Mechanisms of Desflurane-induced Preconditioning in Isolated Human Right Atria In Vitro

Background The authors examined the role of adenosine triphosphate-sensitive potassium (K(ATP)) channels, adenosine A1 receptor, and alpha and beta adrenoceptors in desflurane-induced preconditioning in human myocardium, in vitro. Methods The authors recorded isometric contraction of human right atrial trabeculae suspended in oxygenated Tyrode's solution (34 degrees C; stimulation frequency, 1 Hz). Before a 30-min anoxic period, 3, 6, and 9% desflurane was administered during 15 min. Desflurane, 6%, was also administered in the presence of 10 microm glibenclamide, a K(ATP) channels antagonist; 10 microm HMR 1098, a sarcolemmal K(ATP) channel antagonist; 800 microm 5-hydroxy-decanoate (5-HD), a mitochondrial K(ATP) channel antagonist; 1 microm phentolamine, an alpha-adrenoceptor antagonist; 1 microm propranolol, a beta-adrenoceptor antagonist; and 100 nm 8-cyclopentyl-1,3-dipropylxanthine (DPX), the adenosine A1 receptor antagonist. Developed force at the end of a 60-min reoxygenation period was compared (mean +/- SD). Results Desflurane at 3% (95 +/- 13% of baseline), 6% (86 +/- 6% of baseline), and 9% (82 +/- 6% of baseline) enhanced the recovery of force after 60 min of reoxygenation as compared with the control group (50 +/- 11% of baseline). Glibenclamide (60 +/- 12% of baseline), 5-HD (57 +/- 21% of baseline), DPX (63 +/- 19% of baseline), phentolamine (56 +/- 20% of baseline), and propranolol (63 +/- 13% of baseline) abolished desflurane-induced preconditioning. In contrast, HMR 1098 (85 +/- 12% of baseline) did not modify desflurane-induced preconditioning. Conclusions In vitro, desflurane preconditions human myocardium against simulated ischemia through activation of mitochondrial K(ATP) channels, adenosine A1 receptor, and alpha and beta adrenoceptors.

Download Full-text

Ketamine Preconditions Isolated Human Right Atrial Myocardium

Anesthesiology ◽

10.1097/00000542-200506000-00019 ◽

2005 ◽

Vol 102 (6) ◽

pp. 1190-1196 ◽

Cited By ~ 15

Author(s):

Jean-Luc Hanouz ◽

Lan Zhu ◽

Emmanuel Persehaye ◽

Massimo Massetti ◽

Gerard Babatasi ◽

...

Keyword(s):

Adenosine Triphosphate ◽

Enhanced Recovery ◽

Human Myocardium ◽

Right Atrial ◽

Control Group ◽

Force Of Contraction ◽

Human Right ◽

Adrenoceptor Antagonist ◽

Racemic Ketamine

Background The authors examined the effect of ketamine and its S(+) isomer on isolated human myocardium submitted to hypoxia-reoxygenation in vitro. Methods The authors studied isometric contraction of human right atrial trabeculae suspended in an oxygenated Tyrode's modified solution at 34 degrees C. Ten minutes before a 30-min hypoxic period followed by a 60-min reoxygenation, muscles were exposed for 15 min to racemic ketamine and its S(+) isomer at 10, 10, and 10 m alone or in the presence of 8.10 m 5-hydroxydecanoate, 10 m HMR 1098 (sarcolemmal adenosine triphosphate-sensitive potassium channel antagonist), 10 m phentolamine (alpha-adrenoceptor antagonist), and 10 m propranolol (beta-adrenoceptor antagonist). Force of contraction at the end of the 60-min reoxygenation period was compared between groups (mean +/- SD). Results Ketamine (10 m: 85 +/- 4%; 10 m: 95 +/- 10%; 10 m: 94 +/- 14% of baseline) and S(+)-ketamine (10-6 m: 85 +/- 4%; 10 m: 91 +/- 16%; 10 m: 93 +/- 14% of baseline) enhanced recovery of force of contraction at the end of the reoxygenation period as compared with the control group (47 +/- 10% of baseline; P < 0.001). Ketamine-induced preconditioning at 10 m was inhibited by 5-hydroxydecanoate (60 +/- 16%; P < 0.001), HMR 1098 (60 +/- 14%; P < 0.001), phentolamine (56 +/- 12%; P < 0.001), and propranolol (60 +/- 7%; P < 0.001). Conclusions In vitro, ketamine preconditions isolated human myocardium, at least in part, via activation of adenosine triphosphate-sensitive potassium channels and stimulation of alpha- and beta-adrenergic receptors.

