Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ganglionic Blockers”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 487 records · Page 27Linked to original sources
PubMed1986

Changes in the reactivity of the intrinsic nervous system of the stomach to hexamethonium after transthoracic vagotomy.

Experiments were carried out on seven breedless dogs with chronically implanted electrodes in the stomach. The effect of hexamethonium (in doses of 0.2, 0.3, 0.5, 1, 2, 3, 5, 7 and 10 mg/kg, i. v.) on the migrating myoelectrical complex (MMC) was studied before and after transthoracic vagotomy. Injected on the background of the first MMC phase, hexamethonium in doses of up to 2 mg/kg induces the appearance of spike potentials (SP). Applied on the background of spike activity, hexamethonium induces the appearance of spike activity of the type of the 3rd MMC phase. In a dose exceeding 2 mg/kg, introduced during SP activity, hexamethonium interrupts for different periods of time the SP generation and shortens the duration of the active MMC phases. On the background of increased spike activity characteristic of the stomach after vagotomy, 3 mg/kg hexamethonium have almost no effect on the electrical activity, whereas 10 mg/kg only reduce the percentage of slow waves accompanied by SP. It is probably that after vagotomy the excitability of the intrinsic nerve cells is increased, therefore even the high doses of the ganglionic blocker hexamethonium cannot inhibit entirely the active phases of MMC.

Animals↗
PubMedDate not supplied

Interaction of adrenergic and opioid systems in the short-term regulation of cardiovascular activities.

Endogenous opioid peptides such as methionine enkephalin (met-enkephalin) are known to have a profound cardiovascular action in addition to actions mimicking morphine in many animal models. In the anesthetized rabbit, met-enkephalin, as little as 1 microgram/kg, decreased blood pressure and heart rate upon its intravenous injection. Little is known about the locus of action or the mechanism and the physiological implication of the peptide action. The primary objective of this study was to test influences of adrenergic and cholinergic agents on the cardiovascular effects of the peptide. Pentobarbital (30 mg/kg) anesthetized rabbits were tracheotomized and a femoral artery and vein were cannulated for the measurement of arterial blood pressure and drug injection. Through a left lateral abdominal incision, the left renal nerve was isolated and renal nerve activity (RNA) recorded. Met-enkephalin (1 to 300 micrograms/kg, i.v.) decreased RNA initially and reduced blood pressure and heart rate. The cardiodepressant action of the peptide was antagonized by naloxone (1 mg/kg), but not by naloxone methobromide (1.3 mg/kg). Both phentolamine (4 mg/kg) and prazosin (1 mg/kg) antagonized the cardiovascular effect of met-enkephalin. Both hexamethonium (5 mg/kg) and mecamylamine (2 mg/kg) completely masked most of the depressant cardiovascular effects of metenkephalin by an increase in the duration of RNA suppression. The inability of naloxone methobromide and ganglionic blockers to antagonize the hypotensive action of met-enkephalin suggests that the peptide effect is secondary to its action on the central adrenergic system.

Animals↗
PubMed1986

Ethanol-induced adrenomedullary catecholamine secretion in LS/Ibg and SS/Ibg mice.

