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Artykuły w czasopismach na temat „Adrenergic nerve”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

Powell, Cynthia C., and Charles L. Martin. "Distribution of cholinergic and adrenergic nerve fibers in the lacrimal glands of dogs." American Journal of Veterinary Research 50, no. 12 (1989): 2084–88. https://doi.org/10.2460/ajvr.1989.50.12.2084.

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SUMMARY The distribution of postganglionic autonomic nerve fibers in the lacrimal gland and gland of the third eyelid of dogs was studied by use of histochemical techniques. Adrenergic nerve distribution was identified by use of the sucrose-potassium phosphate-glyoxylic acid technique. A loose network of adrenergic nerves was found throughout the interstitium around acini and blood vessels and in vessel walls. Acetylcholinesterase staining was used to identify cholinergic nerve fibers. A cholinergic distribution pattern around acini and blood vessels similar to the adrenergic pattern was found

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2

Noh, Mi, Hee-Seong Jang, Jinu Kim, and Babu Padanilam. "Renal Sympathetic Nerve-Derived Signaling in Acute and Chronic Kidney Diseases." International Journal of Molecular Sciences 21, no. 5 (2020): 1647. http://dx.doi.org/10.3390/ijms21051647.

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The kidney is innervated by afferent sensory and efferent sympathetic nerve fibers. Norepinephrine (NE) is the primary neurotransmitter for post-ganglionic sympathetic adrenergic nerves, and its signaling, regulated through adrenergic receptors (AR), modulates renal function and pathophysiology under disease conditions. Renal sympathetic overactivity and increased NE level are commonly seen in chronic kidney disease (CKD) and are critical factors in the progression of renal disease. Blockade of sympathetic nerve-derived signaling by renal denervation or AR blockade in clinical and experimental

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3

Pitetti, K. H., G. A. Iwamoto, J. H. Mitchell, and G. A. Ordway. "Stimulating somatic afferent fibers alters coronary arterial resistance." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 6 (1989): R1331—R1339. http://dx.doi.org/10.1152/ajpregu.1989.256.6.r1331.

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We used a constant flow preparation to study the changes in left circumflex coronary arterial (LCCA) pressure and resistance evoked by electrical stimulation of branches of muscle, cutaneous, and mixed nerves in the hindlimb of anesthetized dogs. Stimulation (20 Hz) of all three nerve types at 20, 70, 100, and 200 times the voltage threshold that evoked compound action potentials significantly (P less than 0.05) increased LCCA resistance. Stimulation at three and five times threshold had no effect on this same variable. Cooling the nerve to 2-4 degrees C, temperatures that block myelinated ner

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4

Tangsucharit, Panot, Shingo Takatori, Pengyuan Sun, et al. "Do cholinergic nerves innervating rat mesenteric arteries regulate vascular tone?" American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 11 (2012): R1147—R1156. http://dx.doi.org/10.1152/ajpregu.00317.2012.

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Vascular blood vessels have various types of cholinergic acetylcholine receptors (AChR), but the source of ACh has not been confirmed. Perivascular adrenergic nerves and nonadrenergic calcitonin gene-related peptide (CGRP)-containing (CGRPergic) nerves innervate rat mesenteric arteries and regulate vascular tone. However, function of cholinergic innervation remains unknown. The present study investigated cholinergic innervation by examining effects of cholinesterase inhibitor (neostigmine), a muscarinic AChR antagonist (atropine), and a nicotinic AChR antagonist (hexamethonium) on adrenergic n

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5

Amano, Tatsuro, Naoto Fujii, Yoshimitsu Inoue, and Narihiko Kondo. "Cutaneous adrenergic nerve blockade attenuates sweating during incremental exercise in habitually trained men." Journal of Applied Physiology 125, no. 4 (2018): 1041–50. http://dx.doi.org/10.1152/japplphysiol.00370.2018.

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It remains unknown whether cutaneous adrenergic nerves functionally contribute to sweat production during exercise. This study examined whether cutaneous adrenergic nerve blockade attenuates sweating during incremental exercise, specifically in habitually trained individuals. Accordingly, 10 habitually trained and 10 untrained males (V̇o2max: 56.7 ± 5.4 and 38.9 ± 6.7 ml·kg−1·min−1, respectively; P < 0.001) performed incremental semirecumbent cycling (20 W/min) until exhaustion. Sweat rates (ventilated capsule) were measured at two bilateral forearm skin sites on which either 10 mM bretyliu

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6

Kubes, P., M. Melinyshyn, K. Nesbitt, S. M. Cain, and C. K. Chapler. "Participation of alpha 2-adrenergic receptors in neural vascular tone of canine skeletal muscle." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 6 (1992): H1705—H1710. http://dx.doi.org/10.1152/ajpheart.1992.262.6.h1705.

