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81.
C. Agnisola F. B. Jensen B. Tota T. Mustafa 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》1998,168(2):96-104
The effects of arachidonic acid (AA) and indomethacin (IM) on performance, oxygen consumption and lactate release of the
trout heart were studied in vitro TPa s m−3 using a perfusion system, which allowed the evaluation of the integrated function of ventricle and coronary system by continuously
setting the input coronary flow and pressure proportional to the pressure and flow output of the heart. The heart was working
against a fixed resistance. A reduction of input oxygen partial pressure (PO2) from 175 torr (high PO2) to 76 torr (low PO2) increased the coronary flow (from 0.51 ml min−1 kg−1 to 1.21 ml min−1 kg−1, respectively) due to a strong reduction in coronary resistance (from 0.60 TPa s m−3 to 0.19 TPa s m−3, respectively). Oxygen consumption by the heart was significantly reduced from 20.7 ml min−1 g−1 at high PO2 to 4.6 ml min−1 g−1 at low PO2, while lactate production was increased from 24 μmol h−1 g−1 to 42 μmol h−1 g−1, indicating a higher contribution of anaerobic respiration to mechanical work. Mechanical efficiency was significantly higher
at low than at high PO2. Exogenous AA caused a depression of inotropism and a reduction in the aerobic metabolic rate (by 25–35%), which was not
accompanied by increased lactate production. IM enhanced the depression of both inotropism and aerobic metabolism. The effect
of AA and IM on the heart were amplified at low PO2.
Accepted: 20 October 1997 相似文献
82.
Alexander Pasternak Stephen D. Goble Reynalda K. deJesus Donna L. Hreniuk Christine C. Chung Michael R. Tota Paul Mazur Scott D. Feighner Andrew D. Howard Sander G. Mills Lihu Yang 《Bioorganic & medicinal chemistry letters》2009,19(21):6237-6240
This Letter describes optimization of ghrelin receptor antagonists and inverse agonists starting from a screening hit. 相似文献
83.
Pellegrino D Tota B Randall DJ 《Comparative biochemistry and physiology. Part A, Molecular & integrative physiology》2005,142(2):198-204
The potent vasomodulator adenosine (AD), thanks to the interaction with by A(1) and A(2) receptors, dilates systemic, coronary and cerebral vasculatures but exert a constrictor action in several vessels of respiratory organs. Recent investigations suggest that nitric oxide (NO) contributes to AD effects. In fish, both NO and AD induce atypical effects compared to mammals. Since there is very little information on the role of NO and its involvement in mediating the actions of AD in fish, we have analysed this question in the branchial vasculature of the elasmobranch Squalus acanthias and the teleost Anguilla anguilla using an isolated perfused head and a branchial basket preparation, respectively. In both dogfish and eel, AD dose-response curves showed a biphasic effect: vasoconstriction (pico to nanomolar range) and vasodilation (micromolar range). Both effects were abolished by the classic xanthine inhibitor theophylline (Theo) and also by specific antagonists of A(1) and A(2) receptor subtypes. To analyse the involvement of the NO/cGMP system in the AD responses, we tested a NOS inhibitor, l-NIO, and a specific soluble guanylate cyclase (sGC) blocker, ODQ. In both dogfish and eel preparations l-NIO abrogated all vasomotor effects of AD, whereas ODQ blocked the AD-mediated vasoconstriction without affecting the vasorelaxant response. This indicates that only AD-induced vasoconstriction is mediated by a NO-cGMP-dependent mechanism. By using the NO donor SIN-1, we showed a dose-dependent vasoconstrictory effect which was completely blocked by ODQ. These results provide compelling evidence that the vasoactive role of AD in the branchial circulation of S. acanthias and A. anguilla involves a NO signalling. 相似文献
84.
85.
Sinz C Chang J Lins AR Brady E Candelore M Dallas-Yang Q Ding V Jiang G Lin Z Mock S Qureshi S Salituro G Saperstein R Shang J Szalkowski D Tota L Vincent S Wright M Xu S Yang X Zhang B Tata J Kim R Parmee E 《Bioorganic & medicinal chemistry letters》2011,21(23):7131-7136
In the course of the development of an aminobenzimidazole class of human glucagon receptor (hGCGR) antagonists, a novel class of cyclic guanidine hGCGR antagonists was discovered. Rapid N-dealkylation resulted in poor pharmacokinetic profiles for the benchmark compound in this series. A strategy aimed at blocking oxidative dealkylation led to a series of compounds with improved rodent pharmacokinetic profiles. One compound was orally efficacious in a murine glucagon challenge pharmacodynamic model and also significantly lowered glucose levels in a murine diabetes model. 相似文献
86.