Ethanol, administered i.p., produced a dose-dependent increase in plasma norepinephrine and epinephrine concentrations in LS/Ibg (LS) but not in SS/Ibg (SS) lines of mice. Ethanol-induced elevations of plasma epinephrine in LS mice were approximately 10-fold greater than those observed in SS mice. Plasma epinephrine and norepinephrine attained peak concentrations at 20-min post-ethanol administration at doses ranging from 2.8 to 4.1 g/kg. Plasma catecholamines remained elevated for approximately 1 hr and returned to basal values 2 hr after ethanol administration. Significant correlations were obtained between blood ethanol (r = 0.99), plasma epinephrine (r = 0.92) and plasma glucose (r = 0.98) as a function of ethanol dose in LS mice. Chlorisondamine (3 mg/kg), a ganglionic blocker, abolished completely the ethanol-induced increase in plasma catecholamines. These results confirm previous suggestions that the response is centrally mediated through an increased sympathetic outflow rather than by a direct effect on the adrenal medulla. The increase in plasma epinephrine and associated hyperglycemia produced by ethanol was not observed with pentobarbital or halothane anesthesia. Ethanol-induced hypothermia was diminished markedly (47%) by an elevated ambient temperature (28 degrees C) without reducing the hyperglycemic response to ethanol. These results suggest that ethanol-induced hypothermia does not mediate ethanol-induced adrenomedullary catecholamine secretion and concomitant hyperglycemia. It is proposed that the differential ethanol-induced secretion of adrenomedullary catecholamines in LS and SS mice is due to differential central nervous system sensitivities to ethanol.

Adrenal Medulla↗
PubMed1980

Inhibition and facilitation in parasympathetic ganglia of the urinary bladder.

Neurons in vesical parasympathetic ganglia receive excitatory and inhibitory inputs from both divisions of the autonomic nervous system. Sacral parasympathetic pathways (cholinergic) provide the major excitatory input to these ganglia via activation of nicotinic receptors. Parasympathetic pathways also activate muscarinic inhibitory and excitatory receptors, which may exert a modulatory influence on transmission. Cholinergic transmission is relatively inefficient when preganglionic nerves are stimulated at low frequencies (< 1 Hz). However, excitatory postsynaptic potentials (EPSPs) and postganglionic firing markedly increase during repetitive stimulation at frequencies of 1-10 Hz. It is concluded that enhanced transmitter release accounts for the temporal facilitation and that vesical ganglia function as "high pass filters" that amplify the parasympathetic excitatory input to the detrusor muscle during micturition. Transmission in vesical ganglia is also sensitive to adrenergic inhibitory and facilitatory synaptic mechanisms elicited by efferent pathways in the hypogastric nerves. The effects of exogenous norepinephrine indicate that adrenergic inhibition is mediated by alpha receptors and reflects primarily a presynaptic depression of transmitter release although postsynaptic adrenergic hyperpolarizing and depolarizing effects have also been noted. Adrenergic facilitation is mediated by beta receptors as well as unidentified receptors. Norepinephrine also can inhibit or excite spontaneously active neurons in vesical ganglia. The existence of inhibitory and facilitatory synaptic mechanisms in vesical ganglia provides the basis for a complex ganglionic modulation of the central autonomic outflow to the bladder.

Animals↗
PubMed1981

Nicotine action on rat colon.

A new system for the study of the autonomic actions of nicotine in the rat has been developed. It is the oxotremorine-contracted longitudinal muscle of the rat terminal colon, which relaxes transiently in the presence of nicotine. This effect is mediated by nicotinic cholinergic receptors on neuronal structures since it was blocked by hexamethonium and tetrodotoxin. Other nicotinic agonists also caused the muscle strip to relax. Some of these agents 1) provided a greater maximal effect that nicotine, 2) did not show complete cross-desensitization with nicotine and 3) had tetrodotoxin-insensitive components to their action. These agents therefore do not operate solely through the same receptor nicotine does. Nicotine appears to cause relaxation by releasing a nonadrenergic inhibitory substance since 1) alpha and beta adrenergic antagonists are ineffective against nicotine and 2) nicotine retains activity on preparations from reserpinized animals. Nicotine does not cause relaxation by releasing adenosine or ATP since preparations maximally relaxed by adenosine or ATP relax further with nicotine.

Animals↗
PubMed1981

Non-adrenergic inhibitory and non-cholinergic excitatory neural involvement in DMPP and nicotine action of fowl rectum.

