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At least 433 records · Page 24Linked to original sources
PubMed1986

Stress-induced elevation of testosterone concentration in high ranking baboons: role of catecholamines.

In an ongoing study of wild olive baboons living in a protected reserve in Kenya, the response of the testicular axis to the acute stress of rapid capture and immobilization was studied. The stress suppressed LH and testosterone (T) concentrations; previous work showed this to be due to stress-induced release of opiates and glucocorticoids, acting to inhibit LH release and testicular sensitivity to LH, respectively. There was considerable individual variation in this phenomenon, which was related to the social status of individual males. High ranking males (by reproductive criteria) were less vulnerable to the suppressive effects of stress on T concentrations and, in fact, showed transient increases in T concentrations during the first poststress hour. T concentrations in subordinates, in contrast, declined promptly and continuously. This difference in T profiles occurred despite similar suppressions of LH concentrations in both groups, suggesting a peripheral mechanism for the transient elevation of T concentrations in high ranking males. Part of this distinctive pattern had been shown to be due to the lesser sensitivity of the testes of high ranking males to the suppressive effects of glucocorticoids. The present report suggests an additional mechanism accounting for this rank-related difference. Administration of chlorisondamine, a sympathetic ganglionic blocker which attenuates stress-induced release of epinephrine and norepinephrine, failed to alter any aspect of LH or T profiles in low ranking males or LH profiles in high ranking males. However, it completely eliminated the transient rise in T concentrations in these males. This suggests that sympathetic catecholamines, released during stress and acting peripherally, directly, or permissively lead to increased T concentrations. This could be via increased blood flow through the testes and/or through direct stimulation of T release by catecholamines. The limitation of this sympathetic regulation of the testes to high ranking males suggests either enhanced sympathetic tone during stress in these animals (relative to subordinates) or enhanced target tissue sensitivity to catecholamines.

Animals↗
PubMed1989

Central nervous system-mediated glucagon secretion is enhanced by alpha 2-adrenoreceptor activation.

We assessed the response of the adrenergic receptor in pancreatic glucagon secretion to central nervous system stimulation. Injection of neostigmine (5 x 10(-8) mol) into the third cerebral ventricle in intact rats resulted in increased epinephrine and norepinephrine secretion associated with glucagon secretion. This glucagon secretion was still observed in bilateral adrenalectomized (ADX) rats, although its concentration was significantly lower than that in the intact rats. This glucagon rise was significantly inhibited by ip treatment of ganglionic blocker with hexamethonium. Intraperitoneal injection of alpha-adrenergic receptor antagonist phentolamine (5 x 10(-7) mol), but not of beta-adrenergic receptor antagonist propranolol (1 x 10(-6) mol), reduced the hyperglucagonemic effect of a subsequent neostigmine injection in intact and ADX rats, although these antagonists did not influence epinephrine or norepinephrine secretion in intact rats. In addition, ip injection of the selective alpha 2-receptor antagonist yohimbine (5 x 10(-7) mol), but not of the selective alpha 1-receptor antagonist prazosin (1 x 10(-6) mol), inhibited the neostigmine-induced glucagon secretion in intact and ADX rats. From this evidence it is suggested that central nervous system-mediated glucagon release is enhanced by alpha 2-adrenoreceptor stimulation by either catecholamines or the autonomic nervous system.

Adrenalectomy↗
PubMed2005

Methylisogermabullone isolated from radish roots stimulates small bowel motility via activation of acetylcholinergic receptors.

We have previously reported that extract of radish roots exhibits an increase in gastrointestinal motility through the activation of muscarinic acetylcholine (ACh) receptors. Based on the stimulatory activity-guided fractionation on rat ileal segments, this study isolated methylisogermabullone (MIGB, C23H31O5NS, MW 433) from methanol extracts of radish roots. MIGB caused a significant increase of the isolated rat ileal contraction in a concentration-dependent manner (23-693 microM), and the pattern of MIGB-induced ileal contraction was different in the time course to that produced by ACh. The EC50 value of MIGB, to produce 50% maximum ileal contraction, was estimated to be 45.5 microM. MIGB (230 microM)-induced ileal contractions were enhanced by pretreatment of segments with ACh (0.1 microM). Ileal contractions produced by MIGB (230 microM) or ACh (0.1 microM) at submaximal concentration were partially inhibited by pretreatment of hexamethonium (0.1 mM), a ganglionic blocker, whereas they were almost completely abolished by atropine (10 microM). Oral administration of MIGB to mice stimulated the small intestinal transit of charcoal in a dose-dependent manner (10-100 mg kg(-1)), and MIGB (100 mg kg(-1))-induced stimulation of small intestinal transit was significantly attenuated by co-administration of atropine (50 mg kg(-1)). Taken together, these results demonstrate that MIGB isolated from radish roots stimulates the small bowel motility through the activation of ACh receptors. These findings suggest that MIGB may become a potential regulatory agent for therapeutic intervention in dysfunction of gastrointestinal motility.

