Norepinephrine inducement

Marzan AS, Hungerbuhler HJ, Studer A, Baumgartner RW, Georgiadis D. Feasibility and safety of norepinephrine-induced arterial hypertension in acute ischemic stroke. Neurology 2004 62(7) 1193-1195. 

The endogenous release of the potent vasoconstrictor neuropeptide Y (NPY) is increased during sepsis and the highest levels are detected in patients with shock (A8). NPY is a 36-amino-acid peptide belonging to the pancreatic polypeptide family of neuroendocrine peptides (T2). It is one of the most abundant peptides present in the brain and is widely expressed by neurons in the central and peripheral nervous systems as well as the adrenal medulla (A3). NPY coexists with norepinephrine in peripheral sympathetic nerves and is released together with norepinephrine (LI9, W14). NPY causes direct vasoconstriction of cerebral, coronary, and mesenteric arteries and also potentiates norepinephrine-induced vasoconstriction in these arterial beds (T8). It appears that vasoconstriction caused by NPY does not counterbalance the vasodilatator effects of substance P in patients with sepsis. The properties of vasodilatation and smooth muscle contraction of substance P are well known (14), but because of the morphological distribution and the neuroendocrine effects a possible stress hormone function for substance P was also advocated (J7). Substance P, which is a potent vasodilatator agent and has an innervation pathway similar to that of NPY, shows a low plasma concentration in septic patients with and without shock (A8). 

Martinez-Morales JR, Morales A, Marin R, Hern4ndez-Jim nez JG, Acevedo A, Guerra B, Hernandez G, Ldpez-Coviella I, Prieto L, Alonso R (2001) Estrogen modulates norepinephrine-induced accumulation of adenosine cyclic monophosphate in a subpopulation of immortalized luteinizing hormone-releasing hormone secreting neurons from the mouse hypothalamus. Neurosci Lett 298 61-64... 

Capuano CA, Leibowitz SF, Barr GA. 1992. The pharmaco-ontogeny of the paraventricular alpha 2-noradrenergic receptor system mediating norepinephrine-induced feeding in the rat. Brain Res Dev Brain Res 68(1) 67-74. 

Increased prothrombin time, partial thromboplastin time, platelet aggregation time, platelet count, and factors II, VII, VIII, IX, X, XII, Vll-X complex, ll-VII-X complex, and -thromboglobulin decreased antithrombin III, antifactor Xa increased fibrinogen, plasminogen, norepinephrine-induced platelet aggregability. 

Efferth T, Volm M (1992) Expression of protein kinase C in human renal cell cardnoma cells with inherent resistance to doxorubicin. Anticancer Res 12 2209-2211 Eguchi Y, Srinivasan A, Tomaselli KJ, Shimizu S, Tsujimoto Y (1999) ATP-dependent steps in apoptotic signal transduction. Cancer Res 59 2174-2181 Ek TP, Campbell MD, Deth RC, Gowraganahalli J (1989) Reduction of norepinephrine-induced tonic contraction and phosphoinositide turnover in arteries of spontaneously hypertensive rats. A possible role for protein kinase C. Am J Hy-pertens 2 40-45... 

Delmas P, Abogadie FC, Milligan G, Buckley NJ, Brown DA (1999) Py dimers derived from Go and Gj proteins contribute different components of adrenergic inhibiton of Ca channels in rat sympathetic neurons. J Physiol 518 23-36 Diverse-Pierluissi M, Inglese J, Stoffel RH, Lefkowitz RJ, Dunlap K (1996) G protein-coupled receptor kinase mediates desensitization of norepinephrine-induced Ca channel inhibition. Neuron 16 579-585 Docherty JR (1998) Subtypes of fimctional ap and a2-adrenoceptors. Eur J Pharmacol 361 1-15... 

The release of norepinephrine induced by I at 40 mg/kg was about 1.35 times that produced by the lower dose. The release of norepinephrine induced by tyramlne at 0.5 mg/kg was 1.47 times that by I at 40 mg/kg. The release by nicotine at 0.5 mg/kg was 1.59 times that by the larger dose of I. The action of I In Inducing release of norepinephrine from tissues In which it has been stored, although it Is slightly more prolonged (20 min vs. 15 min) than those of the classical releasers of norepinephrine, Is much weaker than those of tyramlne and nicotine. 

Incubation in 1-20 iM pyridine for 20 min inhibited norepinephrine-induced phasic and tonic contractions in the thoracic aorta, incubated as aortic rings, as well as the endothelium-denuded aorta of Wistar rats (Hsu Lin-Shiau, 1995). These effects were related to inhibition of the calcium influx normally elicited by norepinephrine. 

Rettori, V., Gimeno, M., Lyson, K., and McCann, S. M. (1992). Nitric oxide mediates norepinephrine-induced prostaglandin E2 release from the hypothalamus. Proc. Natl. Acad. Sci. U.S.A. 89, 11543-11546. 

Yuan Q, Harley CW, McLean JH. Mitral cell betal and 5-HT2A receptor colocalization and cAMP coregulation a new model of norepinephrine-induced learning in the olfactory bulb. Learn Mem 2003 10 5-15. 

Yamazaki T, Komuro I, Zou Y, Kudoh S, Shiojima I, Hiroi Y, Mizuno T, Aikawa R, Takano H, Yasaki Y. 1997. Norepinephrine induces the raf-1 kinase/mitogen-activated protein kinase cascade through both alpha 1- and beta-adrenoceptors. Circulation 95 1260-1268. 

