Inhibitory effects of excess sympathetic activity on parasympathetic vasodilation in the rat masseter muscle

2007 ◽  
Vol 293 (2) ◽  
pp. R729-R736 ◽  
Author(s):  
Hisayoshi Ishii ◽  
Takeharu Niioka ◽  
Hidekazu Watanabe ◽  
Hiroshi Izumi
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Activity ◽  
Masseter Muscle ◽  
Lingual Nerve ◽  
Dependent Manner ◽  
Tonic Activity ◽  
Inhibitory Effects ◽  
Cervical Sympathetic ◽  
Dose Dependent ◽  
Stimulation Of

The present study was designed to examine the effect of sympathetic tonic activity on parasympathetic vasodilation evoked by the trigeminal-mediated reflex in the masseter muscle in urethane-anesthetized rats. Sectioning of the superior cervical sympathetic trunk (CST) ipsilaterally increased the basal level of blood flow in the masseter muscle (MBF). Electrical stimulation of the peripheral cut end of the CST for 2 min using 2-ms pulses ipsilaterally decreased in a dependent manner the intensity (0.5–10 V) and frequency (0.1–5 Hz) of the MBF. The CST stimulation for 2 min at <0.5 Hz with 5 V using 2-ms pulses seems to be comparable with the spontaneous activity in the CST fibers innervating the masseter vasculature, because this stimulation restored the basal level of the MBF to the presectioned values. Parasympathetic vasodilation evoked by electrical stimulation of the central cut end of the lingual nerve in the masseter muscle was markedly reduced by CST stimulation for 2 min with 5 V using 2-ms pulses in a frequency-dependent manner (0.5–5 Hz). Intravenous administration of phentolamine significantly reduced the vasoconstriction induced by CST stimulation in a dose-dependent manner (0.1–1 mg/kg), but pretreatment with either phentolamine or propranolol failed to affect the sympathetic inhibition of the parasympathetic vasodilation. Our results suggest that 1) excess sympathetic activity inhibits parasympathetic vasodilation in the masseter muscle, and 2) α- and β-adrenoceptors do not contribute to sympathetic inhibition of parasympathetic vasodilation, and thus some other types of receptors must be involved in this response.

Role of baroreceptor afferents on area postrema-induced inhibition of sympathetic activity

1991 ◽  
Vol 260 (4) ◽  
pp. H1353-H1358
Author(s):  
M. Hay ◽  
E. M. Hasser ◽  
K. P. Undesser ◽  
V. S. Bishop
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Activity ◽  
Area Postrema ◽  
Afferent Input ◽  
Dependent Manner ◽  
Chemical Application ◽  
Renal Sympathetic Nerve Activity ◽  
Before And After ◽  
Stimulation Of

Activation of the area postrema by either electrical stimulation or chemical application of L-glutamate has been shown to result in an enhancement of cardiovascular baroreflexes similar to that seen with systemic infusions of arginine vasopressin (AVP). In addition, it has been found that the effects of AVP on baroreflex inhibition of renal sympathetic nerve activity (RSNA) are similar to those observed with phenylephrine following lesions of the area postrema or after partial denervation of baroreceptor afferents. The present study was undertaken to determine the role of baroreceptor afferent input on area postrema stimulation-induced decreases in sympathetic activity. In anesthetized rabbits, the responses of arterial pressure, heart rate, and RSNA to area postrema electrical stimulation were obtained before and after progressive sinoaortic denervation and vagotomy. Stimulation of the area postrema in carotid sinus-denervated animals consistently decreased RSNA in a frequency-dependent manner. However, following bilateral removal of both the aortic nerves and the vagi, electrical stimulation of the area postrema had no effect on RSNA. These results suggest that the ability of area postrema stimulation to inhibit RSNA is dependent on the presence of baroreceptor afferent input.

scholarly journals Differences in control of parasympathetic vasodilation between submandibular and sublingual glands in the rat