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Studies were carried out in anesthetized, paralyzed, and ventilated dogs to determine whether postsynaptic alpha 2-adrenergic receptors participated in neurally mediated vascular tone in skeletal muscle. Hindlimb skeletal muscle resistance (RL) and blood flow (QL) were determined before, during, and after reversible cold block of the sciatic nerve. This sequence of observations was repeated 30 min after blockade of alpha 1-adrenergic receptors with prazosin. Then the alpha 2-adrenergic receptors were blocked with yohimbine, and the nerve cold block was repeated. When the sciatic nerve was cold

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7

Cohen, RA. "Platelet 5-Hydroxytryptamine and Vascular Adrenergic Nerves." Physiology 3, no. 5 (1988): 185–89. http://dx.doi.org/10.1152/physiologyonline.1988.3.5.185.

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Platelets contain and release large amounts of 5-hydroxytryptamine that can influence the function of vascular adrenergic nerves. The immediate effect on neuronal function of low concentrations of the amine is to inhibit norepinephrine release. 5-Hydroxytryptamine may also be accumulated by the same uptake mechanism that reaccumulates norepinephrine into the adrenergic nerve endings. In diseased blood vessels where platelet aggregation occurs, 5-hydroxytryptamine may therby assume an alternative transmitter role, altering the function of the sympathetic nerves.

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8

Luo, Min, Gregory D. Fink, Keith J. Lookingland, John A. Morris та James J. Galligan. "Impaired function of α2-adrenergic autoreceptors on sympathetic nerves associated with mesenteric arteries and veins in DOCA-salt hypertension". American Journal of Physiology-Heart and Circulatory Physiology 286, № 4 (2004): H1558—H1564. http://dx.doi.org/10.1152/ajpheart.00592.2003.

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The present study tested the hypothesis that there is impaired function of α2-adrenergic autoreceptors and increased transmitter release from sympathetic nerves associated with mesenteric arteries and veins from DOCA-salt rats. High-performance liquid chromatography was used to measure the overflow of ATP and norepinephrine (NE) from electrically stimulated mesenteric artery and vein preparations in vitro. In sham arteries, nerve stimulation evoked a 1.5-fold increase in NE release, whereas in DOCA-salt arteries there was a 3.9-fold increase in NE release over basal levels ( P < 0.05). In c

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9

Danser, A. H., R. van den Ende, R. R. Lorenz, N. A. Flavahan, and P. M. Vanhoutte. "Prejunctional beta 1-adrenoceptors inhibit cholinergic transmission in canine bronchi." Journal of Applied Physiology 62, no. 2 (1987): 785–90. http://dx.doi.org/10.1152/jappl.1987.62.2.785.

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The aim of the present study was to determine in canine bronchi the effects produced by norepinephrine (released from adrenergic nerve terminals) on cholinergic neurotransmission. Electrical stimulation of canine bronchi activates cholinergic and adrenergic nerve fibers. The adrenergic neuronal blocker, bretylium tosylate, inhibited the increase in [3H]norepinephrine overflow evoked by electrical stimulation but did not prevent that caused by the indirect sympathomimetic tyramine. During blockade of the exocytotic release of norepinephrine with bretylium, the pharmacological displacement of th

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10

Nausch, Lydia W. M., Adrian D. Bonev, Thomas J. Heppner, Yvonne Tallini, Michael I. Kotlikoff, and Mark T. Nelson. "Sympathetic nerve stimulation induces local endothelial Ca2+ signals to oppose vasoconstriction of mouse mesenteric arteries." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 3 (2012): H594—H602. http://dx.doi.org/10.1152/ajpheart.00773.2011.

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It is generally accepted that the endothelium regulates vascular tone independent of the activity of the sympathetic nervous system. Here, we tested the hypothesis that the activation of sympathetic nerves engages the endothelium to oppose vasoconstriction. Local inositol 1,4,5-trisphosphate (IP3)-mediated Ca2+ signals (“pulsars”) in or near endothelial projections to vascular smooth muscle (VSM) were measured in an en face mouse mesenteric artery preparation. Electrical field stimulation of sympathetic nerves induced an increase in endothelial cell (EC) Ca2+ pulsars, recruiting new pulsar sit

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11

Chuchkova, N. N., O. L. Polyakova, A. E. Shklyaev, V. M. Chuchkov, M. V. Smetanina, and K. A. Pazinenko. "Microvascular bed and adrenergic nerve endings of the pulp during permanent teeth eruption." Journal of Anatomy and Histopathology 12, no. 2 (2023): 72–78. http://dx.doi.org/10.18499/2225-7357-2023-12-2-72-78.

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The aim of the study was to reveal associations between the number of functioning microvessels and formation of adrenergic control (nerve endings containing catecholamine) of the dental pulp in children and adolescents of Udmurtia during the period of permanent teeth eruption. Material and methods. The study included neurovascular bundle of the pulp of teeth extracted for medical reasons at the age of 5 to 14 years. At the light-optical level, the number of functioning capillaries was counted; an electron microscopic technique was used to qualitative assess the microvascular bed. Identificatio

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12

Jordan, D. A., M. J. Breslow, K. L. Kubos, and R. J. Traystman. "Adrenergic receptors of adrenal medullary vasculature." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 1 (1989): H233—H239. http://dx.doi.org/10.1152/ajpheart.1989.256.1.h233.

