Effects of potassium and ouabain on the vascular reactivity to norepinephrine in the rat mesenteric artery

1979 ◽  
Vol 57 (8) ◽  
pp. 908-912 ◽  
Author(s):  
Kazuoki Kondo ◽  
Tetsuji Okuno ◽  
Konosuke Konishi ◽  
Takao Saruta ◽  
Eiichi Kato
Keyword(s):  
Prostaglandin E2 ◽  
Mesenteric Artery ◽  
Vascular Reactivity ◽  
Potassium Concentration ◽  
Vascular Wall ◽  
Vascular Response ◽  
Vascular Bed ◽  
Rat Mesenteric Artery ◽  
Low Potassium ◽  
Mesenteric Vascular Bed

In the perfused rat mesenteric vascular bed, the effects of potassium and ouabain on the vascular response to norepinephrine were studied. Neither changing the concentration of potassium (1.9 to 7.9 mM) nor adding ouabain (8.6 × 10−7 to 2.2 × 10−4 M) to the perfusate changed the basal pressure. A slight increase in the potassium concentration in the perfusate attenuated the vascular response to norepinephrine, and a slight decrease in the potassium concentration potentiated this response. Ouabain in the perfusate potentiated the vascular response to norepinephrine in a dose-related manner. The effect of potassium on the vascular response was inhibited in the presence of ouabain. In preparations in which vascular reactivity had been abolished by indomethacin and then restored by prostaglandin E2, the effects of potassium and ouabain on the vascular reactivity to norepinephrine were similar to those found in the untreated preparations. These results indicate that a slight change in potassium concentration in the perfusate can affect the vascular response to norepinephrine by changing the activity of a Na+–K+-dependent ATPase. It is also suggested that the potentiating effect of low potassium concentration on the norepinephrine response is, at least in the rat mesenteric vascular bed, not mediated by the synthesis of prostaglandin E2 in the vascular wall.

scholarly journals Levobupivacaine induces vasodilatation, but not vasoconstriction, in rat mesenteric artery

2016 ◽  
Vol 45 (5) ◽  
pp. 258-264 ◽  
Author(s):  
Liciane dos Santos MENEZES ◽  
Liane Maciel de Almeida SOUZA ◽  
Márcio Roberto Viana dos SANTOS ◽  
Patrícia Santos Cunha MENDONÇA ◽  
Ítalo José Alves MOREIRA ◽  
...  
Keyword(s):  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Vascular Reactivity ◽  
Force Transducer ◽  
K Channel ◽  
Independent Manner ◽  
Vasodilator Effect ◽  
Rat Mesenteric Artery ◽  
Male Wistar Rats ◽  
Cotton Threads

Abstract Introduction Levobupivacaine (LEVO) can replace analgesia because it exhibits low toxicity and causes minor vasoconstriction, enabling its use in patients in whom vasoconstrictors are contraindicated. Objective We aimed to evaluate the effects of LEVO in isolated rat superior mesenteric artery by using the vascular reactivity technique and compare its effect to that of lidocaine. Material and method Arterial rings were obtained from the mesenteric artery of male Wistar rats and kept in organ baths. For recording isometric contractions, each ring was suspended by cotton threads from a force transducer, which was connected to a data acquisition system. Result Both lidocaine and LEVO did not show a vasoconstrictor effect on the basal tone of the arterial rings with functional endothelium. However, when the rings were pre-contracted with phenylephrine, both drugs were able to induce concentration-dependent vasodilatation. The vasodilator effect induced by LEVO did not change after removal of the endothelium, or with the addition of tetraethylammonium (1 mM), a non-selective K+ channel blocker. In the rings without functional endothelium, which were pre-contracted with depolarizing Tyrode’s solution (KCl 80 mM), LEVO-induced vasodilatation was not significantly different from that observed in the rings pre-contracted with phenylephrine. Moreover, it did not show a significant additional vasodilator effect compared to the maximal vasodilator effect of nifedipine. Conclusion This study demonstrated that LEVO produces a vasodilator effect in the rat superior mesenteric artery in an endothelium-independent manner. This effect seems to be mediated via Ca2+ channel blockade in the vascular smooth muscle cells.