Alkenes↗
PubMed1979

Influence of arterial blood pressure upon central hemorrhagic necrosis after severe spinal cord injury.

To determine the influence of systemic arterial blood pressure upon the pathogenesis of spinal cord injury, we eliminated the increase in systemic blood pressure normally observed after trauma to the spinal cord with the ganglionic blocker chlorisondamine. Blockade of the pressure response did not influence the development of hemorrhagic necrosis in the spinal cord. We conclude that the transient pressure response accompanying spinal cord injury is probably not a major factor in the pathogenesis of hemorrhagic necrosis at the site of the spinal cord injury.

Animals↗
PubMed1994

Sympathetic mediation of peripheral vasodilation induced by spinal cord stimulation: animal studies of the role of cholinergic and adrenergic receptor subtypes.

Electric spinal cord stimulation (SCS) is widely used as a treatment modality for ischemic pain in peripheral arterial insufficiency. The background for the therapeutic effect may be a temporary inhibition of sympathetically maintained peripheral vasoconstriction. In this series of experiments, the involvement of different types of cholinergic and adrenergic receptor subclasses in the vasodilatory effect was explored in anesthetized rats. The microcirculation in hindlimb skin and hamstring muscle was studied by the laser Doppler technique. The ganglionic blocker hexamethonium as well as the nicotinic receptor antagonist chlorisondamine abolished the effect in both vascular beds, whereas the muscarinic receptor antagonists pirenzepine and atropine were ineffective. Among the adrenergic receptor active compounds, phentolamine, prazosine (an alpha 1-receptor antagonist), and clonidine in high doses suppressed the SCS-induced vasodilation. Yohimbine (an alpha 2-receptor antagonist) did not alter the effect. The beta-adrenergic compounds had a differential effect on muscle and skin perfusion. Atenolol, a beta 1-receptor antagonist, inhibited SCS-induced vasodilation only in the skin, whereas the beta 2-receptor antagonist butoxamine selectively depressed the muscle response. The vasodilatory effect of SCS in the animal model used here seems to a large extent to be mediated by an inhibitory effect on peripheral vasoconstriction maintained via efferent sympathetic activity involving nicotinic transmission in the ganglia and the postganglionic alpha 1-adrenoreceptors. The involvement of beta-receptors seems to be different in skin and muscle, beta 1 being more important for the changes in the skin and beta 2 being more important for those in muscle. The high-intensity antidromic response, earlier believed to explain how SCS exerted its vasodilatory effect, was resistant to cholinergic and adrenergic manipulations and seems to depend on entirely different mechanisms.

Animals↗
PubMed2003

Effects of microinjected carbachol on the antinociceptive response to noxious heat stimuli.

Injecting muscarinic receptor agonists into a specific area of the brainstem produces an antinociceptive response. The present study investigates whether direct injections of the cholinergic agonist, carbachol, into the rat nucleus reticularis gigantocellularis (NRGC)/nucleus reticularis gigantocellularis alpha (NRGCalpha) of the rostral ventrolateral medulla evokes antinociception, and then examines the interference action of cholinergic antagonists in rats. Microinjections of carbachol (0.75, 1.5, 3 micro g/site) prolonged hot plate (HP) and tail flick (TF) responses to noxious heat stimuli in a dose-dependent manner. The level of carbachol-induced antinociception during the HP and TF tests reached a maximum at 5-15 min after carbachol administration in all groups. Thereafter, the peak level progressively decreased and reached the baseline by the end of the experiment. Antinociception induced by carbachol at 3 micro g/site was attenuated by the prior administration of the muscarinic receptor antagonist, atropine (200, 500 ng/site). On the other hand, the nicotinic autonomic ganglion blocker, mecamylamine (1, 3 micro g/site), did not affect subsequent carbachol-induced antinociception. These results suggest that the antinociceptive effects induced by a microinjection of carbachol depend on muscarinic, but not nicotinic, mechanisms within the rat NRGC/NRGCalpha.

Analgesics↗
PubMed1977

Descending release of acetylcholine from the locally distended guinea pig ileum.