2015 ◽  
Vol 309 (11) ◽  
pp. R1432-R1438 ◽  
Author(s):  
Toshiya Sato ◽  
Hisayoshi Ishii
Keyword(s):  
Blood Flow ◽  
Receptor Antagonist ◽  
Recovery Time ◽  
Lingual Nerve ◽  
Laser Speckle ◽  
Dependent Manner ◽  
Antimuscarinic Agent ◽  
Dose Dependent ◽  
Stimulation Of ◽  
Vip Receptor

We examined blood flow in the submandibular gland (SMGBF) and sublingual gland (SLGBF) during electrical stimulation of the central cut end of the lingual nerve (LN) in the urethane-anesthetized rats using a laser speckle imaging flow meter. LN stimulation elicited intensity- and frequency-dependent SMGBF and SLGBF increases, and the magnitude of the SMGBF increase was higher than that of the SLGBF increase. The increase in both glands was significantly inhibited by intravenous administration of the autonomic cholinergic ganglion blocker hexamethonium. The antimuscarinic agent atropine markedly inhibited the SMGBF increase and partly inhibited the SLGBF increase. The atropine-resistant SLGBF increase was significantly inhibited by infusion of vasoactive intestinal peptide (VIP) receptor antagonist, although administration of VIP receptor antagonist alone had no effect. The recovery time to the basal blood flow level was shorter after LN stimulation than after administration of VIP. However, the recovery time after LN stimulation was significantly delayed by administration of atropine in a dose-dependent manner to the same level as after administration of VIP. Our results indicate that 1) LN stimulation elicits both a parasympathetic SMGBF increase mainly evoked by cholinergic fibers and a parasympathetic SLGBF increase evoked by cholinergic and noncholinergic fibers, and 2) VIP-ergic mechanisms are involved in the noncholinergic SLGBF increase and are activated when muscarinic mechanisms are deactivated.

Tofisopam, a new 2,3-benzodiazepine. Inhibition of changes induced by stress loading and hypothalamic stimulation

1983 ◽  
Vol 61 (6) ◽  
pp. 619-625 ◽  
Author(s):  
K. Yamaguchi ◽  
K. Suzuki ◽  
T. Niho ◽  
M. Shimora ◽  
C. Ito ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Immobilization Stress ◽  
Water Immersion ◽  
Hypothalamic Stimulation ◽  
Gastric Ulceration ◽  
Dependent Manner ◽  
Hypothalamic Area ◽  
Autonomic Responses ◽  
Dose Dependent ◽  
Stimulation Of

Effects of tofisopam, a new 2,3-benzodiazepine compound, were investigated on the following: gastric ulceration, induced by water-immersion stress in normal rats and by immobilization stress in olfactory-bulbectomized (OB) rats; and propulsion of the small intestine caused by water-immersion stress in rats and autonomic responses to electrical stimulation of the hypothalamus in rabbits. In the latter, the results were compared with those of diazepam and γ-oryzanol. Tofisopam (30 and 100 mg/kg, po) significantly inhibited the gastric ulceration induced by water-immersion stress in normal rats in a dose-dependent manner. Immobilization-stress loading increased the incidence and average index of gastric ulceration in OB rats, compared with nonstressed rats. Tofisopam (100 mg/kg, po) significantly inhibited the gastric ulceration induced by stress loading in OB rats. Water-immersion stress loading induced a significant increase in intestinal propulsion in rats. This increase was reversed to control levels by tofisopam (100 mg/kg, po). Tofisopam (1.0 mg/kg, iv, or 0.1 mg/kg by intracerebrospinal injection) inhibited the constriction of ear microvessels, the decrease in earlobe temperature, and mydriasis induced by electrical stimulation of the medial hypothalamic area in rabbits. However, diazepam and γ-oryzanol failed to inhibit the autonomic responses to medial hypothalamic stimulation. From these results, it can be concluded that tofisopam restores the autonomic abnormality induced by stress loading possibly via intervention in the central autonomic area, i.e., the hypothalamus, by an action different from that of diazepam.