Baicalin-Induced Vascular Response In Rat Mesenteric Artery: Role Of Endothelial Nitric Oxide

2002 ◽  
Vol 29 (8) ◽  
pp. 721-724 ◽  
Author(s):  
Yu Huang ◽  
Suk Ying Tsang ◽  
Xiaoqiang Yao ◽  
Chi Wai Lau ◽  
Ya Lun Su ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mesenteric Artery ◽  
Vascular Response ◽  
Rat Mesenteric Artery ◽  
Endothelial Nitric Oxide

Vasorelaxant effects of and receptors for atrial natriuretic peptides in the mesenteric artery and aorta of the rat

1988 ◽  
Vol 66 (7) ◽  
pp. 951-956 ◽  
Author(s):  
Jean St-Louis ◽  
Ernesto L. Schiffrin
Keyword(s):  
Natriuretic Peptides ◽  
Mesenteric Artery ◽  
Atrial Natriuretic Peptides ◽  
Binding Assays ◽  
Structural Requirements ◽  
Vascular Bed ◽  
Relaxation Experiments ◽  
Mesenteric Vascular Bed ◽  
Anp Receptors ◽  
Atrial Natriuretic

Vasorelaxant effects of different atrial natriuretic peptides (ANP) were measured on rat aortic strips and mesenteric artery rings. These results were compared with the potency of the same peptides to displace 125I-labelled ANP (101–126) on membrane preparations of aorta and of mesenteric vascular bed. In aortic strips and mesenteric artery rings precontracted with phenylephrine (3 × 10−8 and 10−6 M, respectively), the order of potency of ANP was as follows: ANP (99–126) > ANP (101–126) > ANP (103–126) = ANP(103–125) [Formula: see text] ANP (103–123). In the displacement binding assays, the order of potency of ANP peptides was similar to that of the relaxation experiments: ANP (99–126) = ANP (101–126) > ANP (103–126) = ANP (103–125) [Formula: see text] ANP (103–123). When the vessels were precontracted by a smaller concentration of phenylephrine (10−7 M in mesenteric artery and 10−8 M in aorta), the IC50 of ANP (101–126) was significantly lower than when the higher concentration of phenylephrine was used. These results show that ANP receptors in the mesenteric artery and in the aorta have similar structural requirements, according to the order of potency of different length ANP, both for binding and myotropic responses.

Vascular Actions of Frusemide and Bumetanide on the Rat Superior Mesenteric Vascular Bed: Interactions with Prostaglandins

1976 ◽  
Vol 51 (s3) ◽  
pp. 257s-258s
Author(s):  
D. F. Horrobin ◽  
M. S. Manku ◽  
J. P. Mtabaji
Keyword(s):  
Prostaglandin E2 ◽  
Inhibitory Effect ◽  
Prostaglandin Synthesis ◽  
Inhibitory Effects ◽  
Perfusion Fluid ◽  
Endogenous Prostaglandin ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed

1. The addition of frusemide or bumetanide to perfusion fluid inhibited the response of the isolated mesenteric vascular bed to noradrenaline. 2. Addition of prostaglandin E2 to the perfusion fluid completely restored the response to noradrenaline. 3. Inhibition of prostaglandin secretion by indomethacin with restoration of responses to noradrenaline by the addition of exogenous prostaglandin E2 prevented the inhibitory effect of frusemide or bumetanide on responses to noradrenaline. 4. The inhibitory effects of diuretics on responsiveness to noradrenaline is mediated by blockade of endogenous prostaglandin synthesis.

Potentiation of Pressor Effects of Noradrenaline and Potassium Ions in the Rat Mesenteric Arteries by Physiological Concentrations of Angiotensin II: Effects of Prostaglandin E2 and Cortisol

1977 ◽  
Vol 53 (3) ◽  
pp. 233-239 ◽  
Author(s):  
K. Kondo ◽  
M. S. Manku ◽  
D. F. Horrobin ◽  
R. Boucher ◽  
J. Genest
Keyword(s):  
Angiotensin Ii ◽  
Prostaglandin E2 ◽  
Potassium Chloride ◽  
Prostaglandin Synthesis ◽  
Mesenteric Arteries ◽  
Potassium Ions ◽  
Vascular Bed ◽  
Vasoconstrictor Response ◽  
Mesenteric Vascular Bed

1. In the perfused rat mesenteric vascular bed, the effects of angiotensin II, cortisol and prostaglandin E2 on the vascular responses to noradrenaline or potassium chloride were studied. 2. Angiotensin II in subpressor concentrations potentiated the vasoconstrictor response to noradrenaline and potassium chloride. This effect of angiotensin II was inhibited in the presence of indomethacin and prostaglandin E2. 3. Cortisol in physiological concentrations inhibited the potentiating effect of angiotensin II. 4. Prostaglandin E2 enhanced the vasoconstrictor response to noradrenaline. This effect was not abolished by cortisol. 5. These results suggest that some actions of angiotensin II and cortisol in vivo are mediated by the regulation of prostaglandin synthesis or release.

