Search PubMed⌕ Search

Biomedical subjects

A Anggård

Publications and source records attributed to A Anggård.

At least 37 records · Page 2Linked to original sources
PubMed1986

Effects of VIP, PHM and substance P on blood vessels and secretory elements of the human submandibular gland.

The effects of the neuropeptides VIP, PHM and substance P (SP) on vascular smooth muscle tone, K+ secretion from exocrine elements and tissue content of cyclic AMP (cAMP) in the human submandibular gland were studied in vitro. All three peptides caused relaxation of noradrenaline contracted human submandibular arteries at nM concentrations. SP was slightly more active than VIP and PHM which had a similar potency as vasodilators. Only carbachol but not VIP, PHM or SP stimulated K+ secretion from exocrine elements of the human submandibular gland. Principally similar in vitro effects on K+ secretion were obtained on the cat submandibular gland, but in the rat not only carbachol but also SP stimulated K+ secretion. VIP and PHM increased cAMP production of exocrine elements in the human submandibular gland in nM concentrations. VIP was about 5-fold more potent than PHM with regards to cAMP production. In conclusion, VIP, PHM and SP relaxed human submandibular arteries in vitro. Both VIP and PHM stimulated cAMP production in glandular tissue but none of the three peptides induced K+ secretion from human submandibular gland tissue. This suggests that, in contrast to the situation in the rat, SP does not cause watery salivation in man, while VIP and PHM may modulate protein e.g. amylase content of the saliva.

Adult↗
PubMed1985

Neuropeptide Y-, substance P- and VIP-immunoreactive nerves in cat spleen in relation to autonomic vascular and volume control.

Neuropeptide Y (NPY)-immunoreactive (IR) nerve fibres were found around both arteries and veins and in smooth muscle trabeculae of the cat spleen with the highest density on the arterial side. Considerably more tyrosine hydroxylase (TH)- and dopamine-beta-hydroxylase (DBH)-positive than NPY-IR nerves were seen in the trabeculae and splenic capsule. The NPY-IR nerves in the spleen most likely originated in the coeliac ganglion, since (1) splanchnic nerve sectioning did not change the splenic NPY-IR nerves, (2) most neurones in the coeliac ganglion were NPY-IR, as well as DBH- and TH-positive, and (3) NPY-IR was transported axonally from the coeliac ganglion towards the spleen via the splenic nerve. Local NPY infusion in the isolated, blood-perfused cat spleen caused a marked increase in splenic vascular resistance and a small volume reduction. NA caused a comparatively larger reduction in splenic volume than NPY in addition to vasoconstriction. VIP-IR cell bodies in the coeliac ganglion were NPY- and TH-negative. VIP-IR nerves were seen both around the splenic artery and vein as well as around arterioles and within venous trabeculae of the spleen. VIP infusion caused reduction of splenic perfusion pressure (i.e. vasodilation) as well as an increase in splenic volume. Substance P-IR nerves, most likely of splanchnic afferent origin, were present in the coeliac ganglion around the splenic artery and arterioles of the spleen. Infusion of substance P induced marked reduction in perfusion pressure and a reduction in splenic volume. Enkephalin-immunoreactive nerves of splanchnic origin surrounded some TH- and NPY-positive, coeliac ganglion cells. It is concluded that several vasoactive peptides are located in splenic nerves. NPY is present in noradrenergic neurones and causes mainly increased vascular resistance. VIP occurs in non-adrenergic neurones of sympathetic origin and induces vasodilation and relaxation of the capsule. Finally, substance P is present in peripheral branches of spinal afferent nerves and causes vasodilation and capsule contraction. Stimulation of the splenic nerves may thus release several vasoactive substances in addition to noradrenaline, exerting a variety of actions.

Adrenergic Fibers↗
PubMed1985

Neuropeptide Y and sympathetic vascular control in man.