Effect of Isoflurane on Motor-evoked Potentials Induced by Direct Electrical Stimulation of the Exposed Motor Cortex with Single, Double, and Triple Stimuli in Rats

1996 ◽  
Vol 85 (5) ◽  
pp. 1176-1183 ◽  
Author(s):  
Masahiko Kawaguchi ◽  
Kiyoshi Shimizu ◽  
Hitoshi Furuya ◽  
Takanori Sakamoto ◽  
Hideyuki Ohnishi ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Motor Cortex ◽  
Evoked Potentials ◽  
Success Rate ◽  
Motor Evoked Potentials ◽  
Single Pulse ◽  
Dependent Manner ◽  
Dose Dependent ◽  
Pulse Stimulation ◽  
Stimulation Of

Background The clinical application of intraoperative motor-evoked potentials (MEPs) has been hampered by their sensitivity to anesthetics. Recently, to overcome anesthetic-induced depression of myogenic MEPs, multiple stimulus setups with a paired or a train of pulses for stimulation of the motor cortex were reported. However, the effects of anesthetics on MEPs induced by these stimulation techniques are unknown. Methods Bipolar electrical stimulation of the left motor cortex was carried out in 15 rats anesthetized with thiopental while the compound muscle action potentials were recorded from the contralateral hind limb. After recording of the MEP in response to the single-shock stimulation of the motor cortex, paired pulses (double pulses) or a train of three pulses (triple pulses) with an interstimulus interval of each pulse at 0.3, 0.5, 1.0, 1.5, and 2.0 ms were applied. After control MEP recording, isoflurane was administered at a concentration of 0.25 minimum alveolar anesthetic concentration (MAC), 0.5 MAC, 0.75 MAC, and 1.0 MAC, and the effects of isoflurane on the MEPs induced by single, double, and triple pulses were evaluated. Results In all animals, distinct baseline MEPs were recorded. During the administration of 0.25 MAC and 0.5 MAC isoflurane, MEPs induced by stimulation with a single pulse could be recorded in 87% and 33% of animals, respectively, and MEP amplitude was significantly reduced in a dose-dependent manner. During the administration of 0.75 MAC isoflurane, MEPs after single-pulse stimulation could not be recorded in any animals. By stimulating with paired or triple pulses, the success rate of MEP recording and MEP amplitude significantly increased compared with those after single pulse before and during the administration of isoflurane. Both the success rate of MEP recording and MEP amplitude after double- and triple-pulse stimulation decreased significantly in a dose-dependent manner during the administration of isoflurane. Conclusions Application of double or triple stimulation of the motor cortex increases the success rate of MEP recording and its amplitude during isoflurane anesthesia in rats. However, these responses are suppressed by isoflurane in a dose-dependent manner.

Interaction between amrinone and parathyroid hormone on bone in culture

1982 ◽  
Vol 243 (6) ◽  
pp. E499-E504
Author(s):  
N. S. Krieger ◽  
P. H. Stern
Keyword(s):  
Parathyroid Hormone ◽  
Bone Resorption ◽  
Direct Interaction ◽  
Inhibitory Effects ◽  
Dihydroxyvitamin D3 ◽  
Basal Bone ◽  
Cardiotonic Agent ◽  
Neonatal Mouse Calvaria ◽  
Dose Dependent ◽  
Stimulation Of

