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R Henriksson

Publications and source records attributed to R Henriksson.

At least 181 records · Page 10Linked to original sources
PubMed1987

Beta-adrenoceptor stimulation increases the pH of parotid acinar cells.

To characterize the effect of L-norepinephrine on intracellular pH (pHi) in parotid acinar cells, were measured the accumulation of 14C-labelled 5,5-dimethyloxazolidine-2,4-dione ([14C]DMO), in slices of parotid glands from Sprague-Dawley rats. L-Norepinephrine enhanced the [14C]DMO uptake in a concentration-dependent manner with half-maximal effect at about 1 microM and maximum effect at about 1 mM. The half-maximal effect corresponded to an increase in pHi by 0.08 units and was reduced by 2 microM L-propranolol (beta-adrenoceptor antagonist), but was not affected by 2 microM phentolamine (alpha-adrenoceptor antagonist). The results suggest that L-norepinephrine increases intracellular pH in rat parotid acini and that this effect may be mediated by beta-adrenoceptor stimulation.

Adrenergic beta-Agonists↗
PubMed1987

Iontophoretic study of adrenergic and cholinergic skin vessel reactivity in normal ageing and Alzheimer's disease.

Iontophoresis was used to evaluate the peripheral reactivity of phenylephrine (alpha 1-agonist), isoproterenol (beta-agonist) and metacholine (cholinergic agonist) in patients with Alzheimer's disease (AD). The cutaneous responses--erythema and blanching--were visually recorded. Healthy personnel, medical students and patients with various dermatoses served as controls. A reduced response towards the adrenergic agonists was seen in AD. The reduced sensitivity was highly significant for the beta-agonist isoproterenol (p less than 0.001), in contradistinction the metacholine response did not differ between AD and age-matched controls. Furthermore, increasing age did not seem to significantly influence the cutaneous responses in mentally healthy controls. Thus, a reduced peripheral adrenergic reactivity was observed in the patients suffering from AD.

Adolescent↗
PubMed1986

Isoflurane--a study of its adrenoceptor interaction in the isolated rat parotid gland.

Adrenergic receptor interaction with isoflurane was studied in an in vitro rat parotid gland model in which beta-adrenoceptor agonists evoke amylase release and alpha-adrenoceptor agonists induce potassium secretion from parotid cells. The amylase secretory studies were performed using a batch-incubation technique, and potassium efflux was evaluated using 86Rb+ as a probe for K+. Isoflurane was dissolved in a fat emulsion, which of its own had no secretory effect. Isoflurane induced a dose-dependent amylase release that was unaffected by beta-adrenergic blockade with propranolol and metoprolol. Isoflurane also induced a significant efflux of 86Rb+ that could not be inhibited by the alpha-adrenoceptor antagonist, phentolamine. Dinitrophenol, an uncoupler of oxidative phosphorylation, had no effect on the isoflurane-induced enzyme release, indicating that amylase secretion occurred by passive leakage. It is suggested that isoflurane has no direct action on alpha- or beta-adrenoceptors. Isoflurane, however, induces potent cellular events that might be due to an unspecific effect on the cell membrane, thereby causing changes in membrane permeability.

2,4-Dinitrophenol↗
PubMed1985

Ultrastructural morphometry and secretory behavior of acinic cell carcinoma.

Cells from three parotid acinic cell carcinomas were compared stereologically with normal parotid acinar cells. The morphometric studies revealed that the granular volume density was increased in the tumor cells. The cells contained more granules, but the mean granule diameter was considerably less, compared with normal controls. On the other hand, no difference in cell volume or nuclear volume density could be found. Although morphologically similar to normal acinar cells, the tumor cells had a much lower content of amylase. However, in a batch-incubated system, amylase secretion could be elicited with noradrenaline from the tumor cells. Furthermore, noradrenaline stimulation increases tumor tissue cyclic AMP content dramatically. The current study demonstrated the similarity between normal acinar cells and acinic cell tumor cells: the latter respond to physiologic secretion stimuli with an increased tissue level of cyclic AMP accompanied by amylase release.

Amylases↗
PubMed1985

Differences in dopamine- and noradrenaline-induced amylase release from the rat parotid gland.

