Constant polarization potentials and adsorbent properties of the salivary gland after division and stimulation of the lingual and sympathetic nerves in the rabbit

1967 ◽  
Vol 63 (3) ◽  
pp. 240-241
Author(s):  
�. V. Tsegel'nitskaya
Keyword(s):  
Salivary Gland ◽  
Sympathetic Nerves ◽  
Constant Polarization ◽  
Stimulation Of

Peripheral muscarinic control of norepinephrine release in the cardiovascular system

1980 ◽  
Vol 239 (6) ◽  
pp. H713-H720 ◽  
Author(s):  
E. Muscholl
Keyword(s):  
Physiological Role ◽  
Sympathetic Nerves ◽  
Adrenergic Nerve ◽  
Sequence Of Events ◽  
Adrenergic Response ◽  
Adrenergic Nerve Terminals ◽  
Muscarinic Cholinergic ◽  
Related Compounds ◽  
Stimulation Of

Activation of muscarinic cholinergic receptors located at the terminal adrenergic nerve fiber inhibits the process of exocytotic norepinephrine (NE) release. This neuromodulatory effect of acetylcholine and related compounds has been discovered as a pharmacological phenomenon. Subsequently, evidence for a physiological role of the presynaptic muscarinic inhibition was obtained on organs known to be innervated by the autonomic ground plexus (Hillarp, Acta. Physiol. Scand. 46, Suppl. 157: 1-68, 1959) in which terminal adrenergic and cholinergic axons run side by side. Thus, in the heart electrical vagal stimulation inhibits the release of NE evoked by stimulation of sympathetic nerves, and this is reflected by a corresponding decrease in the postsynaptic adrenergic response. On the other hand, muscarinic antagonists such as atropine enhance the NE release evoked by field stimulation of tissues innervated by the autonomic ground plexus. The presynaptic muscarine receptor of adrenergic nerve terminals probably restricts the influx of calcium ions that triggers the release of NE. However, the sequence of events between recognition of the muscarinic compound by the receptor and the process of exocytosis still remains to be clarified.

Effects of intravenous anesthetic agents on left ventricular function in dogs

1977 ◽  
Vol 232 (1) ◽  
pp. H44-H48
Author(s):  
L. D. Horwitz
Keyword(s):  
Left Ventricular Pressure ◽  
Cardiovascular Effects ◽  
Sympathetic Nerves ◽  
Left Ventricular ◽  
Intravenous Anesthetic ◽  
First Derivative ◽  
Anesthetic Agents ◽  
Thiopental Sodium ◽  
Stimulation Of ◽  
Mean Heart Rate

The cardiovascular effects of ketamine hydrochloride and thiopental sodium were studied in 11 dogs. During anesthesia, mean heart rate rose to 185 beats/min with ketamine and 147 beats/min with thiopental. Cardiac output was increased with ketamine but unchanged by thiopental. The maximum first derivative of the left ventricular pressure (dP/dt max) fell by 14% with thiopental but did not change significantly with ketamine. Propranolol resulted in attenuation of the tachycardia and a fall of 10% in dP/dt max with ketamine but had little effect on the response to thiopental. Phentolamine had no consistent effects on either drug. With pentolinium both drugs decreased dP/dt max. Intracoronary injection of ketamine decreased dP/dt max. Adrenalectomy had little effect on the responses to either anesthetic. The results lead to the conclusion that both ketamine and thiopental have myocardial depressant effects, but, whereas thiopental does not alter sympathetic tone, the depressive effects of ketamine are obscured by stimulation of cardiac sympathetic nerves.

Cardiac arrhythmias of sympathetic origin in the dog

1977 ◽  
Vol 233 (5) ◽  
pp. H535-H540
Author(s):  
L. S. D'Agrosa
Keyword(s):  
Cardiac Arrhythmias ◽  
Sympathetic Nerves ◽  
Nerve Fibers ◽  
Cardiac Contraction ◽  
Cardiac Rate ◽  
Atrioventricular Junction ◽  
Cardiac Nerve ◽  
Sympathetic Nerve Fibers ◽  
Beta Receptors ◽  
Stimulation Of

The effects of ventrolateral and ventromedial cardiac nerve (left sympathetics) stimulation on cardiac force, on rate, and on arrhythmogenic responses were characterized and quantitated. The stimulation of left sympathetic nerves produced augmentation in cardiac contraction in 45% of the experiments, an augmentation of both a cardiac rate and force in 47%, and in cardioacceleration alone in 8%. Two characteristic patterns of arrhythmogenic responses were elicited from stimulations of 100 sympathetic nerves. The two types of neurally induced arrhythmias were atrioventricular junctional or ventricular in origin. The onset and duration of the arrhythmias were quantitated. Both types of neurally induced arrhythmias were prevented either by blocking the beta receptors with propranolol or by preventing the neural release of norepinephrine with bretylium tosylate. The neurally induced arrhythmias were probably the result of enhanced automaticity in the atrioventricular junction area and in the ventricles produced by stimulating the sympathetic nerve fibers. This report thus implicates the ventromedial cardiac nerve in the genesis of cardiac arrhythmias.