The cardiotonic agent amrinone has been postulated to directly affect Na-Ca exchange. Because stimulated bone resorption has been proposed to require Na-Ca exchange, we examined the effects of amrinone on bone. Amrinone inhibited release of Ca from neonatal mouse calvaria in organ culture stimulated by parathyroid hormone (PTH), 1,25-dihydroxyvitamin d3, or prostaglandin E2. Inhibition was dose dependent and maximal at 2 X 10(-4) M. The effect of amrinone differed from the inhibitory effects of calcitonin, ouabain, or nigericin in that 1) 6-h exposure to amrinone alone prevented the effect of subsequently added PTH; 2) amrinone was only partially effective if added after resorption was initiated by 24-h treatment with PTH; 3) coincubation with amrinone and PTH during the first 48 h of culture allowed for a response to PTH after amrinone was removed; no such protection by a stimulator occurred with ouabain or nigericin. Also submaximal concentrations of amrinone plus calcitonin, ouabain, or nigericin gave greater than additive inhibition of Ca release. Amrinone had no effect on basal bone cAMP or on the acute stimulation of cAMP by PTH. The results suggest that amrinone could have a more direct interaction with the pathway involved in stimulated bone resorption than the other inhibitors.

scholarly journals Establishment of a New Device for Electrical Stimulation of Non-Degenerative Cartilage Cells In Vitro

2021 ◽  
Vol 22 (1) ◽  
pp. 394
Author(s):  
Simone Krueger ◽  
Alexander Riess ◽  
Anika Jonitz-Heincke ◽  
Alina Weizel ◽  
Anika Seyfarth ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Electric Fields ◽  
Cartilage Tissue ◽  
Type I ◽  
Dependent Manner ◽  
New Device ◽  
Alternating Electric Fields ◽  
Cartilage Cells ◽  
Stimulation Of

In cell-based therapies for cartilage lesions, the main problem is still the formation of fibrous cartilage, caused by underlying de-differentiation processes ex vivo. Biophysical stimulation is a promising approach to optimize cell-based procedures and to adapt them more closely to physiological conditions. The occurrence of mechano-electrical transduction phenomena within cartilage tissue is physiological and based on streaming and diffusion potentials. The application of exogenous electric fields can be used to mimic endogenous fields and, thus, support the differentiation of chondrocytes in vitro. For this purpose, we have developed a new device for electrical stimulation of chondrocytes, which operates on the basis of capacitive coupling of alternating electric fields. The reusable and sterilizable stimulation device allows the simultaneous use of 12 cavities with independently applicable fields using only one main supply. The first parameter settings for the stimulation of human non-degenerative chondrocytes, seeded on collagen type I elastin-based scaffolds, were derived from numerical electric field simulations. Our first results suggest that applied alternating electric fields induce chondrogenic re-differentiation at the gene and especially at the protein level of human de-differentiated chondrocytes in a frequency-dependent manner. In future studies, further parameter optimizations will be performed to improve the differentiation capacity of human cartilage cells.

scholarly journals Adrenaline Stimulation of Phospholipid Metabolism in Adipocyte Ghosts

1987 ◽  
Vol 40 (4) ◽  
pp. 405
Author(s):  
David Mann ◽  
Audrey M Bersten
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Linoleic Acid ◽  
Adenylate Cyclase ◽  
Phospholipid Metabolism ◽  
Dependent Manner ◽  
Long Chain Fatty Acids ◽  
Membrane Phospholipids ◽  
Dose Dependent ◽  
Stimulation Of

The incorporation of long-chain fatty acids into phospholipids has been detected in adipocyte ghosts that were incubated with [1_14 C] stearic, [1_14 C] linoleic or [l_14C] arachidonic acid. Adrenaline and adenosine activated this incorporation within 15 s of exposure of the ghosts to the hormones and the response was dose dependent. Maximum incorporation of labelled linoleic acid occurred at 10-5 M adrenaline and 10-7 M adenosine. The a-agonist phenylephrine and the ~-agonist isoproterenol were also shown to stimulate the incorporation of fatty acid in a dose dependent manner. Phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine and phosphatidylinositol were each labelled preferentially with linoleic or arachidonic acid. p-Bromophenacylbromide, quinacrine and centrophenoxine inhibited the adrenaline-stimulated incorporation of fatty acids into ghost membrane phospholipids, and p-bromophenacylbromide also reduced the activation of adenylate cyclase by adrenaline. NaF, an activator of adenylate cyclase, like adrenaline, stimulated the incorporation of linoleic acid into ghost membrane phospholipids.

