PubMed Health⌕ Search

Biomedical subjects

J Ekström

Publications and source records attributed to J Ekström.

At least 55 records · Page 3Linked to original sources
PubMed1996

The role of circulating catecholamines in the depletion of parotid acinar granules in conscious rats in the cold.

The possibility that circulating catecholamines might affect parotid gland function during feeding (over a period of 80 min) and cold stress (2-4 degree C) was investigated in rats that had been fasted for 30 h. In the first set of experiments, in which the glands had been sympathectomized by removing both superior cervical ganglia 10-12 days previously, there was a substantial reduction in the density of acinar secretory granules (42% compared with non-fed animals in the cold) and in the total glandular amylase activity (54%). However, similar, or even greater, losses were recorded in rats subjected to additional bilateral adrenal medullectomy and pretreatment with atropine and alpha- and beta-adrenoceptor blockers. The losses were therefore attributed to activation of parasympathetic non-adrenergic, non-cholinergic mechanisms. In a second set of experiments, employing only morphometric assessment, the parasympathetic auriculotemporal nerve was cut on one side in addition to bilateral sympathectomy and, as a further precaution, the animal was atropinized. It was then found that there was a loss of 17% of granules in the parasympathectomized plus sympathectomized gland, but not the contralateral gland, of non-fed cold-exposed rats compared with non-fed animals kept at room temperature. When rats were fed as well as exposed to cold the number of granules in parasympathectomized plus sympathectomized glands fell by 46% compared with similar non-fed animals in the cold and by 55% compared with those at room temperature. After adrenal medullectomy, cold exposure alone had no effect on the granular density of parasympathectomized plus sympathectomized glands but, when combined with feeding, granular loss amounted to 30%. Pretreatment with a combination of alpha- and beta-adrenoceptor blocking agents abolished this effect. Thus circulating catecholamines liberated not only from the adrenal medulla but also from other sources (extraglandular adrenergic nerve terminals and extra-adrenal chromaffin tissue) are able to induce losses in the number of acinar granules in the parasympathectomized plus sympathectomized glands. However, a high degree of sensitization of the parotid acinar cells may be required to allow the response to become manifest.

Animals↗
PubMed1996

Depletion of vasoactive intestinal peptide and substance P in parotid glands of atropinized rats during reflex secretion.

Rats previously starved for 30 h were offered hard chow over a period of 80 min, and the effect of eating on the parotid gland content of vasoactive intestinal peptide (VIP), substance P and neuropeptide Y (NPY) was examined. In rats pretreated with I.P. atropine and alpha- and beta-adrenoceptor blocking agents, the total amounts of VIP and substance P were reduced after feeding by 23 and 42%, respectively; in contrast the NPY content was not significantly affected. Similarly, in animals given atropine alone the VIP content was reduced by 25% and substance P by 40% after feeding. In the absence of autonomic receptor blockade, there was no loss of parotid neuropeptide content in response to feeding. Neither an intact sympathetic innervation nor a capsaicin-sensitive sensory innervation was a prerequisite for depletion of parotid neuropeptides in the presence of atropine and adrenoceptor blockers. The observed decrease in neuropeptide content is thought to reflect an imbalance between peptide release from nerve terminals and their replenishment by axonal transport, this imbalance resulting from the unusually high demands on the parasympathetic non-adrenergic, non-cholinergic (NANC) mechanism. Under normal conditions salivary peptidergic mechanisms are spared as seen in the absence of autonomic receptor blockade.

Adrenergic Antagonists↗
PubMed1996

Nitric oxide and release of the peptide VIP from parasympathetic terminals in the submandibular gland of the anaesthetized cat.

The role of nitric oxide (NO) in mediating various submandibular responses to stimulation of the parasympathetic innervation has been investigated in anaesthetized cats, in which N omega-nitro-L-arginine methyl ester (L-NAME; 30 mg kg-1 I.A.) was used to block the synthesis of NO. L-NAME significantly reduced the vasodilator response and the flow of saliva, together with the output of salivary protein that occurred during stimulation of the chorda lingual nerve (20 Hz for 1 s at 10 s intervals), without significantly reducing the output of vasoactive intestinal peptide (VIP) from the gland. The results show that NO is implicated not only in the release of VIP, as established previously, but also in mediating its actions following release in the submandibular gland of the cat.

Animals↗
PubMed1996

Non-adrenergic, non-cholinergic influences on parotid acinar degranulation in response to stimulation of the parasympathetic innervation in the anaesthetized rat.