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The present study evaluates possible effects of adrenal catecholamines, released by splanchnic nerve stimulation, on adrenal medullary blood flow (MQ) and adrenal catecholamine secretion (CS). Twelve pentobarbital-anesthetized mongrel dogs were subjected to three identical splanchnic nerve stimulations (5 V, 20 Hz, for 3 min) at 30-min intervals, and MQ (radiolabeled microsphere technique) and CS (high-performance liquid chromatography) were measured before and during each nerve stimulation. Animals were assigned to one of three groups and administered either saline, pindolol (1 and 4 mg/kg),

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13

Garfield, R. E. "Structural studies of innervation on nonpregnant rat uterus." American Journal of Physiology-Cell Physiology 251, no. 1 (1986): C41—C54. http://dx.doi.org/10.1152/ajpcell.1986.251.1.c41.

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Whole-mount preparations of the uterus and mesentery from nonpregnant rats were examined after staining with glyoxylic acid or acetylcholinesterase to demonstrate the innervation. Some uterine tissues were also evaluated by electron microscopy. Glyoxylic acid fluorescent nerves were present in the mesentery, mesometrium, and uterine wall exclusively around blood vessels. Acetylcholinesterase positive nerve fibers from Frankenhauser's plexus (cervical ganglia) were associated with blood vessels and muscle in the uterine wall but not in the mesentery. Electron microscopy revealed nerve varicosit

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14

Du, X. J., E. Vincan, D. M. Woodcock, C. A. Milano, A. M. Dart, and E. A. Woodcock. "Response to cardiac sympathetic activation in transgenic mice overexpressing beta 2-adrenergic receptor." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 2 (1996): H630—H636. http://dx.doi.org/10.1152/ajpheart.1996.271.2.h630.

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Transgenic mice have been created with 200-fold overexpression of beta 2-adrenergic receptors specifically in the heart. Cardiac function was studied in these transgenic mice and their controls at baseline and during isoproterenol perfusion or sympathetic nerve stimulation. The model used was an in situ buffer-perfused, innervated heart, and the left ventricle maximal derivative of pressure over time (dP/dtmax) and heart rate (HR) were measured. Basal HR and dP/dtmax were 30-40% higher in hearts from transgenic mice than controls. Electrical stimulation of sympathetic nerves (2, 4, and 8 Hz) o

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15

Bossut, D. F., and E. R. Perl. "Effects of nerve injury on sympathetic excitation of A delta mechanical nociceptors." Journal of Neurophysiology 73, no. 4 (1995): 1721–23. http://dx.doi.org/10.1152/jn.1995.73.4.1721.

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1. The effects of sympathetic stimulation and close arterial injection of norepinephrine were tested on cutaneous myelinated-fiber (A delta) mechanical nociceptors [high-threshold mechanoreceptors-(MyHTMs)] from normal and from partially transsected nerves. 2. Neither sympathetic stimulation nor close arterial injection of norepinephrine (200 ng) excited MyHTMs (18) recorded from the uninjured great auricular nerve of adult rabbits. 3. MyHTMs (58) conducting across the site of partial cut lesions, made 2 to 28 days previously, had threshold and responsiveness to mechanical stimuli, receptive f

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16

Dodd, L. R., and P. C. Johnson. "Antagonism of vasoconstriction by muscle contraction differs with alpha-adrenergic subtype." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 3 (1993): H892—H900. http://dx.doi.org/10.1152/ajpheart.1993.264.3.h892.

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It has been suggested that muscle contraction causes prejunctional inhibition of transmitter release from sympathetic nerves. In accordance with this, we found that second-order (50 microns ID) arterioles of the cat sartorius muscle dilate 40-80% more with muscle contraction during 2-, 4-, or 8-Hz sympathetic nerve stimulation than during equivalent constriction produced by intravenous norepinephrine injection. However, when constriction was to the selective alpha 1-agonist phenylephrine, the magnitude of dilation induced by muscle contraction was similar to that seen with sympathetic nerve st

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17

O'Shea, J. E., and B. K. Evans. "Innervation of bat heart: cholinergic and adrenergic nerves innervate all chambers." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 4 (1985): H876—H882. http://dx.doi.org/10.1152/ajpheart.1985.249.4.h876.

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Adult Miniopterus schreibersii were anesthetized with chloroform, and in vitro preparations of cardiac chambers were prepared. Stimulation of intramural nerves in right ventricles paced at 6 Hz caused an inhibition (56.3 +/- 3.5% decrease on basal force) mediated by cholinergic nerves and an excitation (91.5 +/- 9.9% increase on basal force) mediated by adrenergic nerves. Mean pD2s (-log effective concentration, 50%) for ventricular beta-adrenoceptors and muscarinic cholinoceptors were 6.99 +/- 0.03 and 6.42 +/- 0.07, respectively. The inhibition of ventricular contractility, by nerve stimulat

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18

Woo, Seunghui, Geehoon Chung, Hyunsu Bae, and Sun Kwang Kim. "Suppressive Effects of Bee Venom-Derived Phospholipase A2 on Mechanical Allodynia in a Rat Model of Neuropathic Pain." Toxins 11, no. 8 (2019): 477. http://dx.doi.org/10.3390/toxins11080477.

