A Santos
Keyword(s):  
Cho Cells ◽  
No Production ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Angiotensin I ◽  
Vasorelaxant Effect ◽  
Sprague Dawley Rats ◽  
No Release ◽  
A Minor ◽  
Hydrolysis Of

Angiotensin-(1-9) is a nonapeptide formed by the hydrolysis of angiotensin I by ACE2 that seems to counter-regulate the classical RAS axis. Recent studies suggest that Ang-(1-9) acts via AT2 receptors (AT2R), however the pharmacological tool used to asses this ang-(1-9) /AT2R mediated interaction, is the AT2R antagonist, PD123319, that appears to have a great deal of inespecificity . Two other candidates for the ligation of Ang-(1-9), that have protective effects similar to the AT2R, are the MAS and the recently described MrgD receptor. Thus, in this study we addressed if Ang-(1-9) could be a ligand for AT2, MAS or MrgD receptors using aortic rings taken from AT2 and Mas knockout mice and AT2R or MrgD-transfected CHO cells. Materials and methods: The endothelium-dependent vasodilatory response to Ang-(1-9) was tested in aortic rings taken from Wild-Type, AT2KO and MASKO mice and Sprague-Dawley rats, pre-contracted with phenylephrine (0.1 umoles/L). NO release from AT2R or MrgD stable transfected CHO cells was evaluated using the NO indicator 4-amino-5 methylamino-2, 7 difluorofluorescein diacetate (DAF-FM) after Ang-(1-9) stimulation. Results: In aortic rings from SD rats Ang-(1-9) produced a dose-related relaxation (Emax= 15 ± 2.6) which was not modified by A-779 (Emax=12.9 ± 1.9) , the Mas/MrgD antagonist D-Pro7-Ang-(1-7) (Emax= 15.6 ± 1.7); or by PD123319 (Emax= 22.7 ± 5.4) . In aortic rings taken from MasKO there was a minor attenuation of the Ang-(1-9) vasorelaxant effect when compared to the WT, but the response was not abolished. No difference between AT2KO and WT mice was observed regarding the vasorelaxation produced by Ang-(1-9) (Emax= 20.7±2.4 and 20.9 ± 1.3 respectively). Moreover, the vasorelaxing effect of Ang-(1-9) was not affected by the association of PD123319 and D-Pro7-Ang-(1-7). In addition, the nonapeptide did not stimulate NO production in AT2R-stably transfected CHO cells or MrgD stably transfected cells. Taken together these results suggest that the vasorelaxation produced by Ang-(1-9) in rodent aortic rings is independent of Mas , AT2R or MrgD receptors.

scholarly journals B. anthracisedema toxin increases cAMP levels and inhibits phenylephrine-stimulated contraction in a rat aortic ring model

2013 ◽  
Vol 305 (2) ◽  
pp. H238-H250 ◽  
Author(s):  
Yan Li ◽  
Xizhong Cui ◽  
Steven B. Solomon ◽  
Kenneth Remy ◽  
Yvonne Fitz ◽  
...  
Keyword(s):  
Protective Antigen ◽  
Lethal Factor ◽  
Aortic Ring ◽  
Contractile Force ◽  
Host Cells ◽  
Sprague Dawley ◽  
Adenyl Cyclase Activity ◽  
Ring Model ◽  
Arterial Relaxation ◽  
Rat Aortic Ring Model