In pentobarbitione-anaesthetized rats the parasympathetic auriculotemporal nerve of the parotid gland was continuously stimulated at supramaximal voltage and at maximal frequency (40 Hz) for salivary secretion. The animals were pretreated with phentolamine and propranolol (2 mg kg-1 i.p. of each) and, in some groups, additionally with atropine (2 mg kg-1 i.p.). Morphometric assessment at the light microscopic level (x 100) showed that the numerical density of parotid acinar secretory granules (per 100 microns2 acinar epithelial cytoplasm) was reduced by 30 and 39% after 40 and 80 min, respectively, of stimulation in non-atropinized animals and by 30 and 27% in atropinized animals. The numerical density of acinar granules was not influenced by pretreatment with the protein synthesis inhibitor cycloheximide. The results suggest that most of the parasympathetic nerve-induced degranulation in the absence of muscarinic receptor blockade can be attributed to the action of non-adrenergic, non-cholinergic mechanisms.

Animals↗
PubMed1995

Presence and effects of pituitary adenylate cyclase activating peptide in the submandibular gland of the ferret.

Pituitary adenylate cyclase activating peptide (PACAP), a recently described vasoactive intestinal peptide-like neuropeptide, was found to be present in neurons in the submandibular gland of the ferret, where PACAP-immunoreactive nerve fibers were distributed around blood vessels, acini and ducts. Most of the PACAP-immunoreactive fibres were distinct from those storing vasoactive intestinal peptide. PACAP occurs in tissues as PACAP1-38 and PACAP1-27. PACAP1-38 and PACAP1-27 but not PACAP16-38 displayed biological activity with about the same potency. They exerted vasodilator effects on the submandibular vasculature, which resulted in a greater fall in vascular resistance than an equimolar dose of vasoactive intestinal peptide. The vasodilator response was independent of muscarinic receptor activation. Neither vasoactive intestinal peptide nor PACAP alone evoked any flow of saliva. However, both vasoactive intestinal peptide and PACAP enhanced the fluid response to acetylcholine, and the flow of saliva as well as the output of protein in response to parasympathetic nerve stimulation, vasoactive intestinal peptide being more potent than PACAP. In vitro, protein was released from submandibular gland tissue in response to both vasoactive intestinal peptide and PACAP, vasoactive intestinal peptide being more potent than PACAP. PACAP (and vasoactive intestinal peptide) exerted its in vitro effect following adrenoceptor and muscarinic blockade and following degeneration of sympathetic nerves. Sympathetic denervation combined with parasympathetic preganglionic denervation resulted in supersensitivity to both vasoactive intestinal peptide and PACAP. The fact that PACAP and vasoactive intestinal peptide occur in different nerve fibre populations suggests different roles for the two peptides in the submandibular gland.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1995

Fluid and protein secretion from ferret submandibular and parotid glands in response to sympathetic nerve stimulation or administration of sympathomimetics.

Electrical stimulation of the sympathetic innervation evoked secretion of submandibular and parotid saliva. By changing the mode of stimulation from a continuous to an intermittent one the fluid response increased and glandular blood flow improved. The volumes from the submandibular glands were larger than those from the parotid glands and further, the protein concentration of submandibular saliva was higher than that of parotid saliva. Adrenaline, isoprenaline and phenylephrine evoked larger fluid responses from submandibular than from parotid glands. However, the fluid response was small compared to the parasympathetic one. Substance P-evoked saliva was used as carrier for protein released by sympathetic nerve stimulation or administration of adrenaline and isoprenaline. In vitro tissues of submandibular and parotid glands responded to adrenaline with a dose-dependent release of protein. Taken together, the analytical pharmacology performed in vivo and in vitro, and including the antagonists phentolamine, dihydroergotamine, propranolol and metoprolol, showed that in submandibular glands, alpha(alpha 1)adrenoceptors were predominantly involved in fluid secretion and beta(beta 1)-adrenoceptors predominantly involved in protein secretion. In parotid glands, fluid secretion seemed solely to depend on alpha(alpha 1)-adrenoceptors, while beta(beta 1)-adrenoceptors seemed almost solely involved in protein secretion.

Animals↗
PubMed1995

Nitric oxide synthase-containing neurons in rat parasympathetic, sympathetic and sensory ganglia: a comparative study.