The effects of dopamine and noradrenaline on amylase secretion from rat parotid gland were studied in a batch incubation system. Dopamine effectively caused amylase secretion but the concentration-response curve was shifted to the right in reserpinized animals, suggesting a minor indirect component in the action of dopamine. The noradrenaline-evoked secretion was the same in reserpinized glands as in the controls. Bromocriptine, a dopamine receptor agonist, was without effect on amylase secretion. The dopamine receptor antagonists pimozide, chlorpromazine, haloperidol and droperidol as well as SKF 38393 all effectively inhibited dopamine-induced amylase secretion without affecting the enzyme release caused by noradrenaline. The D-2 antagonist sulpiride was without effect on both dopamine- and noradrenaline-stimulated secretion. The dopamine-induced secretion was also significantly blocked by the non-selective beta-blocker propranolol as well as by beta 1- and beta 2-selective antagonists. Several alpha-antagonists were all partial blockers of dopamine-stimulated amylase secretion. In contrast, the noradrenaline-evoked amylase release was exclusively abolished by propranolol and beta 1-selective antagonists. The results suggest that the dopamine- and noradrenaline-induced amylase secretion are activated via different receptor systems, and that dopamine stimulation is mainly a postsynaptic D-1 effect and only to a minor extent due to presynaptic interaction.

Amylases↗
PubMed1985

Developmental influences of the sympathetic nervous system on rat parotid gland.

In an attempt to evaluate the effect of the sympathetic nervous system on the postnatal maturation of the parotid gland, rats were either sympathetically denervated on one side by avulsion of the superior cervical ganglion within 4 h after birth or treated with various beta-adrenoceptor blocking agents from the day of birth. Four or 9 weeks later the animals were killed and the parotid glands were subjected to quantitative morphological studies. The neonatal denervation caused a significant decrease in parotid acinar cell size and their granule content, whereas chronic beta-adrenoceptor blockade was without any effect. It is suggested that the trophic effect of the sympathetic nervous system may be due to a growth factor released from sympathetic nerve endings, which does not seem to interact with the beta-adrenoceptor system.

Adrenergic beta-Antagonists↗
PubMed1985

Glycoprotein secretion from mouse gallbladder principal cells after chronic variation in parasympathetic activity. A morphometric study after vagotomy and cholinergic superstimulation.

Principal cells of mouse gallbladder epithelium were subjected to quantitative electron microscopic investigation either after superstimulation with pilocarpine for 12 days or 6 weeks after vagotomy at different levels. Cholinergic superstimulation caused a slight hypertrophy of the principal cells, whereas different types of vagotomy induced hypotrophic changes. In the superstimulated animals there was decreased sensitivity to single-dose stimulation with pilocarpine. In contrast, a supersensitivity was recorded in mice subjected to vagotomy. It is concluded that the parasympathetic nervous system is of importance for the regulation of glycoprotein secretion from mouse gallbladder principal cells. The demonstrated vagotomy-induced super-sensitivity may be responsible for an increased glycoprotein release, which in turn may be involved in the formation of gallstones occurring after truncal vagotomy in man.

Animals↗
PubMed1984

Is the modality of the supersensitivity after sympathectomy age and duration dependent?

Sympathetic denervation of the rat parotid gland was performed neonatally or in adult fully developed animals on one side. The contralateral gland served as control. Two and 9 weeks later the glands were used for in vitro amylase secretory studies. The neonatally denervated glands displayed an enhanced response to high concentrations of noradrenaline, without significant changes in the lower concentration range. In adult sympathectomized animals no significant alteration could be recorded in secretory response 9 weeks after denervation. Two weeks after adult ganglionectomy a striking leftward shift of the noradrenaline concentration-response curve was observed without changes in the maximal response. Thus, the modality of the supersensitivity appears to be influenced by the age of the animal when the surgical procedure is performed, as well as by the duration of the denervation.

Aging↗
PubMed1984

Inhomogeneities in glycoprotein cytochemistry of secretory granules in rat-parotid acinar cells after selective beta 1-adrenoceptor stimulation.

The distribution of periodate-positive glycoproteins was studied in parotid acinar cells of the rat after stimulation with the specific beta 1-adrenoceptor agonist prenalterol. After two weeks of daily injections, the majority of secretory granules were larger, less electron dense, and often exhibited a bipartite or pleomorphic PA-CrA-silver staining pattern. A great variation in the staining pattern of the secretory granules was seen among different cells but, within any individual cell, most granules displayed a similar pattern. The staining reaction suggests a mucoid transformation of the granules, or a reorganization of the glycoproteins within the granules. The variation among cells in the staining pattern of granules may suggest that there are different populations of acinar cells or of secretory granules.

Adrenergic beta-Agonists↗
PubMed1984

Chronic propranolol treatment affects parietal cells of the developing rat gastric mucosa.

The nonselective beta-adrenoceptor antagonist propranolol (0.3 mg/kg body weight) was given to rats, twice daily, from the day of birth to 5 weeks of age. The animals were then killed, and sections from gastric mucosa were prepared for light and electron microscopy. Propranolol treatment significantly reduced the thickness of the mucosa as compared with that of the controls. The parietal cell volume density and the number of parietal cells were markedly decreased following propranolol. The volume density of lamina propria and of other epithelial cells in the gastric mucosa were not significantly different from the control group. The secretory canaliculi of the parietal cells seemed markedly increased, indicating enhanced secretory activity. These findings suggest an important role for the adrenergic-sympathetic system in the development of parietal cells in the maturing gastric mucosa.