Download Full-text

Adenosine A1 receptor-mediated inhibition of in vitro prolactin secretion from the rat anterior pituitary

Brazilian Journal of Medical and Biological Research ◽

10.1590/s0100-879x2006001100013 ◽

2006 ◽

Vol 39 (11) ◽

Cited By ~ 1

Author(s):

D.L.W. Picanço-Diniz ◽

M.M. Valença ◽

J. Antunes-Rodrigues

Keyword(s):

Anterior Pituitary ◽

Prolactin Secretion ◽

Adenosine A1 Receptor ◽

Adenosine A1 ◽

A1 Receptor

Download Full-text

Regulation of Na(+)-3HCO3- cotransport in rabbit proximal convoluted tubule via adenosine A1 receptor

AJP Renal Physiology ◽

10.1152/ajprenal.1993.265.4.f511 ◽

1993 ◽

Vol 265 (4) ◽

pp. F511-F519 ◽

Cited By ~ 14

Author(s):

M. Takeda ◽

K. Yoshitomi ◽

M. Imai

Keyword(s):

Basolateral Membrane ◽

Receptor Activation ◽

Proximal Convoluted Tubule ◽

Adenosine A1 Receptor ◽

Intracellular Camp ◽

Dependent Manner ◽

Concentration Dependent Manner ◽

Adenosine A1 ◽

A1 Receptor

We investigated the role of adenosine A1-receptor in the regulation of basolateral Na(+)-3HCO3- cotransporter in the rabbit proximal convoluted tubule (PCT) microperfused in vitro by monitoring basolateral membrane potential and intracellular pH. FK-453, a highly specific A1 antagonist, inhibited basolateral HCO3- conductance in a concentration-dependent manner (10(-10)-10(-5) M). Other A1 antagonists, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) at 10(-5) M and theophylline at 10(-3) M, also had similar effects. N6-cyclohexyladenosine (CHA) at 10(-7) M attenuated the effect of low concentration (10(-8) M) of FK-453. Either enhancement of the degradation of adenosine by 0.1 U/ml adenosine deaminase (ADA) or inhibition of adenosine release from the cells by 10(-6) M S-(4-nitrobenzyl)-6-thioinosine (NBTI) mimicked the effects of A1 antagonists. These observations suggest that endogenous adenosine is released from PCT cells and stimulates Na(+)-3HCO3- cotransporter. Both 10(-4) M 8-(4-chlorophenylthio)-adenosine 3',5'-cyclic monophosphate (CPT-cAMP) and 10(-6) M forskolin also inhibited basolateral HCO3- conductance. Both 10(-6) M FK-453 and 10(-4) M CPT-cAMP decreased the initial rate as well as the magnitude of intracellular acidification induced by reduction of peritubular HCO3- concentration from 25 to 0 mM. Neither 10(-6) M FK-453 nor 10(-7) M CHA changed intracellular Ca2+ concentration as measured by fura-2 fluorescence. These results indicate that adenosine might stimulate HCO3- exit across the basolateral membrane through Na(+)-3HCO3- cotransporter by decreasing intracellular cAMP via A1-receptor activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Download Full-text

Enhancement of adenosine A1 receptor functions by benzoylthiophenes in guinea pig tissues in vitro

Naunyn-Schmiedeberg s Archives of Pharmacology ◽

10.1007/bf00176776 ◽

1995 ◽

Vol 352 (2) ◽

Cited By ~ 6

Author(s):

E. Leung ◽

L.K.M. Walsh ◽

L.A. Flippin ◽

E.J. Kim ◽

D.A. Lazar ◽

...

Keyword(s):

Guinea Pig ◽

Adenosine A1 Receptor ◽

Adenosine A1 ◽

A1 Receptor

Download Full-text

Cordycepin Modulate Body Weight by Reducing Prolactin via an Adenosine A1 Receptor

10.20944/preprints201804.0033.v1 ◽

2018 ◽

Cited By ~ 1

Author(s):

Yuan Li ◽

Yan Li ◽

Xueyan Wang ◽

Hongyue Xu ◽

Chao Wang ◽

...

Keyword(s):

Body Weight ◽

Prolactin Secretion ◽

Adenosine A1 Receptor ◽

Gh3 Cells ◽

Serum Prolactin ◽

Prolactin Release ◽

Adenosine A1 ◽

A1 Receptor

Cordycepin is an extract from the insect fungus Cordyceps. militaris, which is a traditional medicine with various biological function. In previous studies, cordycepin had been reported with excellent anti-obesity effect, but the mechanism is unclear. A large quantity of evidences showed that prolactin plays an important part in body weight regulation, hyperprolactinemia can promote appetite and accelerate fat deposition. In this study, we explored the molecular mechanism of the anti-obesity effect of cordycepin by reducing prolactin release via an adenosine A1 receptor. In vivo, obese rats model was induced by high fat diet for 5 weeks, the serum and liver lipids coupling with serum prolactin were reduced by treatment of cordycepin, the results suggested that cordycepin is a potential drug for therapying obesity which could be related with prolactin. In vitro, cordycepin could inhibit prolactin secretion in GH3 cells via upregulating the expression of adenosine A1 receptor, the inhibition effect could be blocked by an antagonist of adenosine receptor A1 DPDPX, prolactin induced the upregulation of lipogenesis genes PRLR, and P-JAK2 in 3T3-L1 cells. Intriguingly, cordycepin would down-regulate the expression of prolactin receptor (PRLR). Thus, we concluded that cordycepin modulate body weight by reducing prolactin release via an adenosine A1 receptor.