Pharmacological analysis of the mechanical responses of fowl rectum to DMPP and nicotine showed that nicotinic stimulation produced varied responses on different segments. On the whole/distal segment DMPP and nicotine induced relaxations. On the proximal segment, DMPP induced relaxation whereas nicotine produced biphasic response. Termination of the adrenergic function converted the relaxatory responses of DMPP and nicotine to biphasic ones, the contractile component of which was potentiated by neostigmine and partially inhibited by atropine. This response was completely abolished by ganglion blockers. On cooled tissue preparations, neither nicotinic nor electrical stimulations elicited any response. These findings implicate the participation of non-adrenergic inhibitory and non-cholinergic excitatory neural elements besides the adrenergic and cholinergic ones to nicotinic stimulation.

Acetylcholine↗
PubMed1978

Trimethaphan camsylate (Arfonad) and human plasma cholinesterase.

These results for the first time document that the brief duration of action of the ganglionic blocker, Arfonad (trimethaphan camsylate), is not due to inactivation by plasma cholinesterase. Inhibition of the enzyme in vitro by Arfonad was not altered by prior incubation of the drug in plasma at 37 degrees C for up to 16 hours nor by treatment with NaOH at 100 degrees C for 10 minutes. Both procedures inactivated succinylcholine. These results in vitro were confirmed in vivo by finding that the toxicity of Arfonad in mice was not significantly altered by these procedures whereas they rendered succinylcholine inocuous. Arfonad is a noncompetitive whereas succinylcholine is a competitive inhibitor of plasma cholinesterase using benzoylcholine as the substrate. The camphorsulfonate moiety of Arfonad was inactive in vitro but caused mild tremors in mice at relatively high doses.

Binding, Competitive↗
PubMed1995

Cardiovascular responses to cigarette smoke exposure in restrained conscious rats.

The effect of exposure to cigarette smoke on cardiovascular function was examined in conscious, restrained Sprague-Dawley rats. Rats were exposed to 3, 6 and 9 puffs of either air or cigarette smoke during the "break in" period and to 10 puffs on the day of the experiment (day 4). HR, cardiac output and mean arterial pressure were recorded continuously throughout the experimental period. Rats exposed previously to cigarette smoke generated from either low-nicotine (0.16 mg/cig.) or high-nicotine (2.45 mg/cig.) cigarettes showed a dose-related decrease in HR in response to restraint stress. In addition, exposure to cigarette smoke produced a further decrease in HR and cardiac output and an increase in mean arterial pressure. This effect by cigarette smoke was dose-dependent (dependent on the cigarette nicotine content) and was antagonized by intra-arterial pretreatment with the nicotinic antagonists mecamylamine and hexamethonium and also with the ganglionic blocker chlorisondamine. Intra-arterial pretreatment with atropine methyl bromide blocked the bradycardia in response to both restraint stress and cigarette smoke. Furthermore, pretreatment with an arginine vasopressin antagonist, d(CH2)5Tyr(Me)arginine vasopressin, significantly attenuated the increase in mean arterial pressure and total peripheral resistance and the decrease in HR and cardiac output due to cigarette smoke. On the other hand, pretreatment with the opioid receptor antagonist naloxone had no effect on cardiovascular parameters in response parameters in response to cigarette smoke. These results implicate arginine vasopressin, in addition to the activation of both sympathetic and parasympathetic systems, in mediating cardiovascular responses to cigarette smoke.

Animals↗
PubMed1994

[Effect and its mechanism of substance P on contractile activity of isolated antral muscle strips of rat].

The present study was aimed at investigating the effect of substance P (SP) on the contractile activity of isolated antral muscle strips of rat and its underlying mechanism. Isolated strips were incubated in an organ bath into which SP was added with or without pretreatment of some antagonists or inhibitors. The results were as follows: (1) SP increased the contractile amplitude of the strips in a dose-dependent manner from 8 x 10(-11) to 8 x 10(-7) mol. At 4 x 10(-8) mol the amplitude was increased by 160.9 +/- 23.0%, while the automaticity of the strips was not affected. (2) This effect of SP could be partially inhibited by hexamethonium (ganglionic blocker), cyproheptadine (blocker of 5-HT2 receptor), diphenhydramine (blocker of H1 receptor), or aminophylline (inhibitor of phosphodiesterase), but not by atropine, propranolol, phentolamine, haloperidol, or naloxone. These results suggested that SP might be a non-cholinergic excitatory transmitter. Its spasmogenic action might be mediated by activating 5-HT neurons, which elicited release of histamine or directly acted on muscle cells.

