Electrical Stimulation Of Splanchnic Nerves Research Articles

Effects of intravenous magnesium infusion on in vivo release of acetylcholine and catecholamine in rat adrenal medulla

We applied microdialysis technique to the left adrenal medulla of anesthetized rats and examined the effects of intravenous Mg(2+) infusion on presynaptic acetylcholine (ACh) release and postsynaptic catecholamine release induced by electrical stimulation of splanchnic nerves. The dialysis probes were perfused with Ringer's solution containing neostigmine. Low-dose MgSO4 (25 μmol/kg/min for 30 min i.v.) increased mean plasma Mg(2+) concentration to 2.5mM; the administration suppressed norepinephrine (NE) release by approximately 30% and epinephrine (Epi) release by approximately 20%, but did not affect ACh release. High-dose MgSO4 (50 μmol/kg/min for 30 min i.v.) increased mean plasma Mg(2+) concentration to 3.8mM; the administration suppressed ACh release by approximately 25%, NE release by approximately 60% and Epi release by approximately 45%. Administration of Na2SO4 (50 μmol/kg/min for 30 min i.v.) did not change the release of ACh, NE or Epi. Local administration of nifedipine (200 μM) suppressed NE release by approximately 40% and Epi release by approximately 30%, but did not affect ACh release. In the presence of nifedipine, low-dose MgSO4 did not suppress the release of ACh, or further suppress NE or Epi compared to nifedipine alone, but high-dose MgSO4 suppressed ACh release by approximately 25% and further suppressed NE release by approximately 60% and Epi release by approximately 50% compared to nifedipine alone. In conclusion, intravenous administration of Mg(2+) inhibits both presynaptic ACh release and postsynaptic catecholamine release in the adrenal medulla, but L-type Ca(2+) channel-controlled catecholamine release may be more sensitive to Mg(2+) than non-L-type Ca(2+) channel-controlled ACh release.

Role of Ca 2+-activated K + channels in catecholamine release from in vivo rat adrenal medulla

To elucidate the role of Ca 2+-activated K + (K Ca) channels in the presynaptic acetylcholine (ACh) release from splanchnic nerve endings and the postsynaptic catecholamine release from chromaffin cells, we applied microdialysis technique to the left adrenal medulla of anesthetized rats and investigated the effects of local administration of K Ca channel antagonists through dialysis probes on the release of ACh and/or catecholamine, induced by electrical stimulation of splanchnic nerves or local administration of ACh through the dialysis probes. Nerve stimulation-induced release: in the presence of a cholinesterase inhibitor, neostigmine, large-conductance K Ca (BK) channel antagonists, iberiotoxin and paxilline enhanced the presynaptic ACh release and postsynaptic norepinephrine (NE) and epinephrine (Epi) release. Small-conductance K Ca (SK) channel antagonists, apamin and scyllatoxin enhanced the Epi release without any changes in ACh or NE release. In the absence of neostigmine, ACh release was not detected. Iberiotoxin and paxilline enhanced NE and Epi release. Apamin and scyllatoxin had no effect on NE or Epi release. Exogenous ACh-induced release: iberiotoxin and paxilline enhanced the Epi release, but had no effect on the NE release. Apamin and scyllatoxin enhanced both NE and Epi release. In conclusion, BK channels on splanchnic nerve endings play an inhibitory role in the physiological catecholamine release from adrenal medulla by limiting presynaptic ACh release while SK channels do not. BK channels on Epi-storing cells may play an inhibitory role in nerve stimulation-induced Epi release. SK channels on NE- and Epi-storing cells play a minor role in nerve stimulation-induced catecholamine release.

A physiological view of the central and peripheral mechanisms that regulate the release of catecholamines at the adrenal medulla