In rats, the distribution of nerve structures staining for NADPH-diaphorase, and showing immunoreactivities for nitric oxide synthase (NOS), tyrosine hydroxylase and various neuropeptides was studied in sensory ganglia (dorsal root, nodose and trigeminal ganglia), in sympathetic ganglia (superior cervical, stellate, coeliac-superior and inferior mesenteric ganglia), parasympathetic ganglia (sphenopalatine, submandibular, sublingual and otic ganglia), and in the mixed parasympathetic/sympathetic ganglia (major pelvic ganglia). The coincidence of neuronal cell bodies with strong NOS-immunoreactivity and strong NADPH diaphorase reactivity was almost total. The relative proportions of NOS-immunoreactive nerve cell bodies were largest in parasympathetic ganglia and major pelvic ganglia followed by sensory ganglia. In sympathetic ganglia no NOS-immunoreactive neuronal cell bodies could be detected. In parasympathetic and major pelvic ganglia, there was a very significant neuronal co-localization of immunoreactivities for NOS and vasoactive intestinal polypeptide (VIP). This was almost total in major pelvic ganglia, in which NOS-/VIP-immunoreactive nerve cell bodies were separate from sympathetic (tyrosine hydroxylase-/neuropeptide Y-immunoreactive), suggesting that NOS-/VIP-immuno-reactive neurons might also be parasympathetic.

Animals↗
PubMed1994

Parasympathetic non-adrenergic, non-cholinergic reflex secretion of parotid acinar granules in rats pretreated with atropine and adrenoceptor antagonists.

In parotid glands of fasted rats, feeding for 60-90 min reduced numerical density of acinar secretory granules by 52% and total activity of glandular amylase by 38%. In the presence of adrenoceptor antagonists (phentolamine and propranolol, 2 mg/kg, i.p., of each) the corresponding decrease was 31% and 32%, and in combination with atropine (1 mg/kg, i.p.) 32% as to both these indices. These non-adrenergic non-cholinergic (NANC) responses depended on an intact parasympathetic auriculo-temporal nerve since they did not occur following section of this nerve. In anaesthetized animals, electrical stimulation of the sympathetic innervation (50 Hz, 1 s every 10th second) for 60 min caused secretion of parotid saliva and decreases in number of acinar granules, by 65%, and in total amylase activity, by 49%; the adrenoceptor antagonists at the above-mentioned doses completely abolished the expected responses of the parotid gland and thus showing that these antagonists at the dose level chosen achieved an effective receptor blockade. In conclusion, parasympathetic NANC mechanisms are reflexly mobilized in response to eating, and these mechanisms are potentially responsible for the whole parasympathetic response and for the major part of that response in the absence of any antagonists. Under natural reflex conditions adrenergic, cholinergic and non-adrenergic, non-cholinergic mechanisms are most likely engaged to varying extents in order to generate the most purposeful response.

Adrenergic Antagonists↗
PubMed1994

Ontogeny of neuropeptides in the rat urinary bladder.

Urinary bladders of male rats at ages ranging from 1 day to 18 months were analysed for their neuropeptide content. NPY was detected at birth, VIP and CGRP at 1 week, and SP at 2 weeks. There was then a sharp increase in both the total amounts and concentrations of VIP, CGRP and SP until the rats had reached the age of 3-4 weeks. The total amount of NPY increased in two surges, between 2-3 weeks and between 4-5 weeks. The concentration of NPY showed a biphasic course, a decrease during the first two weeks and then an increase. In adults the total amounts of substance P and CGRP were higher than in younger animals, whereas that of VIP was lower. Following peaks at 3-8 weeks, the concentrations of VIP and substance P decreased with age, whereas that of CGRP remained unchanged. NPY was not followed beyond 8 weeks. The present findings offer a framework for future studies aimed at elucidating the functional role of neuropeptides in the regulation of micturition.

Aging↗
PubMed1994

Depletion of secretory granules from the feline parotid gland: action of NANC transmitters per se.

