Adrenergic mechanisms in the bullfrog and turtle

1965 ◽  
Vol 209 (6) ◽  
pp. 1287-1294 ◽  
Author(s):  
Takehiko Azuma ◽  
Alberto Binia ◽  
Maurice B. Visscher
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Low Temperatures ◽  
Environmental Temperature ◽  
Contractile Activity ◽  
Sympathetic Nerve Stimulation ◽  
Sympathetic Transmitter ◽  
Cardiac Sympathetic Denervation ◽  
Large Output

Epinephrine and norepinephrine contents of tissues and perfusates have been measured by fluorimetric methods to ascertain which catecholamine is the sympathetic transmitter in bullfrogs and turtles. Except for adrenal and sympathetic chain, the predominant catecholamine in bullfrogs is epinephrine. In snapping turtles, norepinephrine predominates. During perfusion of bullfrog heart or liver without stimulation, only traces of catecholamine appear in perfusates, whereas during sympathetic nerve stimulation a large output of epinephrine occurs. In the bullfrog epinephrine rather than norepinephrine seems to be the sympathetic mediator. The situation may be the reverse in the turtle. Environmental temperature did not alter bullfrog tissue catecholamine. Cardiac sympathetic denervation did not decrease myocardial catecholamine within 6 weeks at low temperatures, but in animals maintained at 20 C survival was not achieved. Epinephrine levels in bullfrog ventricle were not lowered by 5 hr of contractions induced by electrical stimulation at 30/min compared with controls in arrest. The fact that myocardial catecholamine stores are not depleted by contractile activity may result either from absence of utilization or from equivalence between breakdown and synthesis.

Release of norepinephrine by sympathetic nerve stimulation from rabbit lungs

1978 ◽  
Vol 235 (6) ◽  
pp. H803-H808
Author(s):  
E. Y. Tong ◽  
A. A. Mathe ◽  
P. W. Tisher
Keyword(s):  
Electrical Stimulation ◽  
Pulmonary Artery ◽  
Monoamine Oxidase ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerves ◽  
Systemic Circulation ◽  
Inhibitory Mechanism ◽  
Sympathetic Nerve Stimulation ◽  
Mao Inhibitor

Rabbit lungs were perfused via the pulmonary artery and norepinephrine (NE) measured in the outflows. The basal NE level was approximately 3 ng/min. Electrical stimulation (50 V, 1 ms, 10 Hz) of the sympathetic nerves doubled the NE release. Hexamethonium (10(-4) and 10(-5) M) had no effect on the release of NE. Administration of a monoamine oxidase (MAO) inhibitor, pargyline (70 mg/kg) resulted in a 20-fold NE increase by nerve stimulation, implying that the bulk of the amine does not reach the systemic circulation due to an active MAO. Methacholine (1 and 10 micrograms/ml) inhibited NE release by nerve stimulation. This inhibition was abolished by atropine (5 micrograms/ml). It is suggested that a muscarinic inhibitory mechanism may regulate the NE release in the lung. PGE2 (100 ng/ml), but not PGS2alpha, (100 ng/ml), depressed NE release during nerve stimulation, whereas indomethacin (10 mg/kg) enhanced NE release before, during, and after nerve stimulation in seemingly normal animals. This indicates the existence of another presynaptic inhibitory mechanism for NE release in the lung: a PGE-mediated inhibition.

A novel in vitro technique to study extrinsic neural control of rabbit colonic muscle and epithelial function

1993 ◽  
Vol 265 (6) ◽  
pp. G1064-G1070 ◽  
Author(s):  
J. M. Goldhill ◽  
W. H. Percy
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Neural Control ◽  
Contractile Activity ◽  
Circular Muscle ◽  
Potential Difference ◽  
Pelvic Nerve ◽  
Sympathetic Nerve Stimulation ◽  
In Vitro Technique

