Innervation of cat iris dilator

1964 ◽  
Vol 207 (6) ◽  
pp. 1411-1416 ◽  
Author(s):  
U. Schaeppi ◽  
W. P. Koella
Keyword(s):  
Electrical Stimulation ◽  
Adrenergic Receptors ◽  
Isometric Tension ◽  
Adrenergic Nerve ◽  
Nerve Terminals ◽  
Beta Adrenergic Receptors ◽  
Dilator Muscle ◽  
Adrenergic Nerve Terminals ◽  
Electrical Stimuli

Isometric tension changes of radially oriented iris strips of the cat were investigated in vitro. Electrical stimulation, norepinephrine (NE), and tyramine elicited contraction whereas isoproterenol elicited relaxation. Phentolamine reduced electrically and NE induced contractions and, in large doses, converted them to relaxation. Dichloroisoproterenol decreased this relaxation and the relaxation induced by isoproterenol. After chronic sympathetic denervation, electrical stimuli induced mainly relaxation and tyramine had no effect. These results indicate that contractions and relaxations in normal preparations are preponderantly mediated via excitation of adrenergic nerve terminals and release of adrenergic transmitter acting upon alpha and beta adrenergic receptors, respectively. Neostigmine and atropine had little effect on the electrically induced effects of normal preparations. In chronically denervated dilator strips, neostigmine increased and atropine decreased the relaxations and occasional slight contractions produced by electrical stimuli. These observations are interpreted that cholinergic relaxation mechanisms are also involved in the control of the dilator muscle, and that cholinergic contractions are due to activation of aberrant sphincter fibers contaminating the dilator muscle.

Contractile Responses of Canine Isolated Pulmonary Lobar Arteries and Veins to Norepinephrine, Serotonin, and Tyramine

1975 ◽  
Vol 53 (5) ◽  
pp. 830-838 ◽  
Author(s):  
Paul D. Joiner ◽  
Philip J. Kadowitz ◽  
Linda B. Davis ◽  
Albert L. Hyman
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Nerve ◽  
Nerve Terminals ◽  
Tension Development ◽  
Consistent Effect ◽  
Maximum Tension ◽  
Adrenergic Blocker ◽  
Adrenergic Nerve Terminals ◽  
High Concentrations ◽  
Arteries And Veins

Isolated helical strips of canine intrapulmonary lobar arteries and veins (about 4 mm in diameter) undergo dose-related tension development when exposed to increasing concentrations (10−8 – 10−3 M) of norepinephrine (NE), serotonin or 5-hydroxytryptamine (5-HT) and tyramine (Tyr). Venous segments were generally more sensitive while the maximum tension development was greater in the arterial strips, probably owing to their greater thickness. Both strips were more sensitive to 5-HT than NE and only responded to Tyr at high concentrations. Norepinephrine and 5-HT were nearly equally efficacious, whereas Tyr was less so. Responses to the latter were slow to develop, exhibited tachyphylaxis, and were greatly inhibited by phentolamine (10−8 M), an α-adrenergic blocker. Exposure to cocaine (10−5 M) enhanced submaximal NE responses, inhibited Tyr contractions and had no consistent effect on 5-HT responses. Phentolamine (10−8 M) was also found to inhibit NE responses without altering 5-HT effects, whereas methysergide (10−8 M) inhibited 5-HT responses but not NE contractions. Thus, evidence suggests that NE probably acts on α-adrenergic receptors whereas 5-HT probably acts on other receptors. Tyramine may, in part, act directly on α-adrenergic receptors but may also release NE from surviving adrenergic nerve terminals in the preparation. Cocaine inhibits this effect and potentiates responses to lower levels of NE, presumably by blocking NE uptake into nerve terminals although a post-junctional action cannot be excluded.