Localization of intrahepatic portal vascular resistance

1986 ◽  
Vol 251 (3) ◽  
pp. G375-G381 ◽  
Author(s):  
W. W. Lautt ◽  
C. V. Greenway ◽  
D. J. Legare ◽  
H. Weisman
Keyword(s):  
Pressure Drop ◽  
Portal Vein ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Vena Cava ◽  
Sympathetic Nerves ◽  
Hepatic Veins ◽  
Pressure Changes ◽  
Stimulation Of ◽  
Anesthetized Cat

The pressure drop from the portal vein to the vena cava occurs primarily across a postsinusoidal site localized to a narrow segment (less than 0.5 cm) of hepatic veins (roughly 1.5 mm diam) in the anesthetized cat. Portal venous pressure (PVP = 8.9 +/- 0.3 mmHg) and lobar hepatic venous pressure (LVP = 8.7 +/- 0.4 mmHg) are insignificantly different, and pressure changes imposed from the presinusoidal or postsinusoidal side are equally transmitted to both pressure sites. Several types of experiments were done to validate the LVP measurement. The portal vein, hepatic sinusoids, and hepatic veins proximal to the resistance site are all under a similar pressure. Previously reported calculations of hepatic vascular resistance are in error because of incorrect assumptions of sinusoidal pressure and localization of the portal resistance site as presinusoidal. Stimulation of hepatic sympathetic nerves for 3 min caused LVP and PVP to increase equally, showing that the increased "portal" resistance is postsinusoidal across the same region of the hepatic veins that was previously localized as the site of resistance in the basal state.

Differential pattern of spinal sympathetic outflow in response to stimulation of the caudal medullary raphe

2000 ◽  
Vol 279 (1) ◽  
pp. R210-R221 ◽  
Author(s):  
Peter D. Larsen ◽  
Sheng Zhong ◽  
Gerard L. Gebber ◽  
Susan M. Barman
Keyword(s):  
Stimulus Intensity ◽  
Low Frequency ◽  
Sympathetic Nerves ◽  
Frequency Domain Analysis ◽  
Band Power ◽  
Medullary Raphe ◽  
High Stimulus ◽  
Differential Pattern ◽  
Low Frequency Power ◽  
Stimulation Of

In urethan-anesthetized cats, frequency domain analysis was used to explore the mechanisms of differential responses of inferior cardiac (CN), vertebral (VN), and renal (RN) sympathetic nerves to electrical stimulation of a discrete region of the medullary raphe (0–2 mm caudal to the obex). Raphe stimulation in baroreceptor-denervated cats at frequencies (7–12 Hz) that entrained the 10-Hz rhythm in nerve activity decreased CN and RN activities but increased VN activity. The reductions in CN and RN discharges were associated with decreased low-frequency (≤6 Hz) power and either increased (low stimulus intensity) or decreased (high stimulus intensity) 10-Hz band power. In contrast, VN 10-Hz band power was increased at all stimulus intensities, without changes in low-frequency power. High-frequency (25 Hz) stimulation decreased low-frequency activity of CN and RN discharges in both baroreceptor-denervated and baroreceptor-intact cats, without decreasing VN low-frequency activity. We propose that the differential pattern produced by raphe stimulation involves resonance at the level of the 10-Hz oscillators and differential inhibition of follower circuits that transmit both 10-Hz and low-frequency activity to sympathetic nerves.

Increased activity of carotid sinus baroreceptors by sympathetic stimulation and norepinephrine

1981 ◽  
Vol 240 (4) ◽  
pp. H650-H658 ◽  
Author(s):  
E. Tomomatsu ◽  
K. Nishi
Keyword(s):  
Carotid Sinus ◽  
Sympathetic Innervation ◽  
Sympathetic Nerves ◽  
Nerve Endings ◽  
Discharge Frequency ◽  
Sympathetic Stimulation ◽  
High Concentration ◽  
Excitatory Effect ◽  
Pressure Step ◽  
Stimulation Of