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Bee venom (BV) has a long history of being used in traditional Korean medicine to relieve pain. Here, we investigated the effect of BV-derived phospholipase A2 (bvPLA2), a major component of BV, on peripheral nerve injury-induced neuropathic pain in rats. Spinal nerve ligation (SNL) was performed in Sprague Dawley rats to induce neuropathic pain, and paw withdrawal thresholds were measured using von Frey test. Mechanical allodynia, the representative symptom of neuropathic pain, was manifested following SNL and persisted for several weeks. The repetitive bvPLA2 treatment (0.2 mg/kg/day, i.p.)

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19

Koistinaho, J. "Adrenergic Nerve Fibers in the Human Fetal Sciatic Nerve." Cells Tissues Organs 140, no. 4 (1991): 369–72. http://dx.doi.org/10.1159/000147084.

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Li, Z., D. N. Krause, S. Doolen, and S. P. Duckles. "Ovariectomy eliminates sex differences in rat tail artery response to adrenergic nerve stimulation." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 4 (1997): H1819—H1825. http://dx.doi.org/10.1152/ajpheart.1997.272.4.h1819.

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The influence of gonadal hormones on vasoconstrictor responses to adrenergic nerve stimulation was investigated by comparing tail arteries from intact and gonadectomized male and female Fisher 344 rats. Arterial ring segments from females were significantly less responsive to transmural nerve stimulation (1-8 Hz) than arteries from age-matched males. Significant male-female differences persisted after correcting the contractile responses for sex-related differences in arterial mass, optimal resting tension, and maximal contractile force. Arteries were taken from cycling, intact females in eith

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21

Artico, Marco, Carlo Cavallotti, and Daniela Cavallotti. "Adrenergic nerve fibres and mast cells:." Immunology Letters 84, no. 1 (2002): 69–76. http://dx.doi.org/10.1016/s0165-2478(02)00145-1.

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22

Zochodne, Douglas W., and Phillip A. Low. "Adrenergic control of nerve blood flow." Experimental Neurology 109, no. 3 (1990): 300–307. http://dx.doi.org/10.1016/s0014-4886(05)80021-4.

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23

Tai, T. C., David C. Wong-Faull, Robert Claycomb, and Dona L. Wong. "Nerve Growth Factor Regulates Adrenergic Expression." Molecular Pharmacology 70, no. 5 (2006): 1792–801. http://dx.doi.org/10.1124/mol.106.026237.

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Chen, D. G., X. Z. Dai, and R. J. Bache. "Postsynaptic adrenoceptor-mediated vasoconstriction in coronary and femoral vascular beds." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 5 (1988): H984—H992. http://dx.doi.org/10.1152/ajpheart.1988.254.5.h984.

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This study examined the response to intra-arterial norepinephrine and sympathetic nerve stimulation on perfusion pressure of cannulated dog femoral and left circumflex coronary arteries perfused at constant flow rates. Sympathetic nerve stimulation was delivered through the decentralized inferior cardiac nerve and the lumbar sympathetic chain; beta-adrenergic blockade was maintained with propranolol. In the coronary artery, the vasoconstrictor response to norepinephrine was blunted by alpha 1-adrenergic blockade with prazosin but was abolished by alpha 2-adrenergic blockade with rauwolscine, i

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25

Buchholz, John, та Sue P. Duckles. "Chronic hypoxia alters prejunctional α2-receptor function in vascular adrenergic nerves of adult and fetal sheep". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, № 3 (2001): R926—R934. http://dx.doi.org/10.1152/ajpregu.2001.281.3.r926.

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The impact of development and chronic high-altitude hypoxia on the function of prejunctional α2-adrenoceptors was studied by measuring norepinephrine release in vitro from fetal and adult sheep middle cerebral and facial arteries. Blockade of prejunctional α2-adrenoceptors with idazoxan significantly increased stimulation-evoked norepinephrine release in normoxic arteries. This effect was eliminated after chronic hypoxia in cerebral arteries, with a tendency to decline in fetal facial arteries. After chronic hypoxia, the capacity to release norepinephrine declined in fetal middle cerebral arte

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Westby, J., S. Birkeland, S. E. Rynning, O. L. Myking, J. Lekven, and K. Grong. "Alpha-adrenergic vasoconstriction in normal and hypoperfused myocardium during sympathetic nerve stimulation." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 6 (1992): H1682—H1688. http://dx.doi.org/10.1152/ajpheart.1992.263.6.h1682.