Prejunctional beta 1-adrenoceptors inhibit cholinergic transmission in canine bronchi

1987 ◽  
Vol 62 (2) ◽  
pp. 785-790 ◽  
Author(s):  
A. H. Danser ◽  
R. van den Ende ◽  
R. R. Lorenz ◽  
N. A. Flavahan ◽  
P. M. Vanhoutte
Keyword(s):  
Electrical Stimulation ◽  
Nerve Fibers ◽  
Adrenergic Nerve ◽  
Nerve Terminals ◽  
Adrenergic Blockade ◽  
Bronchial Wall ◽  
Cholinergic Neurotransmission ◽  
Adrenergic Antagonist ◽  
Adrenergic Nerve Terminals ◽  
Stimulation Of

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 the sympathetic neurotransmitter by tyramine significantly decreased the contractions evoked by electrical stimulation but did not affect contractions caused by exogenous acetylcholine. Metoprolol, a beta 1-adrenergic antagonist, abolished and propranolol significantly reduced the effect of tyramine during electrical stimulation. alpha 2-Adrenergic blockade, beta 2-adrenergic blockade, or removal of the epithelium did not significantly affect the response to tyramine. These results suggest that norepinephrine when released from sympathetic nerve endings can activate prejunctional inhibitory beta 1-adrenoceptors to depress cholinergic neurotransmission in the bronchial wall.

Interactions between sustained contractile activity and beta-adrenergic receptors in regulation of gene expression in skeletal muscles

1989 ◽  
Vol 256 (3) ◽  
pp. C506-C514 ◽  
Author(s):  
W. E. Kraus ◽  
T. S. Bernard ◽  
R. S. Williams
Keyword(s):  
Electrical Stimulation ◽  
Steady State ◽  
Oxidative Metabolism ◽  
Adrenergic Receptors ◽  
Contractile Activity ◽  
Mitochondrial Enzymes ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Induced Changes ◽  
Aldolase A

Continuous electrical stimulation for 10-21 days of the motor nerve innervating the anterior compartment muscles of adult rabbits increased both the density of beta-adrenergic receptors (beta-AR) and tissue concentrations of adenosine 3',5'-cyclic monophosphate (cAMP) by two to threefold. Changes in cAMP and in beta-AR occurred in parallel with stimulation-induced adaptations in the specific activity of mitochondrial enzymes (2- to 6-fold increases) and with changes in steady-state concentrations of mitochondrial RNA, beta-F1ATPase mRNA, and myoglobin mRNA (2- to 11-fold increases). These increases in muscle cAMP, in beta-AR, and in expression of protein and mRNA products of genes encoding proteins of oxidative metabolism occurred even in animals receiving high doses of propranolol during the period of electrical stimulation. In contrast to genes that encode proteins of oxidative metabolism, the direction and the time course of activity-induced changes in expression of the glycolytic enzyme aldolase A appeared to be unrelated to changes in muscle cAMP; suppression of steady-state concentrations of aldolase A mRNA was maximal (20-25% of control) at early time points preceding the maximal rise in cAMP. In addition, administration of propranolol attenuated the suppressive effect of continuous contractile activity on expression of aldolase A, even in the absence of an effect of this drug on cAMP in stimulated muscles. We conclude that activity-induced changes in cAMP, in beta-AR, and in expression of genes that encode proteins important for oxidative metabolism occur as a direct consequence of contractile activity and do not require concomitant stimulation of beta-AR.(ABSTRACT TRUNCATED AT 250 WORDS)

Ionomycin stimulates secretion of catecholamines from cat adrenal gland and spleen

1982 ◽  
Vol 242 (3) ◽  
pp. E137-E145 ◽  
Author(s):  
M. H. Carvalho ◽  
J. C. Prat ◽  
A. G. Garcia ◽  
S. M. Kirpekar
Keyword(s):  
Chromaffin Cells ◽  
Adrenal Glands ◽  
Secretory Response ◽  
Adrenergic Nerve ◽  
Nerve Terminals ◽  
Potassium Depolarization ◽  
Calcium Dependent ◽  
Dopamine Beta Hydroxylase ◽  
Adequate Stimulus ◽  
Adrenergic Nerve Terminals

Ionomycin, a polyether antibiotic, stimulated the secretion of catecholamines and dopamine beta-hydroxylase from perfused adrenal glands and [3H]norepinephrine ([3H]NE) from spleens of the cat. Release was calcium dependent, and strontium or barium did not substitute for calcium. Ionomycin failed to release [3H]NE from reserpinized spleens. High magnesium did not interfere in the ionomycin response, but lanthanum and manganese blocked it. Ionomycin response that was pH dependent was not affected by potassium depolarization. The secretory response to ionomycin was enhanced when both glycolysis and oxidative metabolism were inhibited. It is concluded that ionomycin introduces calcium into the chromaffin cells and adrenergic nerve terminals to cause the secretory response and that a rise in intracellular calcium may be an adequate stimulus for secretion.