The effects of local distension of the intestinal wall on the release of acetylcholine (ACh) from the adjacent non-distended part were studied with the segment os isolated guinea pig ileum. Local distension of the intestinal wall induced the increased release of ACh in the distended part and in its anal side but not in its oral side. Such aboral release of ACh by local distension was abolished by tetrodotoxin or atropine in the concentrations which did not block the release in the distended part. When hexamethonium was applied exclusively to the distending part, significant increase of ACh release was observed in both the regions oral to and anal to the distended part. It is suggested that distension stimuli applied to the myenteric plexus are transmitted aborally along the network of the Auerbach's plexus to the anal direction. The release of ACh from the intestine by nicotine or DMPP differed from the occurring during local distension in that the release was localized to the part of the intestine to which the drug was applied.

Acetylcholine↗
PubMed1981

Carotid vascular pain--a simple treatment.

Carotid vascular pain has been misdiagnosed in the past as various other conditions. Various etiologies have been assigned to it without clinical or experimental evidence. Haphazard treatment using ganglion-blockers, nicotinic acid, allergy hyposensitization and steroids have been instituted based on imaginary causes of the problem. This paper intends to show that there is no known cause for carotid pain. A simple, effective, safe and inexpensive form of treatment is presented; namely, explaining the problem to the patient, allaying their apprehension and using aspirin in a more scientific fashion. A three-year follow-up is presented.

Adolescent↗
PubMed1984

Changes in tissue sensitivity to drugs in relation with alteration in receptors by treatment of drugs.

Tissues responses for drugs are often altered by chronic administration of drugs and this alteration is one kind of functional abnormality of the tissues. One mechanism under this functional abnormalities is considered to be in changes in receptors for drugs. In this study, we examined amounts and properties of receptors in sub- and supersensitive states caused by pre-exposure of tissues to drugs and the results obtained were summarized as follows. Long term exposure of tissue to agonists or to conditions which elevate concentration of agonist around the receptor caused reduction in amount of receptor without change in its property. Short term exposure to agonists altered the configuration of the receptor accompanying reduction in sensitivity of the tissue to drugs. But amount of receptor in the tissue was not changed. Heterologous desensitization was observed in some cases by exposure to drugs and no significant change was observed in the receptor of the tissue, qualitatively and quantitatively, indicating dysfunction in the process(es) after activation of the receptor. Denervation and chronic treatments with antagonist and ganglion blocker caused supersensitive state accompanying increase in amount of receptor. But in some cases, qualitative change of receptor, increase in affinity of receptor for agonist, seemed to relate with supersensitive state of tissues.

Acetylcholine↗
PubMed1985

Lasting consistency of cold adaptability in rats reared in cold for many generations.

Wistar rats were successively reared in cold at 5 degrees C from 1969 to 1984. The historical changes observed in these rats were reported. The cold-adapted rats reared in cold for 8 to 11 successive generations (C8-11G) were examined on their cold tolerance and non-shivering thermogenesis. C8-11G rats showed greater nonshivering thermogenesis than that of the warm-adapted control group (W), and rats exposed to cold for periods of 2 to 8 weeks (C). The nonshivering thermogenesis of C8-11G rats was diminished to a similar level to that of W and C rats by administration of a ganglion blocker, of reserpine, or of beta-adrenoceptor blocker. The de-adapted rats reared in warm at 25 degrees C for 3 generations after being reared for many generations in cold (DA-3G) showed much more nonshivering thermogenesis as compared to W rats. Cold tolerance of DA-3G rats was at a level of intermediate between that of W and C rats. Brown adipose tissue (BAT) weight of DA-3G rats was similar to that of C rats, while chemical composition of BAT in DA-3G rats differed from that of C and W rats.

Adaptation, Physiological↗
PubMed1993

Regional vasoconstriction and excessive grooming induced by L-arginine injection into the cisterna magna of conscious rats.

Hemodynamic and behavioral changes caused by intracisternally injected L-arginine which has a pressor effect were studied in conscious rats. One week or more after inserting a cannula into the cisterna magna, electromagnetic flow probes were implanted around the superior mesenteric artery, renal artery, or terminal aorta under anesthesia. A catheter for measurement of blood pressure was inserted into the terminal aorta via a femoral artery or into the common carotid. After recovery from surgery, blood flow, arterial blood pressure, heart rate, and behaviors were observed in the conscious state. Peripheral resistance, calculated as pressure divided by flow, increased an average of 80% in the superior mesenteric artery and 60% in the renal artery when the pressure was increased by 25% following intracisternal injection of 5 mumol of L-arginine. Hindquarter (terminal aortic) resistance showed an insignificant decrease of about 10%. The average heart rate showed no significant change. Grooming, moving, and eating all increased significantly after injection of L-arginine. Circulatory events and behaviors did not always synchronize after the injection. Intravenous chlorisondamine chloride, a ganglion blocker, significantly attenuated the pressor effect caused by intracisternal injection of L-arginine. These findings indicate that centrally injected L-arginine not only specifically triggers vasoconstriction in the viscera presumably through excitation of the regional sympathetic vasoconstrictor fibers to raise blood pressure but also centrally induces excessive grooming. However, the relationship between circulation and behavior caused by intracisternal injection of L-arginine remains unknown.

