Responses of isolated perfused arteries to catecholamines and nerve stimulation

1965 ◽  
Vol 209 (2) ◽  
pp. 376-382 ◽  
Author(s):  
Larry A. Rogers ◽  
Richard A. Atkinson ◽  
John P. Long
Keyword(s):  
Nerve Stimulation ◽  
Mesenteric Artery ◽  
Muscle Tone ◽  
Low Frequency ◽  
Sympathetic Nerves ◽  
Gas Mixture ◽  
Constant Flow ◽  
Pressor Responses ◽  
Resistance Vessels ◽  
Small Resistance

An isolated preparation of the dog's mesenteric artery with branching small resistance vessels and sympathetic nerves attached has been devised. The branching arterial segments were perfused by a constant-flow technique; the pressor responses to intra-arterially injected catecholamine and to nerve stimulation were recorded. The preparation gave reproducible pressor responses to injected catecholamine and to nerve stimulation for periods of several hours. Decreasing the temperature or increasing the pH (by decreasing CO2 in the gas mixture) of the vessel bath increased arterial smooth muscle tone and potentiated the pressor responses to injected catecholamine and to nerve stimulation. Increasing the temperature of the bath decreased the tone and reactivity of this preparation. Low-frequency continuous nerve stimulation potentiated the responses of this preparation to intra-arterially injected catecholamines.

Adenosine modulation of vasoconstrictor responses to stimulation of sympathetic nerves and norepinephrine infusion in the superior mesenteric artery of the cat

1988 ◽  
Vol 66 (7) ◽  
pp. 937-941 ◽  
Author(s):  
W. Wayne Lautt ◽  
Leslie K. Lockhart ◽  
Dallas J. Legare
Keyword(s):  
Superior Mesenteric Artery ◽  
Nerve Stimulation ◽  
Adenosine Receptors ◽  
Mesenteric Artery ◽  
Sympathetic Nerves ◽  
Sympathetic Nerve Stimulation ◽  
Vascular Bed ◽  
Norepinephrine Infusion ◽  
Resistance Vessels ◽  
Stimulation Of

Vasoconstriction induced by sympathetic nerve stimulation and by norepinephrine infusion in the superior mesenteric artery of cats anesthetized with pentobarbital was inhibited by adenosine infusions in a dose-related way. The responses to nerve stimulation were not inhibited to a greater extent than the responses to norepinephrine, thus suggesting no presynaptic modulation of sympathetic nerves supplying the resistance vessels of the feline intestinal vascular bed. Blockade of adenosine receptors using 8-phenyltheophylline did not alter the degree of constriction induced by nerve stimulation or norepinephrine infusion, indicating that in the fasted cat, endogenous adenosine co-released or released subsequent to constriction does not affect the peak vasoconstriction reached. Isoproterenol caused similar degrees of vasodilation as adenosine but did not show significant antagonism of the pooled responses to nerve stimulation or norepinephrine infusion; there was no tendency for the degree of dilation induced by isoproterenol to correlate with the inhibition of constrictor responses. Thus, the effect of adenosine on nerve- and norepinephrine-induced constriction is not secondary to nonspecific vasodilation.

Anoxia and capillary filtration coefficient in the isolated cat hindlimb

1984 ◽  
Vol 246 (2) ◽  
pp. H312-H315 ◽  
Author(s):  
P. D. Watson ◽  
D. R. Scott ◽  
M. B. Wolf
Keyword(s):  
Metabolic Control ◽  
Vascular Resistance ◽  
Filtration Coefficient ◽  
Gas Mixture ◽  
Constant Flow ◽  
Co2 Gas ◽  
Capillary Filtration ◽  
Resistance Vessels ◽  
Capillary Filtration Coefficient

Isolated cat hindlimbs were perfused from a reservoir with an albumin-blood mixture at a constant flow of 20 ml X min-1 X 100 g muscle-1 while alternately bubbling the perfusate with either 95% O2-5% CO2 gas mixture or a 95% N2-5% CO2 mixture for 50- to 60-min periods. Capillary filtration coefficient (CFC), vascular resistance (R), and perfusate O2 content were measured in each period. The arterial O2 content fell from fully equilibrated to 0.25 vol% during the use of N2. R fell from about 6 mmHg X min X 100 g X ml-1 during O2 bubbling to approximately 1.0 with N2. CFC averaged 0.012 +/- 0.002 ml X min-1 X mmHg-1 X 100 g muscle-1 (SD, n = 6) during the 1st O2 period, rising to 0.016 +/- 0.002 (n = 4) in the 3rd O2 period 4 h later. CFC fell by 5% (P less than 0.001) during the periods of N2 bubbling. Papaverine was present in two experiments without effect on the CFC data. It was concluded that CFC was not meaningfully influenced by vascular resistance or anoxia, a finding that is inconsistent with the concept of local metabolic control of CFC by precapillary resistance vessels.