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Coronary vasoconstriction mediated by postjunctional alpha 1- and alpha 2-adrenergic receptors was studied in normally perfused (control group) and left coronary hypoperfused (stenosis group) hearts of vagotomized, beta-blocked (propranolol) cats. Cardiac sympathetic nerve stimulation was combined with alpha 1- and subsequent alpha 2-adrenergic antagonism (doxazosin and SK &F 104078). Coronary perfusion pressure and heart rate were kept constant within groups; regional myocardial blood flow and cardiac output were obtained by means of microspheres with concomitant measurement of left ventr

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27

Lee, Hyung Gon, Ji A. Song, Dong Soo Han, Kyeong Wan Woo, and Myung Ha Yoon. "Antiallodynic Effects of Intrathecal Areca Nut for Spinal Nerve-Ligated and Chemotherapy-Induced Neuropathic Pain in Rats." Pharmacology 102, no. 5-6 (2018): 332–38. http://dx.doi.org/10.1159/000492394.

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This study examined the effects of intrathecal areca nut on spinal nerve-ligated and chemotherapy-induced neuropathic pain (NP), and investigated the relevance of spinal 5-hydroxytryptamine (5-HT) and α2-adrenergic receptors to those effects. For drug administration, intrathecal catheters were inserted into the subarachnoid space of male Sprague-Dawley rats. NP was induced either by spinal nerve ligation (left spinal nerves L5 and L6) or by chemotherapeutic injection (intraperitoneal cisplatin, 2 mg/kg/day, once daily for 4 days). Paw withdrawal thresholds (PWT) were mechanically assessed usin

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Ajijola, Olujimi A., Marmar Vaseghi, Wei Zhou, et al. "Functional differences between junctional and extrajunctional adrenergic receptor activation in mammalian ventricle." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 4 (2013): H579—H588. http://dx.doi.org/10.1152/ajpheart.00754.2012.

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Increased cardiac sympathetic activation worsens dispersion of repolarization and is proarrhythmic. The functional differences between intrinsic nerve stimulation and adrenergic receptor activation remain incompletely understood. This study was undertaken to determine the functional differences between efferent cardiac sympathetic nerve stimulation and direct adrenergic receptor activation in porcine ventricles. Female Yorkshire pigs ( n = 13) underwent surgical exposure of the heart and stellate ganglia. A 56-electrode sock was placed over the ventricles to record epicardial electrograms. Ani

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Richer, Louis-Philippe, Alain Vinet, Teresa Kus, René Cardinal, Jeffrey L. Ardell та John Andrew Armour. "α-Adrenoceptor blockade modifies neurally induced atrial arrhythmias". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, № 4 (2008): R1175—R1180. http://dx.doi.org/10.1152/ajpregu.00840.2007.

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Our objective was to determine whether neuronally induced atrial arrhythmias can be modified by α-adrenergic receptor blockade. In 30 anesthetized dogs, trains of five electrical stimuli (1 mA; 1 ms) were delivered immediately after the P wave of the ECG to mediastinal nerves associated with the superior vena cava. Regional atrial electrical events were monitored with 191 atrial unipolar electrodes. Mediastinal nerve sites were identified that reproducibly initiated atrial arrhythmias. These sites were then restimulated following 1 h (time control, n = 6), or the intravenous administration of

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Kitchen, Amy M., Tadeusz J. Scislo та Donal S. O'Leary. "NTS A2a purinoceptor activation elicits hindlimb vasodilation primarily via a β-adrenergic mechanism". American Journal of Physiology-Heart and Circulatory Physiology 278, № 6 (2000): H1775—H1782. http://dx.doi.org/10.1152/ajpheart.2000.278.6.h1775.

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Previously, we have shown that activation of adenosine A2a receptors in the subpostremal nucleus tractus solitarii (NTS) via microinjection of the selective A2a receptor agonist CGS-21680 elicits potent, dose-dependent decreases in mean arterial pressure and preferential, marked hindlimb vasodilation. Although A2a receptor activation does not change lumbar sympathetic nerve activity, it does markedly enhance the preganglionic adrenal sympathetic nerve activity, which will increase epinephrine release and could subsequently elicit hindlimb vasodilation via activation of β2-adrenergic receptors.

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Ulphani, Joseph S., Rishi Arora, Jack H. Cain, et al. "The ligament of Marshall as a parasympathetic conduit." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 3 (2007): H1629—H1635. http://dx.doi.org/10.1152/ajpheart.00139.2007.

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The objective of the study was to investigate the morphology, distribution, and electrophysiological profile of the autonomic fibers that innervate the ligament of Marshall (LOM). Gross anatomical dissections were performed in 10 dogs. Sections of the left vagus nerve, left stellate ganglion, and the LOM were immunostained to identify adrenergic and cholinergic nerves. Hearts were also stained for acetylcholinesterase to identify epicardial cholinergic nerves. In vivo electropyhsiological studies were performed in another 10 dogs before and after LOM ablation. The anatomical examination reveal

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32

Roth, D. M., F. C. White, O. Mathieu-Costello, et al. "Effects of left circumflex Ameroid constrictor placement on adrenergic innervation of myocardium." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 6 (1987): H1425—H1434. http://dx.doi.org/10.1152/ajpheart.1987.253.6.h1425.

