Effect of Transcutaneous Electrical Stimulation of Nerves on Blood Pressure and Blood Content of Neuropeptide CGRP and Nitric Oxide in Hypertensive Rats with Metabolic Disturbances

2019 ◽  
Vol 166 (4) ◽  
pp. 436-439 ◽  
Author(s):  
V. K. Spiridonov ◽  
Z. S. Tolochko ◽  
T. A. Korolenko
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Electrical Stimulation ◽  
Transcutaneous Electrical Stimulation ◽  
Hypertensive Rats ◽  
Metabolic Disturbances ◽  
Blood Content ◽  
Stimulation Of

scholarly journals Intermittent electrical stimulation of the right cervical vagus nerve in salt-sensitive hypertensive rats: effects on blood pressure, arrhythmias, and ventricular electrophysiology

2015 ◽  
Vol 3 (8) ◽  
pp. e12476 ◽  
Author(s):  
Elizabeth M. Annoni ◽  
Xueyi Xie ◽  
Steven W. Lee ◽  
Imad Libbus ◽  
Bruce H. KenKnight ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Vagus Nerve ◽  
Hypertensive Rats ◽  
The Right ◽  
Stimulation Of

scholarly journals Intermedin in Paraventricular Nucleus Attenuates Sympathetic Activity and Blood Pressure via Nitric Oxide in Hypertensive Rats

Hypertension ◽  
2014 ◽  
Vol 63 (2) ◽  
pp. 330-337 ◽  
Author(s):  
Ye-Bo Zhou ◽  
Hai-Jian Sun ◽  
Dan Chen ◽  
Tong-Yan Liu ◽  
Ying Han ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Paraventricular Nucleus ◽  
Sympathetic Activity ◽  
Hypertensive Rats

Contribution of Vascular Nitric Oxide to Basal Blood Pressure in Conscious Spontaneously Hypertensive Rats and Normotensive Wistar Kyoto Rats

1995 ◽  
Vol 89 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Naoyoshi Minami ◽  
Yutaka Imai ◽  
Jun-Ichiro Hashimoto ◽  
Keishi Abe
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Methyl Ester ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Basal Blood Pressure ◽  
Wistar Kyoto

1. The aim of this study was to clarify the extent to which vascular nitric oxide contributes to basal blood pressure in conscious spontaneously hypertensive rats and normotensive Wistar Kyoto rats. 2. The contribution of vascular nitric oxide to maintenance of blood pressure was estimated by measuring the pressor response to an intravenous injection of nitric oxide synthase inhibitor, Nω-l-arginine methyl ester, given after serial injections of captopril, vasopressin V1-receptor antagonist (V1-antagonist) and ganglion blocker (pentolinium) in conscious spontaneously hypertensive and Wistar Kyoto rats aged 20–28 weeks. To estimate the ‘amplifier property’ of hypertrophied vasculature in spontaneously hypertensive rats, which is known to modulate pressor responses, the lower blood pressure plateau after serial injections of captopril, V1-antagonist and pentolinium and the maximum blood pressure elicited by subsequent injection of increasing doses of phenylephrine were also measured. 3. The serial injections of captopril, V1-antagonist and pentolinium decreased mean arterial pressure from 164 ± 9 mmHg to 67 ± 2 mmHg and from 117 ± 2 mmHg to 49 ± 1 mmHg in spontaneously hypertensive and Wistar Kyoto rats respectively. The subsequent injection of Nω-l-arginine methyl ester restored mean arterial pressure almost to its control levels in both spontaneously hypertensive and Wistar Kyoto rats. The absolute changes in mean arterial pressure elicited by Nω-l-arginine methyl ester were significantly greater in spontaneously hypertensive than in Wistar Kyoto rats (P < 0.01), but there was no significant difference in the responses to Nω-l-arginine methyl ester when they were expressed as percentages of either the lower blood pressure plateau or maximum blood pressure. 4. These results indicate that basal blood pressure in both spontaneous hypertensive and Wistar Kyoto rats is maintained by a balance between vascular nitric oxide and major pressor systems. They also suggest that the vasodilatory effect of vascular nitric oxide does not differ between spontaneously hypertensive and Wistar Kyoto rats, and that the increased pressor effect of Nω-l-arginine methyl ester in spontaneously hypertensive rats is due to a vascular amplifier mechanism.