Anderson WG Cerra MC Wells A Tierney ML Tota B Takei Y Hazon N 《Comparative biochemistry and physiology. Part A, Molecular & integrative physiology》2001,128(1):31-40
In mammals, a principal bioactive component of the renin-angiotensin system (RAS), angiotensin II (ANG II), is known to be vasopressor, dipsogenic, a stimulant of adrenocortical secretion and to control glomerular and renal tubular function. Historically, a RAS analogous to that found in mammals was thought to have first evolved in the bony fishes. Recent research has identified the unusually structured elasmobranch [Asp(1)-Pro(3)-Ile(5)] ANG II. Physiological studies have demonstrated that ANG II in elasmobranchs is vasopressor, and stimulates interrenal gland production of the elasmobranch corticosteroid 1alpha-hydroxycorticosterone. The specific binding of ANG II in elasmobranchs has been reported in gills, heart, interrenal gland, gut and rectal gland. The precise osmoregulatory role ANG II plays in cartilaginous fishes is not yet known; however, putative evidence is emerging for a role in the control of drinking rate, rectal gland secretion, and kidney function. 相似文献
87.
Pellegrino D Acierno R Tota B 《Comparative biochemistry and physiology. Part A, Molecular & integrative physiology》2003,134(2):471-480
The involvement of nitric oxide (NO) in the branchial circulation and cardiac performance of the Antarctic hemoglobinless icefish Chionodraco hamatus was investigated using isolated and perfused head and working heart preparations. In the branchial vasculature under basal (i.e. unstimulated conditions), the nitric oxide synthase (NOS) inhibitor L-NIO (L-N(5)-(1-iminoethyl) ornithine, 10(-5) and 10(-4) M), caused a marked vasoconstriction (20%), indicating a basal nitrergic vasodilator tone, while the dose-response curve of the NO donor SIN-1 (3-morpholinosydnonimine) showed a dose-dependent vasodilator effect. Acetylcholine induced a dose-dependent branchial vasoconstriction mediated by muscarinic receptors, since the effects were abolished by pre-treatment with atropine (10(-4) M). Serotonin (5-HT) induced a dose-dependent branchial methysergide-sensitive vasoconstriction which was abolished by pre-treatment with L-NIO, indicating a NO-dependent mechanism. On the isolated heart, the NOS inhibitor L-NMMA (N(G)-monomethyl-L-arginine) 10(-4) M produced a small, but significant decrease of heart rate and, as a consequence, a decrease of power output, while the NO donor sodium nitroprusside (SNP) 10(-4) M elicited increases of stroke volume, stroke work and power output, suggesting an exogenous NO-dependent positive inotropism. Exposure of the bulbus arteriosus to L-NMMA was without any appreciable effect. In contrast, SNP produced a notable relaxation of the bulbus wall with a marked increase of its stiffness, as indicated by the increase of systolic and diastolic dP/dt max (23 and 104%, respectively). 相似文献
88.
Eleonora Bassino Sara Fornero Maria Pia Gallo Clara Gallina Saveria Femminò Renzo Levi Bruno Tota Giuseppe Alloatti 《PloS one》2015,10(3)
Catestatin (Cst) is a 21-amino acid peptide deriving from Chromogranin A. Cst exerts an overall protective effect against an excessive sympathetic stimulation of cardiovascular system, being able to antagonize catecholamine secretion and to reduce their positive inotropic effect, by stimulating the release of nitric oxide (NO) from endothelial cells. Moreover, Cst reduces ischemia/reperfusion (I/R) injury, improving post-ischemic cardiac function and cardiomyocyte survival. To define the cardioprotective signaling pathways activated by Cst (5 nM) we used isolated adult rat cardiomyocytes undergoing simulated I/R. We evaluated cell viability rate with propidium iodide labeling and mitochondrial membrane potential (MMP) with the fluorescent probe JC-1. The involvement of Akt, GSK3β, eNOS and phospholamban (PLN) cascade was studied by immunofluorescence. The role of PI3K-Akt/NO/cGMP pathway was also investigated by using the pharmacological blockers wortmannin (Wm), L-NMMA and ODQ. Our experiments revealed that Cst increased cell viability rate by 65% and reduced cell contracture in I/R cardiomyocytes. Wm, L-NMMA and ODQ limited the protective effect of Cst. The protective outcome of Cst was related to its ability to maintain MMP and to increase AktSer473, GSK3βSer9, PLNThr17 and eNOSSer1179 phosphorylation, while treatment with Wm abolished these effects. Thus, the present results show that Cst is able to exert a direct action on cardiomyocytes and give new insights into the molecular mechanisms involved in its protective effect, highlighting the PI3K/NO/cGMP pathway as the trigger and the MMP preservation as the end point of its action. 相似文献
89.
90.
Naylor EM Parmee ER Colandrea VJ Perkins L Brockunier L Candelore MR Cascieri MA Colwell LF Deng L Feeney WP Forrest MJ Hom GJ MacIntyre DE Strader CD Tota L Wang PR Wyvratt MJ Fisher MH Weber AE 《Bioorganic & medicinal chemistry letters》1999,9(5):755-758
The cyclopentylpropylimidazolidinone L-766,892 is a potent beta3 AR agonist (EC50 5.7 nM, 64% activation) with 420- and 130-fold selectivity over binding to the beta1 and beta2 ARs, respectively. In anesthetized rhesus monkeys, L-766,892 elicited dose-dependent hyperglycerolemia (ED50 0.1 mg/kg) with minimal effects on heart rate. 相似文献