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At least 145 records · Page 8Linked to original sources
PubMed1982

Bole of adrenals in morphine-induced hyperthermia in restrained rats.

Bole of adrenals in morphine-induced hyperthermia was studied in normal, neurotransmitter antagonist-pretreated, chemical-sympathectomized, adrenalectomized or adrenal-demedullated rats. In restrained female rats, 5 mg/kg morphine produced hyperthermia whereas 20 mg/kg and 40 mg/kg produced hypothermia. Pretreatment with either phenoxybenzamine, propranolol, pentolinium or scopolamine inhibited the hyperthermia. After adrenalectomy, neither 5 mg/kg nor chronic administration of 20 mg/kg morphine produced previously demonstrated hyperthermia. After adrenal-demedullation, a dose of 5 mg/kg morphine also did not produce hyperthermia. In contrast to female rats, restrained male rats showed no significant effect on body temperature after 5 mg/kg morphine, requiring 20 mg/kg and 40 mg/kg morphine to produce hyperthermia. In adrenalectomized male rats, 20 mg/kg morphine did not produce the usual hyperthermia. The results suggest that male rats are more resistant to the hyperthermic effects of morphine than female rats and that in the rat, the adrenals, likely the medulla, play an important role in morphine-induced hyperthermia.

Adrenal Glands↗
PubMed1982

The effects of parasympathetic blocking agents on bladder electromyograms and function in conscious and anaesthetized cats.

Voiding induced in conscious cats by infusion of sterile saline into the bladder via a chronically implanted bladder catheter was stable over many months. Artefact-free recordings of electrical activity obtained from the bladder neck and dome of these preparations during bladder filling and voiding showed characteristic voiding electromyograms but did not permit a functional differentiation. Both voiding and the associated electromyogram were abolished by the ganglion blocking agent, pentolinium. Hyoscine or methyl atropine did not affect the electromyogram but impaired the ability of cats to empty their bladders completely. In anaesthetized cats, ganglion blocking agents prevented a rise in bladder pressure during sacral ventral root stimulation but a hyoscine-sensitive bladder contraction was seen following the period of stimulation. Further stimulation during this post-stimulus rise in intravesical pressure revealed a hyoscine-sensitive stimulus-bound relaxation. Sacral ventral root stimulation relaxed the bladder neck/proximal urethra particularly in the presence of sympathetic tone.

Anesthesia↗
PubMed1988

The hypothermic response of mice to delta-9-tetrahydrocannabinol is enhanced by chlorpromazine, thioxanthenes, alpha-adrenoceptor antagonists and pentolinium but not by SCH 23390 or sulpiride.

Chlorpromazine, given either subcutaneously (0.375 mg/kg) or unilaterally into the preoptic/anterior hypothalamic area through a chronically implanted cannula (20 micrograms), was found to enhance the hypothermic response to delta-9-tetrahydrocannabinol (THC; 5 mg/kg i.p.) in unrestrained adult male MF1 mice, kept at 22 degrees C. In mg/kg terms, chlorpromazine was no more potent when injected into the preoptic/anterior hypothalamic area than when given subcutaneously. Phentolamine (54 micrograms) had no significant effect on hypothermia induced by THC when injected into the hypothalamus although it did enhance this response when given subcutaneously (15 mg/kg). Hypothermia induced by THC was also enhanced by flupentixol (0.375 mg/kg s.c.), piflutixol (23.4 micrograms/kg s.c.), pentolinium (5 mg/kg s.c.), prazosin (0.1875 mg/kg s.c.) and indoramin (6 mg/kg s.c.) but not by SCH 23390 (6 mg/kg s.c.) or sulpiride (40 mg/kg s.c.). When taken together with the results from a previous study, these data support the hypothesis that chlorpromazine enhances hypothermia induced in mice by THC by antagonizing alpha-adrenoceptors so as to decrease the capacity of the animals to minimise peripheral blood flow by vasoconstriction. The present data also support the hypothesis that flupentixol and piflutixol interacted with THC not by antagonizing dopamine at D1 or D2 receptors but rather by blocking alpha-adrenoceptors.

Adrenergic alpha-Antagonists↗
PubMed1978

Uropharmacology: VII. Ganglionic stimulating and blocking agents.