Effects of electrical stimulation of sympathetic nerves to the carotid sinus on the discharge of single active baroreceptor fibers of the rabbit were examined in situ and in functionally isolated carotid sinus preparations with an intact sympathetic innervation under controlled conditions of pressure and temperature. Among 30 single units, 18 units responded to sympathetic stimulation of increasing discharge frequency. The excitatory effect of sympathetic stimulation on baroreceptor activity was not abolished by phentolamine (1 mg/kg iv or 10(-6) g/ml in perfusate). In isolated carotid sinus preparations perfused with Krebs-Henseleit solution, various pressure steps were applied to the sinus, and effects of norepinephrine (NE; 10(-9) and 10(-6) g/ml) on activity of nine single baroreceptor units were examined. In the presence of 10(-9) g/ml NE, discharge frequency of all units significantly increased at a given pressure step when compared with the control, whereas NE at a high concentration (10(-6) g/ml) did not produce significant changes in the discharge frequency. It is concluded that NE released by sympathetic nerve endings most likely acts directly on the baroreceptor nerve endings and sensitizes them.

DOPA, dopamine, and DOPAC concentrations in the rat gastrointestinal tract decrease during fasting

2000 ◽  
Vol 279 (4) ◽  
pp. E815-E822 ◽  
Author(s):  
Ebbe Eldrup ◽  
Erik A. Richter
Keyword(s):  
Gastrointestinal Tract ◽  
Sympathetic Nerves ◽  
Quadriceps Muscle ◽  
Reverse Phase Hplc ◽  
Sulfate Content ◽  
Tissue Concentrations ◽  
Food Content ◽  
Exogenous Origin ◽  
Dual Origin ◽  
Stimulation Of

The aim of the present study was to test the hypothesis that 3,4-dihydroxyphenylalanine (DOPA) and dopamine (DA) in the gastrointestinal tract are to a large extent of exogenous origin and derived from food. Tissue concentrations of norepinephrine (NE), epinephrine (Epi), DA, DOPA, and 3,4-dihydroxyphenylacetic acid (DOPAC), as measured by reverse-phase HPLC with electrochemical detection, were studied in fed and 4-day-fasted Wistar rats as well as in sympathectomized and adrenodemedullated rats. Sympathectomy and adrenal demedullectomy decreased tissue concentrations of NE and Epi, respectively, but had no effect on the level of tissue DOPA. Large amounts of DOPA and DA were present in the gastrointestinal tract. Fasting decreased DOPA and DA in the stomach and DOPA concentrations in the quadriceps muscle but no concentrations in other organs. DOPAC in the heart decreased both in response to sympathectomy and to fasting, whereas DOPAC decreased in plasma after fasting and in skeletal muscle after sympathectomy. We conclude that the food content of DOPA and DA is of major importance for the metabolism of DA and, thus, for the dopamine-sulfate content in the gastrointestinal tract and in plasma. The decrease in muscle DOPA after fasting may be explained by less insulin being available during fasting for stimulation of DOPA uptake in the muscle depot. DOPAC in the organism seems to be of a dual origin, derived partly from DA in the food and partly from DA synthesized in sympathetic nerves.

Response of rat jejunum to angiotensin III: pharmacology and mechanism of action

1983 ◽  
Vol 245 (4) ◽  
pp. G511-G518 ◽  
Author(s):  
N. R. Levens
Keyword(s):  
Intestinal Absorption ◽  
Dose Range ◽  
Physiological Role ◽  
Sympathetic Nerves ◽  
Jejunal Absorption ◽  
Angiotensin Peptides ◽  
Angiotensin Iii ◽  
High Doses ◽  
Potent Antagonist ◽  
Stimulation Of

At low doses angiotensin III (A III) stimulates jejunal fluid absorption in the pentobarbital sodium-anesthetized rat. In contrast, at high doses the hormone inhibits absorption and/or stimulates secretory processes. The stimulation of jejunal absorption in response to A III can be blocked by guanethidine, phentolamine, and prazosin but not by propranolol or yohimbine, suggesting that A III-increased intestinal absorption is secondary to the release of norepinephrine from sympathetic nerves in the jejunum and activation of postsynaptic alpha 1-adrenergic receptors. The A III inhibition of water absorption is not affected by adrenergic antagonists but can be reversed to a net stimulation of transfer after pretreatment of the animals with indomethacin. This suggests that at high doses A III stimulates intestinal prostaglandin biosynthesis. The A III analogue [Ile7]A III is devoid of agonist activity over a wide dose range and behaves as a potent antagonist of both the stimulatory and the inhibitory effects of the parent peptide on jejunal absorption. [Ile7]A III will be a useful tool for investigating the physiological role of angiotensin peptides in the control of intestinal absorption.

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