A novel in vitro technique capable of simultaneously measuring distal colonic epithelial potential difference and muscle contraction is described. Under basal conditions, oscillations in both muscle tone and potential difference were observed. Pelvic nerve stimulation was shown to evoke strong "duration" contractile responses in both the longitudinal and circular muscle layers. Additionally, tonic changes in potential difference extending beyond the train of stimuli were observed, suggesting for the first time that colonic ion transport may be influenced by the pelvic nerves. However, it was unclear whether these were direct effects or indirect actions resulting from muscle contractions causing mechanical stimulation of nerves of the submucosal plexus. Lumbar colonic nerve stimulation inhibited spontaneous contractile activity and reduced basal tone in both muscle layers. However, there was no consistent effect of sympathetic nerve stimulation on transepithelial potential difference. Each of the muscle and epithelial effects of sympathetic nerve stimulation was mimicked by exogenous norepinephrine. Based on these data, it is concluded that colonic function is strongly influenced by the extrinsic innervation. Furthermore, relatively long-term modulation of epithelial function can be achieved by short bursts of pelvic nerve activity.

Effects of cadmium and lead on adrenergic neuromuscular transmission in the rabbit

1977 ◽  
Vol 232 (3) ◽  
pp. C128-C131 ◽  
Author(s):  
G. P. Cooper ◽  
D. Steinberg
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Perfusion Pressure ◽  
Pressor Response ◽  
Ringer Solution ◽  
Bathing Solution ◽  
Sympathetic Nerve Stimulation ◽  
Fourfold Increase ◽  
Lead And Cadmium

The effects of inorganic lead (PbCl2) and cadmium (DdCl2) on the pressor response of rabbit saphenous arteries produced by sympathetic nerve stimulation were examined. A 1- to 3-cm length of artery was removed, placed in a bath containing mammalian Ringer solution, and perfused with the same solution at a constant rate sufficient to maintain a 40-60 mmHg perfusion pressure. Increases in perfusion pressure resulting from electrical stimulation -f periarterial nerve endings were reduced or completely blocked by the addition of 5-20 muM lead or cadmium to the bathing solution for a period of 15-30 min. Responses to norepinephrine or to direct electrical stimulation of the muscle remained relatively unaffected. During lead or cadmium blockade, the response to nerve stimulation could be restored by a fourfold increase in calcium concentration. It is concluded that lead and cadmium reduce the response to sympathetic nerve stimulation primarily through an effect on presynaptic nerve terminals.

Interactive Effects of Verapamil and Sympathetic Nerve Stimulation on the Sinus and AV Nodes in the Canine Hearts.

1992 ◽  
Vol 33 (1) ◽  
pp. 83-93 ◽  
Author(s):  
Katsusuke YANO ◽  
Masanobu HIRATA ◽  
Takao MITSUOKA ◽  
Yoriaki MATSUMOTO ◽  
Tetsuya HIRATA ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Interactive Effects ◽  
Sympathetic Nerve Stimulation

What do antagonists tell us about α-adrenoceptors?

1985 ◽  
Vol 68 (s10) ◽  
pp. 15s-19s ◽  
Author(s):  
G. M. Drew
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Isolated Heart ◽  
Coupling Mechanism ◽  
Sympathetic Nerve Stimulation ◽  
Stimulus Response ◽  
Adrenoceptor Agonist ◽  
Tissue Responses ◽  
Cat Spleen ◽  
Relative Potencies

The early proposals that pre- and post-junctional α-adrenoceptors might be different stemmed largely from two separate observations. Firstly, the orders of potency of a series of agonists at inhibiting the response to sympathetic nerve stimulation and in increasing inotropic activity in the rabbit isolated heart were different [1, 2]. Secondly, phenoxybenzamine was more potent in inhibiting vasoconstrictor responses to sympathetic nerve stimulation than in increasing transmitter overflow from the cat spleen [3]. These experiments illustrate the most fundamental, pharmacological ways of distinguishing between receptors: namely, by comparing the relative potencies of agonists and/or antagonists in producing, or preventing, pharmacological effects. There are, however, difficulties in using agonists to classify receptors because their ability to generate a response depends not only upon their intrinsic properties of affinity for, and efficacy at, the receptors but also upon the capacity of the tissue to translate the stimulus into a response. Thus agonists with a relatively low intrinsic efficacy may produce a small response, or no response at all, in a tissue in which the efficiency of the stimulus-response coupling mechanism is low. The importance of this phenomenon in influencing tissue responses to agonists with low efficacy has been demonstrated for the α-adrenoceptor agonist prenalterol [4] and for the α-adrenoceptor agonist oxymetazoline [5].

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