B. anthracis edema toxin (ET) and lethal toxin (LT) are each composed of protective antigen (PA), necessary for toxin uptake by host cells, and their respective toxic moieties, edema factor (EF) and lethal factor (LF). Although both toxins likely contribute to shock during infection, their mechanisms are unclear. To test whether ET and LT produce arterial relaxation, their effects on phenylephrine (PE)-stimulated contraction in a Sprague-Dawley rat aortic ring model were measured. Rings were prepared and connected to pressure transducers. Their viability was confirmed, and peak contraction with 60 mM KCl was determined. Compared with PA pretreatment (control, 60 min), ET pretreatment at concentrations similar to those noted in vivo decreased the mean (±SE) maximum contractile force (MCF; percent peak contraction) in rings generated during stimulation with increasing PE concentrations (96.2 ± 7.0 vs. 57.3 ± 9.1) and increased the estimated PE concentration producing half the MCF (EC50; 10−7M, 1.1 ± 0.3 vs. 3.7 ± 0.8, P ≤ 0.002). ET inhibition with PA-directed monoclonal antibodies, selective EF inhibition with adefovir, or removal of the ring endothelium inhibited the effects of ET on MCF and EC50( P ≤ 0.02). Consistent with its adenyl cyclase activity, ET increased tissue cAMP in endothelium-intact but not endothelium-denuded rings ( P < 0.0001 and 0.25, respectively). LT pretreatment, even in high concentrations, did not significantly decrease MCF or increase EC50(all P > 0.05). In rings precontracted with PE compared with posttreatment with PA (90 min), ET posttreatment produced progressive reductions in contractile force and increases in relaxation in endothelium-intact rings ( P < 0.0001) but not endothelium-denuded rings ( P = 0.51). Thus, ET may contribute to shock by producing arterial relaxation.

Evidence for uneven distribution of L-type calcium channels in rat pulmonary circulation

1995 ◽  
Vol 269 (6) ◽  
pp. H2051-H2056 ◽  
Author(s):  
B. R. Walker
Keyword(s):  
Calcium Channels ◽  
Pulmonary Circulation ◽  
Venous Pressure ◽  
Physiological Saline ◽  
Sprague Dawley ◽  
Arterial Segment ◽  
Venous Circulation ◽  
Sprague Dawley Rats ◽  
High K ◽  
Physiological Saline Solution

Experiments were performed on isolated, perfused rat lungs to determine the segmental sites of vasoconstriction in response to factors that open voltage-sensitive, L-type calcium channels on vascular smooth muscle cells. Lungs from male Sprague-Dawley rats were perfused at constant flow with a physiological saline solution (PSS) containing albumin. Measurements were made of pulmonary arterial and venous pressure, whereas capillary pressure was estimated by the double-occlusion technique. After equilibration, lungs were constricted with depolarizing PSS containing high K+ (35 or 45 mM). With both stimuli, approximately 80% of the observed increase in vascular resistance occurred on the arterial side of the circulation. Both nifedipine and verapamil reversed this response; however, reversal was more consistent in the arterial segment. In additional experiments, the L-type channel activator (-)BAY K 8644 caused increased resistance in the arterial but not the venous segment. Another group of lungs constricted with the thromboxane mimetic U-46619 demonstrated equal arterial and venous vasoconstriction. In U-46619-constricted lungs, nifedipine caused a 28% reversal of the agonist-induced increase in arterial resistance but was without effect on the venous circulation. These data suggest that a greater density of L-type calcium channels may exist within the arterial segment of the pulmonary circulation than in the veins.

scholarly journals Gabapentin Prevents Delayed and Long-lasting Hyperalgesia Induced by Fentanyl in Rats

2008 ◽  
Vol 108 (3) ◽  
pp. 484-494 ◽  
Author(s):  
Alain C. Van Elstraete ◽  
Philippe Sitbon ◽  
Jean-Xavier Mazoit ◽  
Dan Benhamou
Keyword(s):  
Neuropathic Pain ◽  
Calcium Channels ◽  
Systemic Exposure ◽  
Ruthenium Red ◽  
Sprague Dawley ◽  
Auxiliary Subunits ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Sprague Dawley Rats ◽  
Opioid Induced Hyperalgesia