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We evaluated the adrenergic innervation of the swine and canine myocardium after placement of an Ameroid constrictor around the left circumflex coronary artery (LCX). Fluorescent histochemistry was used to identify adrenergic nerve terminals in the myocardium and coronary vasculature. Ameroid occlusion of the proximal LCX in 10 pigs for 3 wk resulted in 6 +/- 1% infarction as well as myocardial ischemia in the left circumflex region of pigs studied during exercise. However, placement of the Ameroid constrictor did not significantly alter the surface density of the nerve terminals in the LCX re

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Jonson, C., and L. Fandriks. "Splanchnic nerve stimulation inhibits duodenal HCO3- secretion in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 255, no. 6 (1988): G709—G712. http://dx.doi.org/10.1152/ajpgi.1988.255.6.g709.

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Sympathoadrenergic inhibition of HCO3- secretion by the duodenal mucosa was studied in chloralose anesthetized rats. Duodenal HCO3- secretion was measured in situ by pH-stat titration. Direct efferent electrical stimulation of the cut splanchnic nerves (10 Hz, supramaximal intensity) inhibited the duodenal alkaline output by approximately 50%. This inhibitory response was blocked by the administration of either the adrenolytic agent guanethidine or the alpha 2-adrenoceptor antagonist yohimbine. However, neither the alpha 1-adrenoceptor antagonist prazosin nor the beta-adrenoceptor antagonist p

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Holtbäck, Ulla, Yoshiyuki Ohtomo, Petter Förberg, Bo Sahlgren та Anita Aperia. "Neuropeptide Y shifts equilibrium between α- and β-adrenergic tonus in proximal tubule cells". American Journal of Physiology-Renal Physiology 275, № 1 (1998): F1—F7. http://dx.doi.org/10.1152/ajprenal.1998.275.1.f1.

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Renal sympathetic nerves play a central role in the regulation of tubular Na+ reabsorption. Norepinephrine (NE) and neuropeptide Y (NPY) are colocalized in renal sympathetic nerve endings. The purpose of this study is to examine the integrated effects of these neurotransmitters on the regulation of Na+-K+-ATPase, the enzyme responsible for active Na+ reabsorption in renal tubular cells. Studies were performed on proximal tubular segments, which express adrenergic α- and β-receptors, as well as NPY-Y2 receptors. It was found that α- and β-adrenergic agonists had opposing effects on Na+-K+-ATPas

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35

Ali, Z., M. Ringkamp, T. V. Hartke та ін. "Uninjured C-Fiber Nociceptors Develop Spontaneous Activity and α-Adrenergic Sensitivity Following L6 Spinal Nerve Ligation in Monkey". Journal of Neurophysiology 81, № 2 (1999): 455–66. http://dx.doi.org/10.1152/jn.1999.81.2.455.

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Ali, Z., M. Ringkamp, T. V. Hartke, H. F. Chien, N. A. Flavahan, J. N. Campbell, and R. A. Meyer. Uninjured cutaneous C-fiber nociceptors develop spontaneous activity and α-adrenergic sensitivity following L6 spinal nerve ligation in the monkey. J. Neurophysiol. 81: 455–466, 1999. We investigated whether uninjured cutaneous C-fiber nociceptors in primates develop abnormal responses after partial denervation of the skin. Partial denervation was induced by tightly ligating spinal nerve L6 that innervates the dorsum of the foot. Using an in vitro skin-nerve preparation, we recorded from uninjured

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Butler, David Gordon. "Mecamylamine blocks the [Asp1,Val5]-ANG II-induced attenuation of salt gland activity in Pekin ducks." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 3 (1999): R836—R842. http://dx.doi.org/10.1152/ajpregu.1999.277.3.r836.

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An intravenous injection of 2 μg of [Asp1,Val5]-ANG II attenuated fluid secretion by the nasal salt glands of Pekin ducks. Ganglionic blockade with mecamylamine stopped salt gland secretion. Flow was reestablished by intravenous methacholine bromide during ganglionic blockade. A second injection of 2 μg of [Asp1,Val5]-ANG II failed to attenuate secretion during ganglionic blockade, showing that the peptide acts via the central nervous system and postganglionic parasympathetic nerves that supply the salt glands. Sympathetic nerves are located in the walls of blood vessels within the salt glands

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Cohen, R. A., and R. M. Weisbrod. "Endothelium inhibits norepinephrine release from adrenergic nerves of rabbit carotid artery." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 5 (1988): H871—H878. http://dx.doi.org/10.1152/ajpheart.1988.254.5.h871.

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The overflow of endogenous norepinephrine caused by transmural electrical stimulation or depolarization with potassium was smaller in superfused segments of the rabbit carotid artery with intact endothelium than in segments denuded of endothelium. In segments preincubated with [3H]norepinephrine, the lesser overflow was found to be partially due to metabolism by the endothelium of the neurotransmitter. Even after treatment to block the disposition of norepinephrine, the endothelium acted as a partial physical barrier to the overflow of norepinephrine into the lumen of arteries superfused and p

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Kenney, M. J., and C. K. Ganta. "Autonomic Nervous System and Immune System Interactions." Comprehensive Physiology 4, no. 3 (2014): 1177–200. https://doi.org/10.1002/j.2040-4603.2014.tb00574.x.