scholarly journals Global Cerebral Vasodilatation Elicited by Focal Electrical Stimulation within the Dorsal Medullary Reticular Formation in Anesthetized Rat

1983 ◽  
Vol 3 (3) ◽  
pp. 270-279 ◽  
Author(s):  
Costantino Iadecola ◽  
Masatsugu Nakai ◽  
Ehud Arbit ◽  
Donald J. Reis
Keyword(s):  
Electrical Stimulation ◽  
Reticular Formation ◽  
Medial Longitudinal Fasciculus ◽  
Medullary Reticular Formation ◽  
Tissue Samples ◽  
The Central Nervous System ◽  
Cerebral Vasodilatation ◽  
Cervical Sympathetic ◽  
Global Increase ◽  
Stimulation Of

We examined the effects of electrical stimulation of a restricted area of the dorsal medullary reticular formation (DMRF) on regional cerebral blood flow (CBF) in anesthetized (by chloralose), paralyzed (by curare) rats. CBF was measured in tissue samples by the Kety principle, with 14C-iodoantipyrine as indicator. Stimulation of DMRF elicited a widespread, significant increase in CBF in 12 of 13 areas. The increase in flow was greatest in cerebral cortex, up to 240% of control. However, it was also substantially increased in selected regions of telencephalon, diencephalon, mesencephalon, and lower brainstem, but not cerebellum. In contrast, electrical stimulation of the midline (interstitial nucleus of the medial longitudinal fasciculus) 1 mm medial to the DMRF did not change CBF. The increase in CBF evoked by DMRF stimulation persisted after transection of the spinal cord at C1 or cervical sympathetic trunk. We conclude that excitation of neurons originating in or passing through the DMRF can elicit a potent and virtually global increase of CBF. The effect appears to be mediated by intrinsic pathways of the central nervous system.

Interaction of adenosine with vasopressin in the inner medullary collecting duct

1990 ◽  
Vol 259 (4) ◽  
pp. F679-F687 ◽  
Author(s):  
Y. Yagil
Keyword(s):  
Pertussis Toxin ◽  
Receptor Agonist ◽  
Collecting Duct ◽  
Phosphodiesterase Inhibitor ◽  
Inhibitory Effects ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct ◽  
Camp Levels ◽  
Dose Dependent ◽  
Stimulation Of

Administration of adenosine (Ado) into rat renal artery induces dose-dependent diuresis that is independent of changes in glomerular filtration rate or renal blood flow, suggesting a direct effect on tubule H2O reabsorption. To test the hypothesis that Ado modulates cellular action of arginine vasopressin (AVP) as a tubular mechanism for the diuretic effect of Ado, interaction of Ado with AVP was studied in primary cell culture of rat inner medullary collecting duct (IMCD) epithelium. Stimulation of cells with 10(-6) M AVP in presence of 0.1 mM Ro 20-1724, a nonmethylxanthine phosphodiesterase inhibitor that has no effect on Ado receptors, increased adenosine 3',5'-cyclic monophosphate (cAMP) levels twofold or more above baseline. Stimulation of cells with the A1 Ado-receptor agonist N6-cyclohexyladenosine (CHA), the A2-receptor agonist 5'-(N-ethylcarboxamido)-adenosine (NECA), or with the P-site agonist 2',5'-dideoxyadenosine (DDA) significantly inhibited the AVP-stimulated cAMP response. Preincubation with pertussis toxin abolished the inhibitory effects of CHA and NECA, but not of DDA. The data suggest that, in the rat IMCD, Ado modulates AVP action by interfering with its ability to stimulate formation of its second messenger, cAMP. This effect is mediated by the extracellular Ado receptors A1 and A2 and by the intracellular P-site. It occurs by at least two pathways, one sensitive and the other insensitive to pertussis toxin.

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