Animals↗
PubMed1996

Tracheal, circulatory, and respiratory responses to femoral nerve stimulation.

Tracheal, circulatory, and respiratory responses to electrical stimulation of the afferent nerve from the hindlimb were analyzed in decerebrate, paralyzed, and mechanically ventilated dogs. Tension of the tracheal smooth muscle (TSM), arterial blood pressure, and phrenic nerve activity (PNA) were measured during stimulation of the proximal end of the transected femoral nerve (FNS) with train pulses (duration; 0.5 ms, frequency; 40 Hz). With low intensity (e.g., 0.62 V) FNS, TSM exhibited relaxation, arterial pressure decreased, and neural respiratory output (NRO) was reduced (3 of 8 dogs) or unchanged (5 of 8 dogs). With increases in stimulus intensity, TSM always exhibited relaxation while arterial pressure and NRO exhibited excitatory responses almost at the same thresholds (approximately 5 V). The TSM relaxation and the excitatory NRO and arterial responses augmented with increases in stimulus intensity up to 16 times of threshold of the excitatory NRO response. TSM response was blocked by intravenous atropine but pressor response and phrenic response were not. The arterial response disappeared after administration of a ganglionic blocker. These findings suggest that TSM, arterial pressure, and PNA may be controlled by one neuronal mechanism during high intensity FNS, but that arterial pressure and PNA may be modified by another mechanism in an inhibitory direction when the stimulus intensity is low. This study suggested the existence of a neural mechanism which controls the airway and cardiorespiratory systems properly to execute exercise. Physiological significance of the responses to low intensity femoral nerve stimulation was uncertain.

Animals↗
PubMed2003

Central administration of ghrelin stimulates pancreatic exocrine secretion via the vagus in conscious rats.

Ghrelin, a novel growth-hormone releasing peptide, was originally isolated from rat and human stomach. Immunohistochemical analyses revealed that ghrelin-immunoreactive neurons were localized in the hypothalamic arcuate nucleus. The function of the digestive organs is controlled from the central nervous system, and the vagus nerve plays an important role. Intracerebroventricular and intravenous administration of ghrelin significantly increased gastric acid secretion, and its effect was abolished by vagotomy. In the present study, the effect of centrally injected ghrelin on pancreatic exocrine secretion was examined in conscious rats. Moreover, an electrophysiologic study was conducted in anesthetized rats to examine whether the excitation of vagal efferent nerve could be induced by ghrelin. To determine the pancreatic exocrine secretion, rats were prepared with cannulae draining bile and pancreatic juice separately. The experiments were conducted in conscious rats on day 4 or 5 after the operation. To exclude the involvement of gastric acid, a proton pump inhibitor omeprazole (5 micromol/kg) was administered into the duodenum 1 h before ghrelin injection. An intracerebroventricular administration of ghrelin (12, 60, and 300 pmol/10 microl) significantly increased pancreatic fluid and protein output in a dose-dependent manner. Pretreatment with the ganglion blocker hexamethonium and with atropine completely abolished the stimulatory effect of central ghrelin. In contrast, an intravenous injection of ghrelin (300 pmol/10 microl) had no effect. Centrally administered ghrelin stimulated the vagal efferent nerve in anesthetized rats. In conclusion, centrally administered ghrelin stimulates pancreatic exocrine secretion through the vagal efferent nerve, and the stimulatory action is independent of gastric acid secretion.

Animals↗
PubMed1991

Continuous alprenolol infusion for control of hypertension in the acute stage of ruptured intracranial aneurysms.

The clinical benefits and hemodynamic effects of continuous alprenolol infusion for control of hypertension in the acute stage of ruptured cerebral aneurysms were investigated. Twenty-five patients manifesting systemic hypertension (greater than 160/100 mmHg) were treated with alprenolol, a beta-adrenergic antagonist, phentolamine, an alpha-adrenergic antagonist, and trimethaphan camsilate, a ganglionic blocker, given intravenously. All drugs decreased the mean arterial blood pressure significantly. However, alprenolol decreased the heart rate and cardiac index while phentolamine increased them. Alprenolol also decreased arterial catecholamine and renin activity, but caused no change in central venous pressure, pulmonary capillary wedge pressure, pulmonary vascular resistance, and systemic vascular resistance. The results indicate the usefulness of continuous alprenolol infusion for the control of acute hypertension in hemorrhagic cerebrovascular disease. The mode of action of alprenolol is also discussed.

Adult↗