Adenosine modulation of hepatic arterial but not portal venous constriction induced by sympathetic nerves, norepinephrine, angiotensin, and vasopressin in the cat

1986 ◽  
Vol 64 (4) ◽  
pp. 449-454 ◽  
Author(s):  
W. Wayne Lautt ◽  
Dallas J. Legare
Keyword(s):  
Smooth Muscle ◽  
Hepatic Artery ◽  
Nerve Stimulation ◽  
Adenosine Receptors ◽  
Sympathetic Nerves ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Resistance Vessels ◽  
Basal Tone ◽  
Intrinsic Regulation

Intrinsic regulation of hepatic arterial blood flow depends upon local concentrations of adenosine. The present data show that i.a. infusions of adenosine cause dilation of the hepatic artery and inhibition of arterial vasoconstriction induced by norepinephrine, vasopressin, angiotensin, and hepatic nerve stimulation. Vasoconstriction induced by submaximal nerve stimulation (2 Hz) and norepinephrine infusions (0.25 and 0.5 μg∙kg−1∙min−1, i.p.v.) were equally inhibited by adenosine. Supramaximal nerve stimulation (8 Hz) was inhibited to a lesser extent. The data are consistent with the hypotheses that (a) adenosine causes nonselective inhibition of vasoconstrictor influences on the hepatic artery; and (b) adenosine antagonizes neurally induced vasoconstriction by a purely postsynaptic effect and does not decrease norepinephrine release. In contrast with the hepatic artery, the intrahepatic portal resistance vessels are not affected by even large doses of adenosine; neither responses in basal tone nor antagonism of vasoconstrictor effects of nerve stimulation, norepinephrine, or angiotensin could be demonstrated. The data are consistent with the hypothesis that the smooth muscle of the portal resistance vessels does not contain adenosine receptors, whereas adenosine receptors on the smooth muscle of the hepatic arterial resistance vessels are of major regulatory importance. Whether endogenous levels of adenosine can reach sufficient concentration to modulate endogenous constrictors remains to be determined.

Effect of adenosine and glucagon on hepatic blood volume responses to sympathetic nerves

1991 ◽  
Vol 69 (1) ◽  
pp. 43-48 ◽  
Author(s):  
W. Wayne Lautt ◽  
Joshua Schafer ◽  
Dallas J. Legare
Keyword(s):  
Blood Volume ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerves ◽  
Liver Weight ◽  
Maximal Response ◽  
Venous Capacitance ◽  
Resistance Vessels ◽  
Capacitance Vessels

Hepatic blood volume responses were studied in cats using in vivo plethysmography. The maximal response (Rmax) to sympathetic nerve stimulation and to infusions of norepinephrine into the hepatic artery or portal vein was similar (12–14 mL expelled per liver in 2.9-kg cats; average liver weight, 76.8 ± 6.8 g). The ED50 for norepinephrine intraportal (0.44 ± 0.13) and intrahepatic arterial infusions (0.33 ± 0.08 μg∙kg−1∙min−1) were similar indicating equal access of both blood supplies to the capacitance vessels. Adenosine (2.0 mg∙kg−1∙min−1) did not cause significant volume changes but produced a mild (27%) suppression of Rmax due to nerve stimulation with no change in the frequency (3.4 Hz) needed to produce 50% of Rmax. Rmax tended (not statistically significant) to decrease during glucagon (1.0 μg∙kg−1∙min−1) infusion but the nerve frequency needed to produce 50% of Rmax rose to 5.6 Hz. Thus both adenosine and glucagon produced modulation of sympathetic nerve-induced capacitance responses without having significant effects on basal blood volume. Adenosine, by virtue of its marked effects on arterial resistance vessels (at substantially lower doses than those used here) and the relative lack of effect on venous capacitance vessels, may be useful for producing clinical afterload reduction without venous pooling.Key words: blood volume, capacitance, sympathetic nerves, adenosine, glucagon.