Background Opioid-induced hyperalgesia can develop rapidly after opioid exposure. Neuropathic pain and opioid-induced hyperalgesia share common pathophysiologic mechanisms. Gabapentin is effective for the management of neuropathic pain and may therefore prevent opioid-induced hyperalgesia. This study tested the effectiveness of gabapentin for prevention of long-lasting hyperalgesia induced by acute systemic fentanyl in uninjured rats. Involvement of the alpha2delta auxiliary subunits of voltage-gated calcium channels in the prevention of opioid-induced hyperalgesia by gabapentin also was assessed. Methods Hyperalgesia was induced in male Sprague-Dawley rats with subcutaneous fentanyl (four injections, 20, 60, or 100 microg/kg per injection at 15-min intervals). Intraperitoneal (30, 75, 150, or 300 mg/kg) or intrathecal (300 microg) gabapentin was administered 30 min before or 300 min after (intraperitoneal 150 mg/kg) the first fentanyl injection. Sensitivity to nociceptive stimuli (paw-pressure test) was assessed on the day of the experiment and for several days after injections. The effects combining gabapentin with intrathecal ruthenium red (20 ng) also were assessed. Results Fentanyl administration was followed by an early increase (analgesia) and by a later and sustained decrease (hyperalgesia) in nociceptive thresholds. Gabapentin did not significantly modify the early analgesic component but dose-dependently prevented the delayed decrease in nociceptive threshold. Ruthenium red partially, but significantly, opposed the prevention of opioid-induced hyperalgesia by gabapentin. Conclusions Intraperitoneal and intrathecal gabapentin prevents the development of hyperalgesia induced by acute systemic exposure to opioids. This prevention may result, at least in part, from binding of gabapentin to the alpha2delta auxiliary subunits of voltage-gated calcium channels.

Ultrastructural Investigation of Spontaneous Pituitary Adenomas in Aging Sprague-Dawley Rats

1982 ◽  
Vol 40 ◽  
pp. 216-217
Author(s):  
D. J. McComb ◽  
J. Beri ◽  
F. Zak ◽  
K. Kovacs
Keyword(s):  
Microscopic Study ◽  
Pituitary Adenomas ◽  
Wistar Rats ◽  
Microscopic Level ◽  
Sprague Dawley ◽  
Prolactin Cells ◽  
Light Microscopic Level ◽  
Ultrastructural Investigation ◽  
Sprague Dawley Rats ◽  
Long Evans

Investigation of the spontaneous pituitary adenomas in rat have been limited mainly to light microscopic study. Furth et al. (1973) described them as chromophobic, secreting prolactin. Kovacs et al. (1977) in an ul trastructural investigation of adenomas of old female Long-Evans rats, found that they were composed of prolactin cells. Berkvens et al. (1980) using immunocytochemistry at the light microscopic level, demonstrated that some spontaneous tumors of old Wistar rats could contain GH, TSH or ACTH as well as PRL.

Early Development of Drug-Induced Hepatic Necrosis

1971 ◽  
Vol 29 ◽  
pp. 576-577
Author(s):  
F. G. Zaki ◽  
E. Detzi ◽  
C. H. Keysser
Keyword(s):  
Early Development ◽  
Hepatic Necrosis ◽  
Screening Tests ◽  
Dense Matrix ◽  
Sprague Dawley ◽  
Electron Microscopic ◽  
Drug Induced ◽  
Hepatocellular Damage ◽  
Sprague Dawley Rats ◽  
Microscopic Studies

This study represents the first in a series of investigations carried out to elucidate the mechanism(s) of early hepatocellular damage induced by drugs and other related compounds. During screening tests of CNS-active compounds in rats, it has been found that daily oral administration of one of these compounds at a dose level of 40 mg. per kg. of body weight induced diffuse massive hepatic necrosis within 7 weeks in Charles River Sprague Dawley rats of both sexes. Partial hepatectomy enhanced the development of this peculiar type of necrosis (3 weeks instead of 7) while treatment with phenobarbital prior to the administration of the drug delayed the appearance of necrosis but did not reduce its severity.Electron microscopic studies revealed that early development of this liver injury (2 days after the administration of the drug) appeared in the form of small dark osmiophilic vesicles located around the bile canaliculi of all hepatocytes (Fig. 1). These structures differed from the regular microbodies or the pericanalicular multivesicular bodies. They first appeared regularly rounded with electron dense matrix bound with a single membrane. After one week on the drug, these vesicles appeared vacuolated and resembled autophagosomes which soon developed whorls of concentric lamellae or cisterns characteristic of lysosomes (Fig. 2). These lysosomes were found, later on, scattered all over the hepatocytes.

Sign in / Sign up

Export Citation Format

Share Document