A classification of the various ganglionic stimulants and blockers is presented, and their pharmacologic effects on the urinary bladder and urethra are discussed. Ganglionic stimulating drugs are of considerable interest in investigational work but are not presently used therapeutically. Ganglionic blockers include hexamethonium, tetraethylammonium, mecamylamine emepronium, pentolinium, chlorisondamine, and pemipidine. Of the numerous ganglionic blocking drugs that have appeared on the therapeutic scene, only mecamylamine, pentolinium, and trimethaphan are currently official.

Animals↗
PubMed1991

Studies of reflexogenic effects of capsaicin and neuropeptides on neural afferents in the dog parietal pericardium.

Stimulation of neural afferents in the parietal pericardium of anaesthetized, open-chest dogs by local application of capsaicin (0.1-100 micrograms) consistently induced dose-related pressor effects and tachycardia, whereas the application (0.1-1 microgram) of neuropeptides substance P (SP), neurokinin A (NKA), neurokinin B (NKB) or calcitonin gene-related peptide (CGRP) had no cardiovascular effect. Capsaicin-induced reflex responses were not affected by vagotomy, but were abolished by bilateral sectioning of the upper thoracic (T1-T4) white rami communicantes and stellectomy. Capsaicin-induced reflex tachycardia could also be abolished by a beta-adrenoceptor blockade with propranolol (0.5 mg/kg, IV), while ganglionic blockade with pentolinium (0.5 mg/kg, IV) eliminated both the tachycardia and pressor effects. Intravenous treatment with the cyclo-oxygenase inhibitors, indomethacin (5 mg/kg) or aspirin (100 mg/kg) had no effect on reflex pressor and heart rate responses to pericardial capsaicin. Also local treatment of the pericardium with either indomethacin (1 microgram/ml) or dual cyclooxygenase/lipoxygenase inhibitor, BW755C (10 micrograms/ml) failed to affect the responses to capsaicin. We conclude that (i) capsaicin-sensitive afferents which are present in the dog pericardium have a spinal origin and can initiate sympathetically-mediated reflex cardiovascular changes; (ii) the reflexogenic action of capsaicin on pericardial afferents does not depend on local production of eicosanoids; (iii) neuropeptides appear to be without reflexogenic effects on neural afferents in the dog parietal pericardium.

Afferent Pathways↗
PubMed1985

Entero-pancreatic reflexes revealed by duodenal anesthesia in the dog.

This study was designed to improve our understanding of duodeno-pancreatic reflexes, the existence of which was suggested by the previous observation of a reduction in secretin-stimulated pancreatic secretion during local anesthesia of the duodenal mucosa. The effects on this reduction in secretin-stimulated secretion of cholinergic or adrenergic blocking agents (alone or in combination) and of truncal vagotomy, were studied in conscious dog with gastric and pancreatic fistulae. For each agent and for secretin alone in normal and vagotomized dogs, a comparison was made of pancreatic secretion with and without lignocaine anesthesia of the duodenal mucosa. Lignocaine reduced pancreatic secretion with secretin alone, and stimulated it during infusion of atropine. The changes in both protein bicarbonate secretion were blocked by pentolinium and by phenoxybenzamine whereas propranolol mainly blocked the effects on bicarbonate output. The effect of truncal vagotomy resembled that of atropine. These results suggest the existence of two enteropancreatic reflex mechanisms; an excitory cholinergic vagal reflex and an inhibitory, atropine-resistant non-vagal reflex. Both are blocked by pentolinium (a ganglion blocker) and by phenoxy-benzamine, suggesting the involvement of alpha-adrenergic receptors probably also at the level of the ganglion cell. Beta-adrenergic receptors are also involved in the regulation of bicarbonate and fluid secretion.

Anesthesia↗
PubMed1988

Cardiovascular consequences of water deprivation in female Long Evans and Brattleboro rats.