Animals↗
PubMed1977

Cardiovascular reactivity and neurogenic tone in hypertension derived from renal artery stenosis and contralateral nephrectomy in the rat.

In the current study a) cardiovascular reactivity (CR) to norepinephrine (NE) and b) the effect of a ganglionic blocker (pentolinium, P) during the early (2nd week) and a later period (10th week) of hypertension elicited by unilateral renal ischemia and contralateral nephrectomy in the rat have been described. Neither the threshold doses nor the dose-pressor response curves have shown a greater reactivity of the cardiovascular system to NE in this type of hypertension. An increase in the activity of the nervous system apparently contributes to hypertension in the early period but would disappear when the one-kidney renovascular hypertension is chronically established; in both phases some other still undefined factor/s are present for fuller development of high arterial pressure.

Animals↗
PubMed1993

Effects of L-NG-nitro arginine on cholinergic transmission in the gastric muscle of the rabbit.

In the circular muscle of the rabbit gastric corpus, the nitric oxide-synthesis inhibitor L-NG-nitro arginine (L-NOARG), enhanced the neurally-induced cholinergic responses evoked by electrical field stimulation (EFS) and ganglionic stimulating agents (nicotine, dimethylphenyl piperazinium iodide). The muscular contractions caused by acetylcholine (Ach) and methacholine were not influenced by the nitric oxide-synthesis inhibitor. The nitric oxide-releasing compound sodium nitroprusside (SNP) did not affect the Ach-induced muscular responses. Our results suggest that L-NOARG enhances gastric cholinergic responses by removing an inhibitory influence exerted at the prejunctional level in the nerve-muscle pathway.

Acetylcholine↗
PubMed1993

Effects of neuropeptide Y, peptide YY and sigma ligands on ion transport in mouse jejunum.

The effects of putative sigma ligands and two neuropeptides on intestinal ion transport were evaluated in isolated sheets of whole mouse jejunum mounted in Ussing flux chambers. Serosal administration of neuropeptide Y (NPY), peptide YY (PYY), (+)-N-cyclopropylmethyl-N-methyl-1,4- diphenyl-1-ethyl-but-3-en-1-ylamine hydrochloride (JO 1784), di(ortho-tolyl)guanidine (DTG) and (+)- or (-)-N-allyl-normetazocine (NANM) produced concentration-related decreases in short-circuit current (Isc) without changes in tissue conductance. Although NPY and PYY were active in nanomolar concentrations, JO 1784, DTG and (+)- and (-)-NANM were active in micromolar concentrations; the rank order of potency in inhibiting Isc was PYY > NPY >> JO 1784 = (-)-N- cyclopropylmethyl-N-methyl-1,4-diphenyl-1-ethyl-but-3-en-1-ylamine hydrochloride > DTG > (+)-NANM = (-)-NANM. Serosal application of tetrodotoxin effectively blocked the decrease in Isc associated with all of the ligands tested. The activity of the serosally applied ligands was blocked by prior application of chlorisondamine, a ganglionic blocker. The effects of JO 1784 and NPY were evaluated using antagonists of several receptor types. Although application of serosal haloperidol had no effect alone up to concentrations of 1 microM, this compound produced a rightward displacement in both the NPY and JO 1784 concentration-effect curves. In contrast, sulpiride, SCH-23390, naloxone, yohimbine and prazosin failed to antagonize the effects of NPY or JO 1784.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