Here we review the tight neural control of the differential secretion into the circulation, of the adrenal medullary hormones adrenaline and noradrenaline. One or the other catecholamines are differentially released on various stress conditions. This is specifically controlled by central nervous system nuclei at the cortex, hypothalamus and spinal cord. Different firing patterns of splanchnic nerves and nicotinic or muscarinic receptors cause the selective release of noradrenaline or adrenaline, to adapt the body to the 'fight or flight' reaction, or during severe hypoglycaemia, haemorrhage, cold, acute myocardial infarction or other severe stressful conflicts. Endogenously acetylcholine (ACh) released at the splanchnic nerve-chromaffin cell synapse, acting on muscarinic and nicotinic receptors, causes membrane depolarization and action potentials (AP) in chromaffin cells. These changes vary with the animal species, the cell preparation (intact bisected adrenal, adrenal slices, or isolated fresh or cultured cells) or the recording technique (intracellular microelectrodes, patch-clamp, perforated-patch, cell-attached). Conflicting results leave many open questions concerning the actions of ACh on chromaffin cell excitability. The use of adrenal slices and field electrical stimulation will surely provide new insights into these mechanisms. Chromaffin cells have been thoroughly used as models to study the relationship between Ca2+ entry, cytosolic Ca2+ signals, exocytosis and endocytosis, using patch-clamp and amperometric techniques. Cells have been stimulated with single depolarizing pulses (DPs), DP trains and with simulated AP waveforms. These approaches have provided useful information but we have no data on APs generated by pulsatile secretory quanta of ACh, trying to mimic the intermittent and repetitive splanchnic nerve discharge of the neurotransmitter. We present some recent experiments using ultrashort ACh pulses (25 ms), that cause non-desensitizing repetitive APs with each ACh pulse, at low ACh concentrations (30 microM). Ultrashort pulses of a high ACh concentration (1000 microM) causes a single AP followed by a prolonged depolarization. It could be interesting trying to correlate these 'patterns of splanchnic nerve discharge' with Ca2+ signals and exocytosis. This, together with the use of adrenal slices and transmural electrical stimulation of splanchnic nerves will provide new physiologically sound data on the regulation of adrenal medullary secretion.

Biophysical and histological determinants underlying natural firing behaviors of splanchnic sympathetic preganglionic neurons in neonatal rats

Isolated thoracic spinal cords of neonatal rats spontaneously generate splanchnic sympathetic nerve discharge (SND) with a quasiperiodic rhythm ∼1-Hz. Using in vitro nerve-cord preparations that retained T6–T12 spinal segments, we investigated whether the natural firing behavior of sympathetic preganglionic neurons (SPNs) encoded the SND rhythm and what were the main biophysical and histological determinants of SPN firing. Under extracellular recording conditions, electrical stimulation of splanchnic nerves elicited antidromic responses in 212 SPNs. Among them, 92 SPNs were quiescent; 120 active SPNs had an average firing rate of 0.72±0.04 Hz, which was close to the quasiperiodic rhythm of SND. SPNs with rhythmic burst firing were rare. Probability plots of interspike intervals were constructed to extract mathematical features underlying SPN firing. Most active SPNs (88%) had a firing well described by unimodal Gaussian, suggesting a predominantly tonic pattern with normal variations. Biophysical properties of 112 SPNs were measured under whole-cell recording conditions. The charging time constant, τ, is positively correlated with the average firing rate. Histological properties were examined in 45 SPNs with intracellular diffusion of Lucifer Yellow or biocytin. SPNs with pyramidal somata and multipolar dendrites tend to be spontaneously active. In contrast, those with bipolar somata and fewer dendritic branches were quiescent in firing. These observations suggest that activity levels of SPNs are correlated with their capacity for temporal and spatial summation of synaptic inputs. How the seemingly tonic firing of individual SPNs is integrated into whole-nerve SND with quasiperiodic rhythms is discussed.

Activation of adrenal medullary L-arginine: nitric oxide pathway by stimuli which induce the release of catecholamines

The activation of the L-arginine: nitric oxide (NO) pathway in the cat adrenal medulla by different stimuli which induce the release of catecholamines was studied. Stimuli that evoke catecholamine release, such as electrical stimulation of splanchnic nerves (50 V, 5 Hz, 1 ms), methacholine (100 μM), dimethyl-4-phenylpiperazinium iodide (DMPP; 10 μM), high K + (35 mM) and alamethicin (15 μg ml −1) also caused a rise in cyclic GMP in the perfused cat adrenal medulla. N G-nitro-L-arginine methyl ester (L-NAME; 1 mM) abolished the rise in cyclic GMP induced by these stimuli without affecting the catecholamine release. Bovine adrenal medulla cytosol contained an NO synthase which was L-arginine- and Ca 2+-dependent. In conclusion cat and bovine adrenal medulla stimulated with a variety of secretagogues synthesize NO from L-arginine to activate the soluble guanylate cyclase. The present data do not rule out a role for cyclic GMP in the regulation of catecholamine secretion; however, it seems more plausible that cyclic GMP may play a role in controlling local blood flow and thus the access of the released catecholamines to the systemic circulation during stressful conflicts.