Animals↗
PubMed1984

Beta 1- and beta 2-adrenoceptor-mediated secretion of amylase from incubated rat parotid gland.

The present in vitro investigation was undertaken in an attempt to obtain further information on beta-adrenoceptor specificity and action in the rat parotid gland, with regard to amylase secretion. The beta 1-selective agonist prenalterol was roughly 800 times more potent than the beta 2-agonist terbutaline, and about 5 times more effective than noradrenaline in evoking amylase release . Propranolol was the most effective inhibitor of amylase release in all experiments. The beta 1-selective antagonist metoprolol and H104 /08 were also effective blockers of maximal noradrenaline- and prenalterol-induced release. The inhibition curves displayed biphasic shapes when amylase secretion was induced by noradrenaline, but not when prenalterol was the secretagogue. The beta 2-antagonist H35 /25 was without effect on maximal noradrenaline- and prenalterol-stimulated secretion. The amylase release evoked by submaximal concentration of terbutaline was inhibited by the two antagonists H35/25 and IPS 339. In another series of experiments propranolol and metoprolol clearly shifted the noradrenaline concentration-response curve to the right, whereas H35/25 was without effect. The results further demonstrate the major importance of the beta 1-adrenoceptor (noradrenaline-activated) in eliciting amylase release from the rat parotid gland. However, it is also suggested that the beta 2-adrenoceptors (terbutaline-activated) may to some extent serve the same function.

Adrenergic beta-Agonists↗
PubMed1983

Ultrastructural changes in rat parotid acinar cells after selective beta 1-adrenoceptor agonist treatment.

Administration of the selective beta 1-adrenoceptor agonist, prenalterol, affects the acinar cell of the rat parotid in a manner similar to that observed after isoprenaline (IPR) treatment. Sixty minutes after injection of prenalterol, many cells are depleted of their zymogen granules and there is evidence of secretory protein resynthesis. Long term treatment leads to cellular hypertrophy and marked structural changes in the granule population. The cellular alterations are, however, not as pronounced as those observed after IPR injections. This may be due to the combined beta 1- and beta 2-adrenoceptor effect of IPR. With prenalterol, cell damage is obvious in acute experiments. In long term treated animals numerous characteristic autophagic vacuoles are observed, reflecting a reorganization of cytoplasmic components in superstimulated glands. Although prenalterol and IPR give rise to rather similar structural changes in parotid glands, marked differences between effects of the two drugs on gland biochemistry have been noted. It seems evident that different biochemical pathways involved in secretory activity have actions in common with respect to effects on submicroscopical structures.

Adrenergic beta-Agonists↗
PubMed1982

Effects of neonatal sympathetic denervation on amylase secretion in the adult rat parotid gland: difference in beta 1- and beta 2-adrenoceptor response.

Changes in amylase secretion and cyclic AMP accumulation in response to various secretagogues were studied in parotid glands of adult rats subjected to neonatal sympathetic denervation by unilateral excision of the superior cervical ganglion. Denervation decreased the gland content of amylase and both basal and the stimulated levels of cyclic AMP were elevated. The secretory cells of neonatally denervated glands exhibited enhanced maximal enzyme discharge in response to beta-adrenoceptor agonists. However, the selective beta 1-agonist, prenalterol was not effective in this respect whereas an enhanced maximal secretory response to the beta 2-selective agonist, terbutaline, was particularly prominent. DBcAMP was also more efficient in inducing amylase release from the denervated gland. The result of the present study demonstrate that the usual dominance of the beta 1-adrenoceptor subtype in eliciting amylase release is lost, implying that the differentiation of the beta-adrenoceptor into its subtypes is altered by neonatal sympathetic denervation.

Amylases↗
PubMed1982

Dissociation of beta-adrenoceptor-induced effects on amylase secretion and cyclic adenosine 3', 5' monophosphate accumulation.

By using a multi-channel microperifusion system the effects of noradrenaline, the beta1-adrenoceptor agonist prenalterol, and the beta2-selective agonist terbutaline were studied on amylase pig submandibular glands. 2 Noradrenaline caused significant amylase discharge and cyclic AMP accumulation. 3 Prenalterol was as effective as noradrenaline in causing amylase release but did not significantly affect the cyclic AMP content. 4 Terbutaline stimulated cyclic AMP accumulation, but had little effect on amylase secretion. 5 The present study reveals that there is a dissociation of the beta-adrenoceptor-induced amylase release and cyclic AMP formation, and that this dissociation may be due to different beta-adrenoceptor subtypes.

Amylases↗