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AbstractThe present review assesses the current state of literature defining integrative autonomic‐immune physiological processing, focusing on studies that have employed electrophysiological, pharmacological, molecular biological, and central nervous system experimental approaches. Central autonomic neural networks are informed of peripheral immune status via numerous communicating pathways, including neural and non‐neural. Cytokines and other immune factors affect the level of activity and responsivity of discharges in sympathetic and parasympathetic nerves innervating diverse targets. Multi

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Musaeva, M. S., and R. S. Hajiyeva. "REPRODUCTIVE HORMONE LEVELS IN WOMEN WITH THALASSEMIA." "The Medicine and Science" scientific-practical journal named after A.Aliyev 2, no. 32 (2023): 84–89. http://dx.doi.org/10.61775/2413-3302.v2i32.13.

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Using histological, and histochemical methods, morphological changes in the intramural nerve elements of the urinary bladder were studied in 6 patients suffering from diabetic cystopathy and who died from various complications of diabetes mellitus. The control group consisted of 4 practically healthy persons who died as a result of a car accident. For histological examination, tissue pieces of the nerve elements of the bladder were fixed with 12% formalin and impregnated according to the method of Bilshchovsky-Gross and Rasskazov. Adrenergic nerve structures were detected by incubation of sect

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Mirzayeva, T. N., E. Ch Akbarov, R. P. Hasanov, and M. I. Mirzayev. "STRUCTURE OF INTRAMURAL NERVE ELEMENTS OF THE URINARY BLADDER IN PATIENTS WITH DIABETIC CYSTOPATHY." "The Medicine and Science" scientific-practical journal named after A.Aliyev 2, no. 32 (2023): 79–83. http://dx.doi.org/10.61775/2413-3302.v2i32.12.

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Using histological, and histochemical methods, morphological changes in the intramural nerve elements of the urinary bladder were studied in 6 patients suffering from diabetic cystopathy and who died from various complications of diabetes mellitus. The control group consisted of 4 practically healthy persons who died as a result of a car accident. For histological examination, tissue pieces of the nerve elements of the bladder were fixed with 12% formalin and impregnated according to the method of Bilshchovsky-Gross and Rasskazov. Adrenergic nerve structures were detected by incubation of sect

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Dekhkanov, T. D., and F. S. Oripov. "Morphological and functional charakteristics of histogenetically related structures - producers of monoamines - in the local regulatory apparatus of the large duodenal papilla." Genes & Cells 16, no. 1 (2021): 60–63. http://dx.doi.org/10.23868/202104009.

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Purpose of the study. Study of the morphology of open-type fluorescent cells and adrenergic nerve structures of the major duodenal papilla. Material and research methods. The material for the study was the area of the large duodenal papilla of 12 rabbits and 5 dogs. Fluorescent endocrine cells and adrenergic nerve structures were revealed by processing cryostat sections of the material with a gly-oxylic acid solution. Research results. It has been established that the fluorescent cells of the diffuse endocrine (APUD) system contain serotonin and catecholamines, the shade of their luminescence

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Cho, Arthur K., and Glenn S. Takimoto. "Irreversible inhibitors of adrenergic nerve terminal function." Trends in Pharmacological Sciences 6 (January 1985): 443–47. http://dx.doi.org/10.1016/0165-6147(85)90209-3.

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Hutchison, S. M., A. E. Tietz, K. A. Trostel, and L. P. Schramm. "Uterine arterial vasoconstrictions mediated by ovarian nerves in virgin and postpartum rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 1 (1997): R318—R325. http://dx.doi.org/10.1152/ajpregu.1997.272.1.r318.

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In most mammals, including humans, pregnancy results in the loss of most uterine vasomotor fibers. These experiments determined whether, despite this denervation, sympathetic nerves mediated uterine vasoconstrictions in the rat 24 h after delivery. Both virgin and uniparous postpartum rats were anesthetized with urethan. Femoral vessels were cannulated for measurement of arterial pressure and intravenous administration of fluids and drugs. Blood flow was measured in a uterine artery after ligation of all anastomotic ovarian vessels. Electrical stimulation of ovarian nerve efferents elicited fr

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Repasky, Elizabeth, and Hemn Mohammadpour. "Targeting nerve growth factor: an Achilles’ heel for tumors?" Journal for ImmunoTherapy of Cancer 13, no. 5 (2025): e011609. https://doi.org/10.1136/jitc-2025-011609.

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A tumor’s ability to attract innervation is a critical factor in tumor progression and immune escape, with the sympathetic nervous system playing a major role. Catecholamines released by sympathetic nerves activate adrenergic receptors on tumor cells, enhancing growth and resistance to therapies, while activation of adrenergic receptors on immune cells triggers immunosuppressive activity in the tumor microenvironment. Nerve growth factor (NGF) produced by tumor cells is a key driver of tumor innervation, making it a promising target for novel therapeutic strategies. In this commentary, we high

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Pelayo, J. C. "Modulation of renal adrenergic effector mechanisms by calcium entry blockers." American Journal of Physiology-Renal Physiology 252, no. 4 (1987): F613—F620. http://dx.doi.org/10.1152/ajprenal.1987.252.4.f613.