A parotid acinar degranulation of approximately 60 and 40% was observed in cats under pentobarbitone anaesthesia after a 90-min period of continuous stimulation of the parasympathetic auriculo-temporal nerve at 10 Hz in the absence and presence of atropine, respectively. Atropine completely abolished the large fluid response of the gland to the nerve stimulation. In the non-atropinized cats, bethanechol, infused into the carotid artery at a dose rate evoking a salivary flow similar to that in response to parasympathetic nerve stimulation, caused an acinar degranulation of approximately 25% and acinar vacuolation. Vasoactive intestinal peptide (VIP; 0.5 microgram kg-1 min-1 also infused into the carotid artery for 90 min) caused an acinar degranulation of the same magnitude as the parasympathomimetic drug but the peptide did not give rise to any fluid secretion or vacuole formation. The experiments were performed in the presence of alpha- and beta-adrenoceptor blockers. Thus, in parotid glands of the cat, producing no overt secretion of fluid, non-adrenergic, non-cholinergic (NANC) mechanisms may be at work causing exocytosis of the acinar granules. These mechanisms are also likely to contribute to the secretion of granules in response to parasympathetic nerve activity in the absence of blockade of the classical autonomic receptors.

Adrenergic alpha-Antagonists↗
PubMed1994

Developmental studies on vasoactive intestinal peptide, substance P and calcitonin gene-related peptide in salivary glands of postnatal rats.

The development of vasoactive intestinal peptide, substance P and calcitonin gene-related peptide in parotid, submandibular and sublingual glands of the male rat was followed by immunochemistry and immunocytochemistry. The total amounts of these peptides increased in surges during the first 8 weeks of the animal's life; one within 2-4 weeks and the other beginning 1-2 weeks later. Nerve fibres containing these peptides were present at birth showing a pattern of distribution similar to that in adults. During the first 4 weeks the nerve fibres increased in number.

Animals↗
PubMed1994

Masticatory-salivary reflexes mobilize non-adrenergic, non-cholinergic secretory mechanisms in parotid glands of conscious rats.

All rats were maintained on liquid diet, prepared from their ordinary hard pelleted diet, for a week, then fasted 32-33 h and subsequently either fed liquid or pelleted diet for 60-90 min or serving as non-fed controls. Both the fed and the non-fed animals had received atropine and alpha- and beta-adrenoceptor antagonists 15 min before the test. The rats given the liquefied chow consumed about twice as much as those given the hard chow. In the parotid glands of the rats given hard chow the number of acinar granules and the total amylase activity were reduced, by 50 and 70%, respectively, as compared with the glands of control rats. In the parotid glands of the rats given liquefied chow the number of acinar granules and the total activity of amylase remained unchanged. The results suggest that non-adrenergic, non-cholinergic secretory mechanisms of the rat parotid gland participate in masticatory-salivary reflexes.

Adrenergic alpha-Antagonists↗
PubMed1994

Electrophoretic analysis of cat parotid saliva in response to parasympathetic stimulation or infusion of bethanechol.

The protein constituents of cat parotid saliva evoked by parasympathetic stimulation or the infusion of bethanechol have been compared by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE). The SDS-PAGE patterns were highly reproducible for an individual cat and revealed up to 30 polypeptide bands in microlitre volumes of unconcentrated saliva. Only minor and predominantly quantitative differences were detected in the salivary protein composition of different cats. SDS-PAGE demonstrates quantitative rather than qualitative changes in the protein composition of saliva evoked in response to different stimuli. The latter included preliminary observations on the effect of vasoactive intestinal peptide (VIP) on the bethanechol-evoked response.

Animals↗
PubMed1993

Electrophoretic analysis of stimulated cat parotid saliva.

The proteins of parasympathetically stimulated cat parotid saliva were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and high resolution two-dimensional electrophoresis (2-DE). SDS-PAGE revealed up to 30 polypeptide bands in microliter volumes of unconcentrated saliva. The patterns were highly reproducible and characterized by prominent bands of M(r) 57,000, M(r) 30,000 and M(r) 15,000. The major protein (M(r) 30,000) appeared as a dimer (M(r) 60,000) when electrophoresed under non-reducing conditions but dissociated into its monomeric form when the SDS concentration of the denatured samples was increased from 1 to 5%. This indicates a noncovalent association. The protein patterns of saliva from different cats differed slightly but sequential samples from the same cat (collected during 90 min of stimulation) showed little change in protein pattern apart from a fall in total protein content. Following 2-DE, the major protein (M(r) 30,000) appeared as a complex array of at least eight spots in two tiers (pI 5.2-6.2; M(r) 28,000 and 32,000). The characteristics of this protein are discussed with reference to allergy to cats.

Animals↗
PubMed1993

Effects of long-term treatment with estrogen and progesterone on in vitro muscle responses of the female rabbit urinary bladder and urethra to autonomic drugs and nerve stimulation.