A parallel increase in systemic plasma levels of neuropeptide Y (NPY)-like immunoreactivity (LI) and noradrenaline (NA) was found during thoracotomy and surgery involving cardiopulmonary bypass in man. Thus, plasma levels of NPY-LI increased from 29 +/- 4 pmol/l before anaesthesia to 59 +/- 10 after thoracotomy and to 87 +/- 8 pmol/l upon cardiopulmonary bypass. The corresponding NA levels increased from 1.3 +/- 0.1 nmol/l before anaesthesia to 3.0 +/- 0.6 and 4.2 +/- 5 nmol/l after thoracotomy and cardiopulmonary bypass, respectively. A significant correlation was found between plasma levels of NPY-LI and NA during the operation but not between NPY-LI and adrenaline. The NPY-LI in human plasma was found to be similar to synthetic porcine NPY on reversed phase high performance liquid chromatography. Human submandibular arteries contained high levels of NPY-LI (24 +/- 3 pmol/g). In in vitro experiments on isolated human submandibular arteries, NPY in low concentrations (1000 pmol/l) was found to potentiate the contractile effects of NA or transmural nerve stimulation and to exert vasoconstrictor activity per se in higher concentrations. The calcium-entry antagonist nifedipine abolished both the NPY-induced contractions and the enhancement of NA-evoked contractions. NPY depressed the nerve stimulation-evoked 3H-NA release from human submandibular arteries via a prejunctional mechanism which was resistant to nifedipine. NPY contracted human mesenteric veins and renal arteries, but not mesenteric arteries. In conclusion, NPY seems to be co-released with NA upon sympathetic activation in man. Furthermore, NPY exerts both pre- and postjunctional effects on sympathetic control of human blood vessels.

Adult↗
PubMed1984

Corelease of vasoactive intestinal polypeptide and peptide histidine isoleucine in relation to atropine-resistant vasodilation in cat submandibular salivary gland.

Parasympathetic nerve stimulation of the submandibular salivary gland in the cat caused salivary secretion, vasodilation and a corelease of vasoactive intestinal polypeptide (VIP) and peptide histidine isoleucine (PHI) immunoreactivities (IR) into the venous effluent, as indicated by an increase in output. The ratio between the released VIP-IR and PHI-IR was close to 1:1. Gel-permeation chromatography of plasma from the submandibular venous effluent indicated that the released VIP-IR and PHI-IR were very similar to porcine VIP and PHI, respectively. Atropine pretreatment enhanced output of both VIP-IR and PHI-IR during the parasympathetic nerve stimulation to a similar extent (about 5-fold) compared to control stimulations. This increase could be due to an inhibitory presynaptic muscarinic receptor regulation of VIP and PHI release. Since VIP and PHI are present in the same postganglionic parasympathetic nerves in the gland and both peptides have vasodilator activity, the present data suggest that both VIP and PHI may contribute to the atropine-resistant vasodilation seen upon stimulation of the chorda-lingual nerve. The parasympathetic control of salivary gland function may thus involve, a multimessenger system with the classical transmitter acetylcholine and the peptides VIP and PHI.

Acetylcholine↗
PubMed1984

Guanethidine-sensitive release of neuropeptide Y-like immunoreactivity in the cat spleen by sympathetic nerve stimulation.

Splenic nerve stimulation (10 Hz for 2 min) caused a perfusion-pressure increase, a volume reduction and an increase in the output of neuropeptide Y-like immunoreactivity (NPY-LI) from the isolated blood-perfused cat spleen. Gel-filtration HPLC analysis revealed that plasma NPY-LI collected during nerve stimulation was similar to the NPY-LI in the spleen and synthetic porcine NPY. Combined propranolol and phenoxybenzamine pretreatment enhanced NPY output upon nerve stimulation by about 60%. Forty percent of the perfusion-pressure increase and 25% of the volume reduction seen during control stimulations remained after adrenoceptor blockade. Guanethidine abolished the release of NPY-LI, the perfusion-pressure increase and the volume reduction normally seen upon splenic nerve stimulation. Infusion of synthetic porcine NPY caused a long-lasting increase in perfusion pressure and a relatively moderate volume reduction. Noradrenaline (NA) both increased perfusion pressure and induced a marked volume reduction. The NPY effects were resistant to adrenoceptor antagonists in doses which abolished the NA response. In conclusion, the present data show that NPY-LI is released upon sympathetic nerve stimulation by a guanethidine-sensitive mechanism. Furthermore, the sympathetic response is partially resistant to adrenoceptor antagonists and NPY has powerful vasoconstrictor effects. This provides further evidence for a role of NPY in sympathetic vascular control.