The effect of transcranial magnetic stimulation on the excitability of the motor neuron pools of the muscles of the lower extremities

2021 ◽  
Author(s):  
S.S. Ananiev ◽  
D.A. Pavlov ◽  
R.N. Yakupov ◽  
V.A. Golodnova ◽  
M.V. Balykin
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Transcranial Magnetic Stimulation ◽  
Motor Cortex ◽  
Magnetic Stimulation ◽  
Primary Motor Cortex ◽  
Lower Extremities ◽  
Transcutaneous Electrical Stimulation ◽  
Stimulation Of

The study was conducted on 22 healthy men aged 18-23 years. The primary motor cortex innervating the lower limb was stimulated with transcranial magnetic stimulation. Using transcutaneous electrical stimulation of the spinal cord, evoked motor responses of the muscles of the lower extremities were initiated when electrodes were applied cutaneous between the spinous processes in the Th11-Th12 projection. Research protocol: Determination of the thresholds of BMO of the muscles of the lower extremities during TESCS; determination of the BMO threshold of the TA muscle in TMS; determination of the thresholds of the BMO of the muscles of the lower extremities during TESCS against the background of 80% and 90% TMS. It was found that magnetic stimulation of the motor cortex of the brain leads to an increase in the excitability of the neural structures of the lumbar thickening of the spinal cord and an improvement in neuromuscular interactions. Key words: transcranial magnetic stimulation, transcutaneous electrical stimulation of the spinal cord, neural networks, excitability, neuromuscular interactions.

Dependence of Respiratory Reaction on the Intensity of Locomotor Response to Transcutaneous Electrical Stimulation of the Spinal Cord

2019 ◽  
Vol 45 (3) ◽  
pp. 262-270 ◽  
Author(s):  
A. V. Minyaeva ◽  
S. A. Moiseev ◽  
A. M. Pukhov ◽  
N. A. Shcherbakova ◽  
Yu. P. Gerasimenko ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Transcutaneous Electrical Stimulation ◽  
Locomotor Response ◽  
Stimulation Of

Mechanism underlying the response to vasodilator nerve stimulation in isolated dog and monkey cerebral arteries

1990 ◽  
Vol 259 (5) ◽  
pp. H1511-H1517 ◽  
Author(s):  
N. Toda ◽  
T. Okamura
Keyword(s):  
Nitric Oxide ◽  
Electrical Stimulation ◽  
Coronary Artery ◽  
Substance P ◽  
Nerve Stimulation ◽  
Cerebral Arteries ◽  
Inhibitory Effect ◽  
Synthesis Inhibitor ◽  
Transmural Stimulation ◽  
Stimulation Of

Relaxant responses to transmural electrical stimulation and nicotine of cerebral artery strips obtained from dogs and Japanese monkeys were abolished by tetrodotoxin and hexamethonium, respectively, and suppressed by treatment with NG-monomethyl-L-arginine (L-NMMA), a nitric oxide (NO) synthesis inhibitor. The inhibitory effect was prevented and reversed by L-arginine but not by D-arginine. The relaxations suppressed by L-NMMA were not increased by exogenously applied NO. Endothelium denudation did not alter the response to transmural stimulation and nicotine or the inhibitory effect of L-NMMA. D-NMMA did not inhibit the response to vasodilator nerve stimulation. Dog coronary artery relaxations caused by transmural stimulation were not inhibited by L-NMMA but reversed to contractions by propranolol. Relaxations caused by substance P of dog cerebral arteries treated with indomethacin were dependent on endothelium and inhibited by L-NMMA, whereas those by NO and nitroglycerin, endothelium-independent relaxations, were unaffected. It is concluded that chemical and electrical stimulation of vasodilator nerves relaxes dog and monkey cerebral arteries, possibly by a mediation of NO rather than a stimulating action of NO on the release of vasodilator transmitter. Endothelium-dependent relaxations by substance P of dog cerebral arteries appear to be mediated by NO.

Neurogenically derived nitrosyl factors mediate sympathetic vasodilation in the hindlimb of the rat

1997 ◽  
Vol 272 (5) ◽  
pp. H2369-H2376 ◽  
Author(s):  
R. L. Davisson ◽  
O. S. Possas ◽  
S. P. Murphy ◽  
S. J. Lewis
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Sympathetic Neurons ◽  
Specific Inhibitor ◽  
No Synthase ◽  
Systemic Administration ◽  
Sympathetic Chain ◽  
Low Intensity ◽  
Stimulation Of

Skeletal muscle vasculature of the hindlimb is innervated by a sympathetic noncholinergic vasodilator system. The aim of this study was to determine whether this vasodilator system may represent postganglionic lumbar sympathetic neurons that synthesize and release nitric oxide (NO) or related NO-containing factors. We examined whether NO synthase (NOS)-positive postganglionic lumbar nerves innervate the hindlimb vasculature of the rat and whether the hindlimb vasodilation produced by electrical stimulation of the lumbar sympathetic chain of anesthetized rats is reduced after the systemic administration of the specific inhibitor of neuronal NOS 7-nitroindazole (7-NI). Subpopulations of lumbar sympathetic cell bodies stained intensely for NOS. Postganglionic fibers and varicosities within the iliac and femoral arteries also stained for NOS. Double ligation of the lumbar chain demonstrated that NOS was transported from the cell bodies toward the peripheral terminals. Low-intensity electrical stimulation of the lumbar chain produced a pronounced hindlimb vasodilation that was markedly diminished by pretreatment with 7-NI (45 mg/kg i.v.). In contrast, the vasodilator potency of acetylcholine and S-nitrosocysteine were augmented by 7-NI. These results suggest that postganglionic lumbar sympathetic neurons may synthesize and release NO-containing factors.

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