Ovariectomized virginal rabbits were treated with either estrogen or progesterone for 4 to 6 months. In vitro responses of muscle strips of the bladder and circular urethra were examined. Estrogen resulted in bladder contractions in response to noradrenaline and phenylephrine, whereas these agonists were without effect or evoked weak relaxations in castrated animals (and normals). Estrogen also caused a rightward shift of the frequency-contraction curve to nerve stimulation. Progesterone increased bladder sensitivity to contraction-evoking bethanechol. Contractile urethral responsiveness to bethanechol increased after both steroids. Urethral sensitivity to noradrenaline, evoking contraction, increased following estrogen. Further, estrogen abolished the marked relaxatory urethral response to nerve stimulation of castrated (and normal) rabbits and caused contraction only, which was abolished by a combination of alpha-adrenoceptor antagonists and scopolamine. When comparing the present results with those of other studies, it is evident that hormone-induced changes become manifest at an early stage. The present animal study gives support for the use of estrogen in the therapy of stress incontinence and, further, it provides no objections to the use of progesterone in combination with estrogen in this condition.

Animals↗
PubMed1993

Effects of luminal stimuli on polyamine metabolism in the small intestine of the rat: the role of enteric nerves.

The aim of this study was to investigate to what extent polyamine metabolism in the small intestine of the rat is controlled by the enteric nervous system. Polyamine metabolism was followed by measuring the activity of ornithine decarboxylase (ODC) and in some instances also the content of polyamines (putrescine, spermidine and spermine). ODC activity in the intestine was increased when intraluminal pressure was increased and 3 h after placing cholera toxin in the intestinal lumen. Cholera toxin also increased the tissue putrescine content. Atropine or hexamethonium given i.v. did not influence the evoked changes of ODC activity. The pressure induced changes were not decreased by placing lidocaine on the serosal surface. On the other hand, the ODC activity of control segments were decreased by hexamethonium or atropine. The presence of glucose in the intestinal perfusate did not augment tissue ODC activity, neither did the heat stable enterotoxin from Escherichia coli (STa). It is concluded that the effect on polyamine metabolism evoked by luminal pressure or cholera toxin seems not to be mediated via nerves, while nerves seem to influence ODC activity during control conditions. The experiments with enterotoxins suggest that cAMP is the intracellular second messenger controlling intestinal ODC activity.

Animals↗
PubMed1993

Parasympathetic non-adrenergic, non-cholinergic mechanisms in reflex secretion of parotid acinar granules in conscious rats.

1. Female adult rats were subjected to sympathetic denervation of the parotid glands by bilateral removal of the superior cervical ganglion 10-12 days before acute experiments. The sympathectomy was in some of the experimental groups combined with either bilateral adrenal medullectomy, treatment with the sensory neurotoxin capsaicin or parasympathetic denervation of the gland by cutting the auriculotemporal nerve. 2. Food but not water was withheld for 29-32 h before acute experiments. All animals were given an intraperitoneal injection of phentolamine (2 mg kg-1) and propranolol (1 mg kg-1) and, when appropriate, also atropine (1 mg kg-1). Then the experimental animals were fed their ordinary food of hard chow for 60-90 min. Thereafter, these animals and their non-fed controls were killed, and the parotid glands were removed and used for either morphometric assessment or measurement of amylase activity. 3. In the atropinized rats subjected to sympathectomy alone, eating reduced the numerical density of acinar secretory granules by 50% and the total activity of amylase by 55%; the corresponding figures were, when sympathectomy was combined with adrenal medullectomy, 51 and 63%. Also, in atropinized animals subjected to sympathectomy and capsaicin pretreatment, eating reduced the numerical density of acinar granules and the total amylase activity, in this case by 45 and 35%, respectively. 4. In the atropinized rats subjected to sympathectomy and parasympathectomy, eating caused no change in the numerical density of acinar granules but reduced the total amylase activity by 35%. 5. In the non-atropinized rats subjected to sympathectomy alone, eating reduced the numerical density of acinar granules by 22%, while there was no change in the total amylase activity. 6. In conclusion, eating evoked a reflex activation of the sympathectomized parotid gland that engaged non-adrenergic non-cholinergic receptors of the acinar cells. The present results give weight to a physiological role for non-adrenergic non-cholinergic parasympathetic mechanisms in salivary secretion under reflex conditions.

Adrenal Medulla↗