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Micropuncture studies in anesthetized Munich-Wistar rats were undertaken to investigate the effects of calcium channel blockade on the glomerular hemodynamic responses to 3-Hz renal nerve stimulation. Stimulation alone increased afferent and efferent arteriolar resistances by 85 and 35%, respectively. Because of these increases both single nephron plasma flow and glomerular capillary hydrostatic pressure difference fell to levels significantly below control, leading to a 26% reduction in single nephron filtration rate (P less than 0.005). These changes, however, were largely attenuated during

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Paqueron, Xavier, Xinhui Li, Carsten Bantel, Joseph R. Tobin, Mary Lou Voytko, and James C. Eisenach. "An Obligatory Role for Spinal Cholinergic Neurons in the Antiallodynic Effects of Clonidine after Peripheral Nerve Injury." Anesthesiology 94, no. 6 (2001): 1074–81. http://dx.doi.org/10.1097/00000542-200106000-00023.

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Background Indirect evidence supports a role of spinal cholinergic neurons in tonically reducing response to noxious mechanical stimulation and in effecting analgesia from alpha2-adrenergic agonists. This study directly assessed the role of cholinergic neurons in regulating the level of mechanical allodynia and in participating in the antiallodynic effect of the clinically used alpha2-adrenergic agonist, clonidine, in an animal model of neuropathic pain. Methods Allodynia was produced in rats by ligation of the left L5 and L6 spinal nerves. Rats received a single intrathecal injection of salin

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Malvin, G. M., and C. Riedel. "Autonomic regulation of cutaneous vascular resistance in the bullfrog Rana catesbeiana." Journal of Experimental Biology 152, no. 1 (1990): 425–39. http://dx.doi.org/10.1242/jeb.152.1.425.

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To gain a better understanding of the regulation of cutaneous blood flow in the bullfrog, the vascular innervation, vasoactivity and adrenoceptor types of the cutaneous vasculature were investigated using a pump-perfused skin preparation. Stimulation of cranial nerve I, the vagal ganglion, sympathetic ganglion 1 and sometimes sympathetic ganglion 2 caused cutaneous vascular resistance (CVR) to increase. Stimulation of cranial nerve IX and spinal nerves 1 and 2 had no effect on CVR. The response to stimulation of sympathetic ganglion 1 was antagonized by phentolamine but not by atropine. Phento

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Silverman, Deborah A., Shamima Akhter, Tongxin Xie, et al. "Abstract PO-076: Adrenergic regulation of the anti-tumor immune response in p53-deficient tumors." Clinical Cancer Research 29, no. 18_Supplement (2023): PO—076—PO—076. http://dx.doi.org/10.1158/1557-3265.aacrahns23-po-076.

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Abstract Several previous studies have shown that β2-adrenergic signaling pathway promotes tumor progression, whereas others have shown the opposite effect. The role of β2-adrenergic activation in oral squamous cell carcinoma (OSCC) remains largely unknown. Our previous study showed that the loss of p53 leads to increased adrenergic tumor innervation in OSCC, resulting in transcriptional programs that establish new neuronal identity. We hypothesized that tumor immunity in OSCC is regulated by adrenergic signaling. The aim of the present study was to determine the influences of adrenergic signa

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Rosas-Ballina, Mauricio, Mahendar Ochani, Peder Olofsson, Sergio Valdés-Ferrer, Sangeeta Chavan, and Kevin Tracey. "Neural control of acetylcholine release by T cells attenuates TNF production in endotoxemia (138.24)." Journal of Immunology 184, no. 1_Supplement (2010): 138.24. http://dx.doi.org/10.4049/jimmunol.184.supp.138.24.

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Abstract The cholinergic anti-inflammatory pathway regulates pro-inflammatory cytokine production through vagus nerve signaling via the α7 subunit of the nicotinic acetylcholine receptor expressed on macrophages. Vagus nerve stimulation requires an intact splenic nerve to attenuate TNF production by spleen macrophages. Despite exhaustive search, cholinergic fibers have not been observed in spleen. Here, we used transgenic mice that express enhanced green fluorescent protein (eGFP) under control of transcriptional regulatory elements of choline acetyltransferase, the enzyme that synthesizes ace

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Burnstock, Geoffrey. "The Concept of Cotransmission: Focus on ATP as a Cotransmitter and its Significance in Health and Disease." European Review 22, no. 1 (2014): 1–17. http://dx.doi.org/10.1017/s1062798713000586.

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The concept of cotransmission, including sympathetic nerve release of noradrenaline and ATP, was formalised in 1976, which challenged the accepted view known as ‘Dale's Principle’ that one nerve released only one transmitter. ATP was also shown to be a cotransmitter with acetylcholine in parasympathetic nerves supplying the urinary bladder and as a cotransmitter with nitric oxide in non-adrenergic, non-cholinergic inhibitory nerves supplying the intestine. It is now recognised that ATP is a cotransmitter in most, if not all, nerves in the peripheral and central nervous systems. The physiologic

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