Animals↗
PubMed1984

Local and systemic capsaicin pretreatment inhibits sneezing and the increase in nasal vascular permeability induced by certain chemical irritants.

The effects of local exposure to chemical irritants and mechanical stimulation on sneezing reflexes have been studied in normal and capsaicin-pretreated, conscious guinea-pigs. The influence of local and systemic capsaicin pretreatment on vascular permeability to plasma proteins and the cardiovascular effects of local application of capsaicin to the nasal mucosa have also been studied in anaesthetized animals. Local application of capsaicin (threshold dose 3 microM), nicotine (threshold dose 300 microM) or formalin to the nasal mucosa induced reflex sneezing discharges. Systemic or local capsaicin pretreatment abolished or reduced the sneezing responses to capsaicin and formalin. The response to nicotine was also reduced following local pretreatment with capsaicin, while the response to systemic pretreatment with capsaicin was only slightly affected. The sneezing response to mechanical stimulation was not affected by capsaicin pretreatment. Pretreatment with a local anaesthetic induced a similar dose-dependent inhibition of the sneezing responses to both capsaicin and nicotine. Local application of disodium cromoglycate to the nasal mucosa reduced the sneezing response to capsaicin, but not that to nicotine. Local pretreatment with the 3 mM and 30 mM capsaicin solution inhibited the increase in vascular permeability to plasma proteins in the nasal mucosa induced by i.v. capsaicin. Local pretreatment with capsaicin did not result in any reduction in the capsaicin-induced permeability in the ureter, suggesting that such treatment did not have any major systemic toxic effects. However, a small, acute increase in respiratory insufflation pressure, indicating broncho constriction, was seen when the 30 mM capsaicin solution was applied to the nasal mucosa.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Inhibition of cigarette smoke-induced oedema in the nasal mucosa by capsaicin pretreatment and a substance P antagonist.

The effect of cigarette smoke on vascular permeability in the rat nasal mucosa was studied using the Evans blue extravasation method. Exposure to smoke from cigarettes induced a significant extravasation of Evans blue in the nasal mucosa of normal rats, suggesting an increased vascular permeability to plasma proteins. The oedema response was correlated to tar, nicotine and vapour phase components in the smoke. The smoke-induced permeability effect was abolished in rats pretreated neonatally with capsaicin. Also, systemic or local pretreatment with [D-Arg, D-Pro, D-Trp, Leu]Substance P, a substance P antagonist, inhibited the permeability response to cigarette smoke. Insertion of a glass-fibre filter, which removes the particulate phase of the smoke (including nicotine), did not significantly reduce the permeability response. The present findings suggest that the smoke-induced oedema in the rat nasal mucosa is not caused by nicotine but by vapour-phase irritants, which activate capsaicin-sensitive C-fibre afferents. These neurons then release agents such as substance P or a related tachykinin which increase permeability to plasma proteins.

Animals↗
PubMed1984

Orally administered decongestant drugs in disorders of the upper respiratory passages: a survey of clinical results.

Side-effects of peroral mucous membrane decongesting agents have been described in recent years while at the same time documentation of the efficiency of these preparations is sparse. The prescription of the agents is very frequent. This article reviews the literature on the use of oral sympathomimetic agents for the treatment of diseases in the upper respiratory passages. The survey was initially instituted by the Swedish National Board of Health and Welfare to consider the indications for the prescription of these drugs. The article concludes with some suggested indications for these preparations.

Acute Disease↗