Female Long Evans and Brattleboro rats were studied while water-replete and after water deprivation sufficient to cause hypovolaemia of similar degree in the two strains. A comparison was made of the blood chemistry and cardiovascular status in the two conditions, and the ability of the renin-angiotensin system, sympathoadrenal activity and (in Long Evans rats) vasopressin to influence blood pressure were assessed by pharmacological blockade of these systems. Under water-replete conditions there were significant differences between plasma variables in the two strains (Long Evans: vol., 3.67 +/- 0.07 ml/100 g b. wt., sodium, 142 +/- 0.3 mmol/l; osmolality, 290 +/- 1 mosmol/kg; Brattleboro: vol., 3.89 +/- 0.07 ml/100 g b. wt.; sodium 148 +/- 0.4 mmol/l; osmolality 304 +/- 2 mosmol/kg). Inhibition of the renin-angiotensin system (with captopril) had a slightly greater hypotensive effect in Brattleboro than in Long Evans rats. In both strains the hypotensive effects of captopril were enhanced markedly in the presence of pentolinium, and, under those conditions there was a vasopressin-dependent recovery of blood pressure in Long Evans rats that was absent in Brattleboro rats. Water deprivation caused a greater proportional reduction in body weight, and increase in plasma sodium and osmolality in Brattleboro than in Long Evans rats, although resting cardiovascular statuses were not markedly different. Despite Brattleboro rats having substantial hypernatraemia (156 +/- 1.0 mmol/l), that should have acted to inhibit renin release, they showed a profound hypotensive response to captopril that was not apparent in Long Evans rats. Thus, the absence of vasopressin in female Brattleboro rats severely affects cardiovascular adaptation to water deprivation. Comparison of the present results with published data obtained from male Long Evans and Brattleboro rats shows marked sex differences in the response to the same water deprivation protocol, and indicates that data obtained from males and females should not be cumulated.

Animals↗
PubMed1988

Regional haemodynamic effects of neuropeptide Y, vasopressin and angiotensin II in conscious, unrestrained, Long Evans and Brattleboro rats.

The regional haemodynamic responses to equipressor doses of neuropeptide Y (NPY), vasopressin (AVP) and angiotensin II (AII) were assessed in conscious Long Evans and Brattleboro rats, chronically instrumented with miniaturized, pulsed Doppler probes. NPY caused particularly potent renal vasoconstrictions in intact rats of both strains. However, there were differential changes in regional vascular sensitivity of NPY following administration of pentolinium and captopril, indicating that 'buffer' mechanisms were an important determinant of responses to NPY. A marked mesenteric and low renal sensitivity to AVP was seen in both strains in all conditions. AVP was the most potent of the 3 pressor agents, and no evidence was found for it interacting uniquely with buffer mechanisms. The pressor action of AII was offset by a tendency towards hindquarters vasodilatation that was converted to a marked vasoconstriction when pentolinium and captopril were administered. It is feasible that, in the intact rat, AII stimulated adrenal medullary adrenal release which caused beta-adrenoceptor-mediated vasodilatation that acted to offset the direct vasoconstrictor effects of AII.

Angiotensin II↗
PubMed1990

Cardiovascular responses elicited by chemical stimulation of the rostral ventrolateral medulla in conscious, unrestrained rats.

The cardiovascular effects of microinjection of L-glutamic acid into the rostral ventrolateral medulla have been investigated in anaesthetized and in conscious, unrestrained rats. In conscious rats L-glutamic acid (0.36, 1.2 and 2.4 nmol) produced significant increases in blood pressure, generally accompanied by a bradycardia. A lower dose of L-glutamic acid (0.12 nmol) had no effect on blood pressure or heart rate. The cardiovascular responses elicited by L-glutamic acid (2.4 nmol) were completely abolished by intravenous infusion of the ganglion blocker, pentolinium. However, in urethane-anaesthetized rats, the pressor response (+27 +/- 2/+21 +/- 2 mmHg) to microinjection of L-glutamic acid (2.4 nmol) was markedly less than that seen in conscious rats (+64 +/- 6/+47 +/- 3 mmHg) and there was a tachycardia (+21 +/- 2 beats/min) rather than a bradycardia. These results corroborate previous studies, carried out in anaesthetized animals, indicating that stimulation of the rostral ventrolateral medulla provides direct and/or indirect excitatory drive to the preganglionic sympathetic neurons of the spinal cord to increase blood pressure, but demonstrate a marked difference in sensitivity in conscious vs urethane-anaesthetized animals.

Animals↗