Stimulating actions of various prostaglandins and noradrenaline in strips of rabbit renal artery

1978 ◽  
Vol 56 (2) ◽  
pp. 321-323 ◽  
Author(s):  
F. Rioux ◽  
G. Gagnon ◽  
D. Regoli
Keyword(s):  
Renal Artery ◽  
Renal Arteries ◽  
Adrenergic Nerve ◽  
Prostaglandin E ◽  
Physiological Salt Solution ◽  
Nerve Terminals ◽  
Release Of Noradrenaline ◽  
Vasoconstrictor Effect ◽  
Adrenergic Nerve Terminals ◽  
Prostaglandins E

The myotropic effects of prostaglandins E1, E2, F2α, A1, and noradrenaline were evaluated in spirally cut strips of rabbit renal arteries suspended in a physiological salt solution maintained at 37 °C. The four prostaglandins as well as noradrenaline elicited contractions of the isolated rabbit renal artery. At concentrations higher than 1.0 × 10−7 g ml−1 the contracting effect of prostaglandin E1 diminished. The vasoconstrictor actions of prostaglandins E2 and F2α were potentiated by cocaine and inhibited by phentolamine. On the other hand, phentolamine did not inhibit the vasoconstrictor effect of prostaglandins E2 and F2α on strips of rabbit renal arteries removed from rabbits pretreated with reserpine. These results were taken as an indication that part of the contractile effects of prostaglandins E2 and F2α on the isolated rabbit renal artery may be due to the release of noradrenaline from adrenergic nerve terminals.

scholarly journals Autoradiographic visualization of beta-adrenergic receptors in normal and denervated skeletal muscle.

1979 ◽  
Vol 27 (10) ◽  
pp. 1308-1311 ◽  
Author(s):  
B Lavenstein ◽  
W K Engel ◽  
N B Reddy ◽  
S Carroll
Keyword(s):  
Skeletal Muscle ◽  
Blood Vessels ◽  
Adrenergic Receptors ◽  
Cellular Localization ◽  
Muscle Fibers ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Adrenergic Blocker

Autoradiographic localization of beta-adrenergic receptors in rat skeletal muscle in vivo was achieved utilizing [125I]-iodohydroxybenzylpindolol, a potent beta-adrenergic blocker with high affinity and specificity for those receptors. In normal muscle the beta-adrenergic receptors were localized mainly to blood vessels, arterioles greater than venules, with much less concentration of grains over the fascicles of muscle fibers. One week after denervation there was an increase in binding both to blood vessels and muscle fibers, more so in soleus and gactrocnemius than in extensor digitorum longus. While these results parallel in vitro biochemical studies, they dictate caution when inferring cellular localization of beta-adrenergic receptors (and other molecules) solely on the basis of biochemical techniques applied to subcellular fractions of whole-organ homogenates.

Adrenergic neuron blocking action of dehydrocorydaline isolated from Corydalis bulbosa

1976 ◽  
Vol 54 (3) ◽  
pp. 287-293 ◽  
Author(s):  
Kazuyoshi Kurahashi ◽  
Motohatsu Fujiwara
Keyword(s):  
Pulmonary Artery ◽  
Nerve Stimulation ◽  
Inhibitory Action ◽  
Adrenergic Nerve ◽  
Active Principle ◽  
Nerve Terminals ◽  
Inhibitory Effects ◽  
Electrical Nerve Stimulation ◽  
Adrenergic Neuron ◽  
Adrenergic Nerve Terminals

Dehydrocorydaline, an active principle of Corydalis bulbosa alkaloids, in concentrations of 10−5M to 5 × 10−5M inhibited relaxation and the concomitant release of [3H]-noradrenaline caused by 10−4M nicotine and electrical perivascular nerve stimulation in the taenia caecum of guinea pig. The same inhibitory effects were observed on contraction and release of [3H]noradrenaline in the sympathetic nerve – pulmonary artery preparation of rabbit. On the other hand, neither relaxation nor contraction caused by exogenously applied noradrenaline was affected. These results suggest that the inhibitory action of dehydrocorydaline on the relaxation or contraction, produced by nicotine and electrical nerve stimulation, is due to blockade of noradrenaline release from the adrenergic nerve terminals in both the taenia caecum and pulmonary artery. Participation of the adrenergic neuron blocking action of dehydrocorydaline in preventing experimental ulceration is discussed.

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