Download Full-text

Cordycepin Modulates Body Weight by Reducing Prolactin Via an Adenosine A1 Receptor

Current Pharmaceutical Design ◽

10.2174/1381612824666180820144917 ◽

2018 ◽

Vol 24 (27) ◽

pp. 3240-3249 ◽

Cited By ~ 4

Author(s):

Yuan Li ◽

Yan Li ◽

Xueyan Wang ◽

Hongyue Xu ◽

Chao Wang ◽

...

Keyword(s):

Body Weight ◽

Liver Lipid ◽

Adenosine A1 Receptor ◽

Gh3 Cells ◽

Serum Prolactin ◽

Lipid Levels ◽

Adenosine A1 ◽

A1 Receptor

Background: Cordycepin is an extract from the insect fungus Cordyceps. militaris with various biological function. In previous studies, cordycepin has demonstrated an excellent anti-obesity effect, but the mechanism is unclear. It was also demonstrated that prolactin played an important role in body weight regulation and hyperprolactinemia can promote appetite and accelerate fat deposition. In this study, we explored the molecular mechanism of the anti-obesity effect of cordycepin. Methods: In Vivo, the obese rat model was induced by high fat diet for five weeks, and the serum and liver lipid levels coupled with the serum prolactin levels were reduced following cordycepin treatment (P<0.01). Results: The results suggested that cordycepin is a potential drug that lowers blood and liver lipid levels and reduces body weight related to prolactin. Cordycepin also protects adipocytes from enlargement and hepatocytes from lipotoxicity-induced inflammation. In vitro, cordycepin inhibited prolactin secretion in GH3 cells via upregulating the expression of adenosine A1 receptor, and the inhibition effect was blocked by an antagonist of adenosine receptor A1 DPDPX, demonstrating that cordycepin may work as an adenosine agonist. Additionally, cordycepin inhibited the ERK/AKT/PI3K pathway in GH3 cells. At the same time, cordycepin blocked prolactininduced upregulation of lipogenesis genes PRLR, and phosphorylation of JAK2 in 3T3-L1 cells. In an in vivo study, cordycepin downregulated the expression of prolactin receptor (PRLR) but not the phosphorylation of JAK2. Conclusion: Thus, it was proved that cordycepin modulates body weight by reducing prolactin release via an adenosine A1 receptor.

Download Full-text

Mechanisms of Sevoflurane-induced Myocardial Preconditioning in Isolated Human Right Atria In Vitro

Anesthesiology ◽

10.1097/00000542-200307000-00008 ◽

2003 ◽

Vol 99 (1) ◽

pp. 27-33 ◽

Cited By ~ 31

Author(s):

Alexandra Yvon ◽

Jean-Luc Hanouz ◽

Benoît Haelewyn ◽

Xavier Terrien ◽

Massimo Massetti ◽

...

Keyword(s):

Potassium Channels ◽

Potassium Channel ◽

Adenosine Triphosphate ◽

Human Myocardium ◽

Right Atrial ◽

Human Right ◽

Myocardial Preconditioning ◽

Right Atria

Background The authors examined the role of adenosine triphosphate-sensitive potassium channels and adenosine A(1) receptors in sevoflurane-induced preconditioning on isolated human myocardium. Methods The authors recorded isometric contraction of human right atrial trabeculae suspended in oxygenated Tyrode's solution (34 degrees C; stimulation frequency, 1 Hz). In all groups, a 30-min hypoxic period was followed by 60 min of reoxygenation. Seven minutes before hypoxia reoxygenation, muscles were exposed to 4 min of hypoxia and 7 min of reoxygenation or 15 min of sevoflurane at concentrations of 1, 2, and 3%. In separate groups, sevoflurane 2% was administered in the presence of 10 microm HMR 1098, a sarcolemmal adenosine triphosphate-sensitive potassium channel antagonist; 800 microm 5-hydroxy-decanoate, a mitochondrial adenosine triphosphate-sensitive potassium channel antagonist; and 100 nm 8-cyclopentyl-1,3-dipropylxanthine, an adenosine A(1) receptor antagonist. Recovery of force at the end of the 60-min reoxygenation period was compared between groups (mean +/- SD). Results Hypoxic preconditioning (90 +/- 4% of baseline) and sevoflurane 1% (82 +/- 3% of baseline), 2% (92 +/- 5% of baseline), and 3% (85 +/- 7% of baseline) enhanced the recovery of force after 60 min of reoxygenation compared with the control groups (52 +/- 9% of baseline). This effect was abolished in the presence of 5-hydroxy-decanoate (55 +/- 14% of baseline) and 8-cyclopentyl-1,3-dipropylxanthine (58 +/- 16% of baseline) but was attenuated in the presence of HMR 1098 (73 +/- 10% of baseline). Conclusions In vitro, sevoflurane preconditions human myocardium against hypoxia through activation of adenosine triphosphate-sensitive potassium channels and stimulation of adenosine A(1) receptors.

Download Full-text