Long Term Effects of Low Frequency (10 Hz) Vagus Nerve Stimulation on EEG and Heart Rate Variability in Crohn's Disease: A Case Report

2014 ◽  
Vol 7 (6) ◽  
pp. 914-916 ◽  
Author(s):  
Didier Clarençon ◽  
Sonia Pellissier ◽  
Valérie Sinniger ◽  
Astrid Kibleur ◽  
Dominique Hoffman ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Crohn’S Disease ◽  
Case Report ◽  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Low Frequency ◽  
Long Term Effects

scholarly journals Median nerve stimulation induces analgesia via orexin-initiated endocannabinoid disinhibition in the periaqueductal gray

2018 ◽  
Vol 115 (45) ◽  
pp. E10720-E10729 ◽  
Author(s):  
Yi-Hung Chen ◽  
Hsin-Jung Lee ◽  
Ming Tatt Lee ◽  
Ya-Ting Wu ◽  
Yen-Hsien Lee ◽  
...  
Keyword(s):  
Pain Management ◽  
Median Nerve ◽  
Nerve Stimulation ◽  
Antinociceptive Effect ◽  
Low Frequency ◽  
Periaqueductal Gray ◽  
Orexin A ◽  
Median Nerve Stimulation ◽  
Opioid Receptor Antagonists ◽  
Nociceptive Responses

Adequate pain management remains an unmet medical need. We previously revealed an opioid-independent analgesic mechanism mediated by orexin 1 receptor (OX1R)-initiated 2-arachidonoylglycerol (2-AG) signaling in the ventrolateral periaqueductal gray (vlPAG). Here, we found that low-frequency median nerve stimulation (MNS) through acupuncture needles at the PC6 (Neiguan) acupoint (MNS-PC6) induced an antinociceptive effect that engaged this mechanism. In mice, MNS-PC6 reduced acute thermal nociceptive responses and neuropathy-induced mechanical allodynia, increased the number of c-Fos–immunoreactive hypothalamic orexin neurons, and led to higher orexin A and lower GABA levels in the vlPAG. Such responses were not seen in mice with PC6 needle insertion only or electrical stimulation of the lateral deltoid, a nonmedian nerve-innervated location. Directly stimulating the surgically exposed median nerve also increased vlPAG orexin A levels. MNS-PC6–induced antinociception (MNS-PC6-IA) was prevented by proximal block of the median nerve with lidocaine as well as by systemic or intravlPAG injection of an antagonist of OX1Rs or cannabinoid 1 receptors (CB1Rs) but not by opioid receptor antagonists. Systemic blockade of OX1Rs or CB1Rs also restored vlPAG GABA levels after MNS-PC6. A cannabinoid (2-AG)-dependent mechanism was also implicated by the observations that MNS-PC6-IA was prevented by intravlPAG inhibition of 2-AG synthesis and was attenuated inCnr1−/−mice. These findings suggest that PC6-targeting low-frequency MNS activates hypothalamic orexin neurons, releasing orexins to induce analgesia through a CB1R-dependent cascade mediated by OX1R-initiated 2-AG retrograde disinhibition in the vlPAG. The opioid-independent characteristic of MNS-PC6–induced analgesia may provide a strategy for pain management in opioid-tolerant patients.

The coordinate roles of branchial nerve activity and potassium in the stimulation of ciliary activity in Mytilus edulis: observations with phenoxybenzamine, bromolysergic acid and fluorescence histochemistry

1976 ◽  
Vol 65 (1) ◽  
pp. 109-116
Author(s):  
A. A. Paparo
Keyword(s):  
Mytilus Edulis ◽  
Nerve Stimulation ◽  
High Frequency ◽  
Low Frequency ◽  
Ciliary Activity ◽  
Nerve Activity ◽  
Basal Rate ◽  
Potassium Effect ◽  
Branchial Nerve ◽  
Stimulation Of

Potassium concentrations in excess of 30 mM increase the rate of beating of lateral cilia on the gill of Mytilus edulis. Cilioexcitation produced by low frequency (5 beats/s) electrical stimulation was potentiated with potassium but blocked with bromolysergic acid (a serotonergic inhibitor). Cilioinhibition produced by high frequency (50 beats/s) stimulation was decreased with potassium and phenoxybenzamine (a dopaminergic inhibitor). Phenoxybenzamine enhanced the cilioexcitation produced by potassium. Potassium doses incapable of maintaining a basal rate of beating (less than 30 mM) could increase ciliary activity if phenoxybenzamine was also added. After transection of the branchial nerve, the yellow-fluorophore (serotonergic storage) and cilioexcitatory effect of potassium gradually decrease. This study shows that the potassium effect on ciliary activity (a) increase with low frequency nerve stimulation, presumably through the release of serotonin and (b) decreases with high frequency nerve stimulation, presumably through the release of dopamine.

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