Effects of Dopamine and Other Catecholamines on the Splanchnic Circulation

1972 ◽  
Vol 50 (6) ◽  
pp. 594-602 ◽  
Author(s):  
Linda L. Shanbour ◽  
Don Parker
Keyword(s):  
Blood Flow ◽  
Hepatic Artery ◽  
Mesenteric Artery ◽  
Splanchnic Circulation ◽  
Blood Flows ◽  
Vascular Bed ◽  
Competitive Action ◽  
Responses To Dopamine ◽  
Mesenteric Vascular Bed ◽  
Dose Levels

Studies were conducted to evaluate the effects of dopamine (3, 4-dihydroxyphenylethylamine) and other catecholamines on the mesenteric vascular bed in dogs. Mesenteric and hepatic artery blood flows were measured with electromagnetic blood flow transducers. Catecholamines were infused intra-arterially into a branch-of the mesenteric artery. Dopamine consistently decreased mesenteric and hepatic artery blood flows at all dose levels studied (5–100 mg/kg). Phenoxybenzamine (12.5 mg/kg) blocked the effects of norepinephrine (0.05–1.0 μg/kg) and reversed the responses to dopamine in the mesenteric bed to those of pure vasodilation (no transient constriction was observed) but failed to abolish the constrictor action of dopamine on the hepatic artery. Propranolol or haloperidol, when administered with the phenoxybenzamine, did not attenuate the mesenteric responses to dopamine. Haloperidol prevented the hepatic artery vasoconstriction produced by dopamine but did not alter isoproterenol-induced hepatic artery vasodilation. No competitive action was observed between dopamine and norepinephrine or isoproterenol. These results suggest that (1) dopamine produces selective vasodilation of the mesenteric bed which is not blocked by haloperidol, and (2) dopamine has a unique action on the hepatic vascular bed which is blocked by haloperidol.

scholarly journals Grape-Derived Polyphenols Prevent Doxorubicin-Induced Blunted EDH-Mediated Relaxations in the Rat Mesenteric Artery: Role of ROS and Angiotensin II

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Noureddine Idris-Khodja ◽  
Paola Di Marco ◽  
Mona Farhat ◽  
Bernard Geny ◽  
Valérie B. Schini-Kerth
Keyword(s):  
Angiotensin Ii ◽  
Mesenteric Artery ◽  
Vascular Reactivity ◽  
Mesenteric Arteries ◽  
At1 Receptors ◽  
Expression Levels ◽  
Rat Mesenteric Artery ◽  
Male Wistar Rats ◽  
Wine Polyphenols ◽  
Calcium Activated Potassium Channels

This study determined whether doxorubicin, an anticancer agent, impairs endothelium-dependent relaxations mediated by nitric oxide (NO) and endothelium-derived hyperpolarization (EDH) in the mesenteric artery and, if so, the mechanism underlying the protective effect of red wine polyphenols (RWPs), a rich natural source of antioxidants. Male Wistar rats were assigned into 4 groups: control, RWPs, doxorubicin, and doxorubicin + RWPs. Vascular reactivity was assessed in organ chambers; the vascular formation of reactive oxygen species (ROS) using dihydroethidine and the expression levels of small and intermediate conductance calcium-activated potassium channels (SKCa,IKCa) and connexin 40 (Cx40), which are involved in EDH-type relaxations, endothelial NO synthase (eNOS), angiotensin II, and AT1 receptors by immunofluorescence. The doxorubicin treatment impaired EDH-mediated relaxations, whereas those mediated by NO were minimally affected. This effect was associated with reduced expression levels ofSKCa,IKCa, and Cx40, increased expression levels of eNOS, angiotensin II, and AT1 receptors, and formation of ROS in mesenteric arteries. RWPs prevented both the doxorubicin-induced blunted EDH-type relaxations and the increased vascular oxidative stress, and they improved the expression levels of target proteins. These findings suggest that polyphenol-rich natural products might be of interest in the management of doxorubicin-induced vascular injury possibly by improving the vascular angiotensin system.

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