He J-R, Molnar J, Barraclough CA (1994) Evidence that amplification of norepinephrine-induced LH release by morphine is indirectly due to suppression of tuberoinfundibular dopamine secretion. Brain Res 652 1-8. Hentschel K, Cheung S, Moore KE, Lookingland KJ (1998) Pharmacological evidence that neurotensin mediates prolactin-induced activation of tuberoinfundibular dopamine neurons. Neuroendocrinology 65 71-76. Hentschel K, Will YM, McMahon CD, Moore KE, Lookingland KJ (1999) Prolactin induces Fos-related antigen expression in neurotensin (NT)-IR neurons and increases numbers of NT-IR neurons in the arcuate nucleus. Soc Neurosci Abstr 25 1185. 

Ischemic AKI may be induced by intrarenal norepinephrine injection or by renal artery clamping. There are similarities between these two models of ischemic renal failure. In the norepinephrine model of renal failure, as in the arterial clamping model, there is the same degree of tubular injury except for a slightly greater frequency of tubular casts at 48 hours in ischemic model [32]. In both models, calcium channel-blockers, improve renal function [33, 34]. The major difference is that in the renal artery clamping model, morphology at 48 hours showed smooth muscle necrosis in half of the resistance vessels, but in less than 10% of those in norepinephrine-induced model. 

Calcium antagonist (aranidipine) Dilates both afferent and efferent arterioles during norepinephrine-induced constriction [252]... 

The effect of acetylcholine, dopamine, and bradyki-nin on vascular tone has been examined in interlobular arteries and superficial afferent and efferent arterioles isolated from rabbit kidney [141]. Acetylcholine caused a dose-dependent relaxation of norepinephrine-induced tone in all three vessel types. Significant relaxation was observed with 10(-8) M acetylcholine and higher concentrations caused complete relaxation. In afferent and efferent arterioles dopamine caused a dose-dependent relaxation that was indistinguishable from the one caused by acetylcholine. Dopamine was much less effective on interlobular arteries. In afferent arterioles atropine blocked the effect of acetylcholine, and metoclopramide selectively inhibited dopamine-induced relaxation. Bradykinin caused a dose-dependent relaxation of norepinephrine- induced tone only in efferent arterioles. Bradykinin, either in the bath or lumen, had no effect on the preglomerular microves-... 

As shown in "Fig. (2) and Fig. (3)", adenosine and pyroglutamic acid inhibited norepinephrine-induced lipolysis dose-dependently. 

Fig. (7). Effects of euciyphin, beigenin and astilbin on norepinephrine-induced lipolysis in rat fat cells...

Arger P H, Sehgal C M, Pugh C R et ai 1999 Evaiuation of change in blood flow by contrast-enhanced power Doppler imaging during norepinephrine-induced renal vasoconstriction. Journal of Ultrasound in Medicine 18 843-851... 

The primary mechanism of terbutaline is the stimulation of adenylcyclase, which catalyzes cyclic adenosine monophosphate (AMP) from adenosine triphosphate (ATP). In the liver, buildup of cyclic AMP stimulates glycogenolysis and an increase in serum glucose. In skeletal muscle, this process results in increased lactate production. Direct stimulus of sodium/potassium AT-Pase in skeletal muscle produces a shift of potassium from the extracellular space to the intracellular space. Relaxation of smooth muscle produces a dilation of the vasculamre supplying skeletal muscle, which results in a drop in diastolic and mean arterial pressure (MAP). Tachycardia occurs as a reflex to the drop in MAP or as a result of Pi stimulus. )Si-Adrenergic receptors in the locus ceruleus also regulate norepinephrine-induced inhibitory effects, resulting in agitation, restlessness, and tremor. 

Gu H, Trajkovic S, Labelle EF. Norepinephrine-induced phosphatidylcholine hydrolysis by phospholipase-D and phospholipase-C in rat tail artery. Am J Physiol 1992 262 C1376-C1383. 

Pheochromocytoma a-Antagonists Reduce norepinephrine-induced vasoconstriction Phenoxybenzamine... 

Marino TA, Cassidy M, Marino DR, Carson NL, Houser S. Norepinephrine-induced cardiac hypertrophy of the cat heart. Anat Rec 1991 229 505-510. 

In contrast to arARs, the effects of a2-AR stimulation on gene expression have not been well studied with DNA microarrays. Laifenfeld et al. (50) used DNA microarrays to identify gene expression changes that accompany norepinephrine-induced neuronal differentiation in SH-SY5 Y cells that endogenously express o -ARs. However, much more work is needed to understand fully the effects of (Xj-AR stimulation on gene expression. 

Isocorydine was observed to significantly decrease the frequency of spontaneous contraction and muscle tension, but not the amplitude of contraction on the isolated isthmus of the oviduct of the rabbit The tension and frequency of spontaneous contraction was suppressed by the alkaloid at concentrations of 3-300 pmol/1, but the amplitude of contraction was decreased only at 300 pmol/1. The alkaloid antagonized the norepinephrine-induced contraction of the oviduct, and the transport of ova through the oviduct was delayed by isocorydine [285]. 

Preischemic activation of a-adrenergic signaling also results in cardioprotection. Pretreatment with norepinephrine induces bimodal (early and delayed) myocardial functional adaptation to ischemia in rats. PKC appears to be involved in the early response. Delayed protection was shown to be associated with the expression of genes encoding fetal contractile proteins (increase in P-MHC mRNA).94 However, a-receptor agonists can trigger arrhythmias in the setting of ischemia and reperfusion.55... 

Hydergine also partially inhibits norepinephrine-induced activation of neuronal Na+-K+ ATPase by a similar anti-adrenergic mechanism -. 

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