Authors Jan L. Brozek, MD, PhD – Department of Clinical Epidemiology & Biostatistics and Medicine, McMaster University, Hamilton, Canada Jean Bousquet, MD, PhD – Service des Maladies Respiratoires, Hopital Arnaud de Villeneuve, Montpellier, France, INSERM, CESP U1018, Respiratory and Environmental Epidemiology Team, France, and WHO Collaborating Center for Rhinitis and Asthma Carlos E. Baena-Cagnani, MD – Faculty of Medicine, Catholic University of Cordoba, Cordoba, Argentina Sergio Bonini, MD – Institute of Neurobiology and Molecular Medicine – CNR, Rome, Italy and Department of Medicine, Second University of Naples, Naples, Italy G. Walter Canonica, MD – Allergy & Respiratory Diseases, DIMI, Department of Internal Medicine, University of Genoa, Genoa, Italy Thomas B. Casale, MD – Division of Allergy and Immunology, Department of Medicine, Creighton University, Omaha, Nebraska, USA Roy Gerth van Wijk, MD, PhD – Section of Allergology, Department of Internal Medicine, Erasmus Medical Centre, Rotterdam, the Netherlands Ken Ohta, MD, PhD – Division of Respiratory Medicine and Allergology, Department of Medicine, Teikyo University School of Medicine, Tokyo, Japan Torsten Zuberbier, MD – Department of Dermatology and Allergy, Charite Universitatsmedizin Berlin, Berlin, Germany Holger J. Schunemann, MD, PhD, MSc – Department of Clinical Epidemiology & Biostatistics and Medicine, McMaster University, Hamilton, Canada

/pdf/allergic-rhinitis-and-its-impact-on-asthma-20b4c7y0pr.pdf

Allergic Rhinitis and Its Impact on Asthma

Natural products afford a window of opportunity to study important biology. If the natural product is used or abused by human beings, finding its biological target(s) is all the more significant. Hot pepper is eaten on a daily basis by an estimated one-quarter of the world’s population and

Vanilloid (Capsaicin) Receptors and Mechanisms

Local effector functions of capsaicin-sensitive sensory nerve endings : involvement of tachykinins, calcitonin gene-related peptide and other neuropeptides

The renal nerves are the communication link between the central nervous system and the kidney. In response to multiple peripheral and central inputs, efferent renal sympathetic nerve activity is altered so as to convey information to the major structural and functional components of the kidney, the vessels, glomeruli, and tubules, each of which is innervated. At the level of each of these individual components, information transfer occurs via interaction of the neurotransmitter released at the sympathetic nerve terminal-neuroeffector junction with specific postjunctional receptors coupled to defined intracellular signaling and effector systems. In response to normal physiological stimuli, changes in efferent renal sympathetic nerve activity contribute importantly to homeostatic regulation of renal blood flow, glomerular filtration rate, renal tubular epithelial cell solute and water transport, and hormonal release. Afferent input from sensory receptors located in the kidney participates in this reflex control system via renorenal reflexes that enable total renal function to be self-regulated and balanced between the two kidneys. In pathophysiological conditions, abnormal regulation of efferent renal sympathetic nerve activity contributes significantly to the associated abnormalities of renal function which, in turn, are of importance in the pathogenesis of the disease.

Neural Control Of Renal Function

These parameters were developed by the Joint Task Force on Practice Parameters, representing the American Academy of Allergy, Asthma & Immunology; the American College of Allergy, Asthma and Immunology; and the Joint Council of Allergy, Asthma and Immunology. The American Academy of Allergy, Asthma & Immunology (AAAAI) and the American College of Allergy, Asthma and Immunology (ACAAI) have jointly accepted responsibility for establishing "The diagnosis and Management of Rhinitis: An Updated Practice Parameter." This is a complete and comprehensive document at the current time. The medical environment is a changing environment, and not all recommendations will be appropriate for all patients. Because this document incorporated the efforts of many participants, no single individual, including those who served on the Joint Task Force, is authorized to provide an official AAAAI or ACAAI interpretation of these practice parameters. Any request for information about or an interpretation of these practice parameters by the AAAAI or ACAAI should be directed to the Executive Offices of the AAAAI, the ACAAI, and the Joint Council of Allergy, Asthma and Immunology. These parameters are not designed for use by pharmaceutical companies in drug promotion.

The diagnosis and management of rhinitis: An updated practice parameter

In immunohistochemical studies, substance P-immunoreactivity (SP-IR) was found in a population of trigeminal ganglion cells in guinea pig, rat and cat. SP-IR nerve endings were found in the spinal trigeminal nucleus, around sphenopalatine ganglion cells, around blood vessels, as well as under and within the epithelium of the nasal mucosa. Ligation and denervation experiments in the cat indicated that the SP-IR nerves in the sphenopalatine ganglion and the nasal mucosa are of trigeminal origin. Capsaicin pretreatment of guinea pigs and rats resulted in a selective loss of the SP-IR nerves in the nasal mucosa and sphenopalatine ganglion, while the parasympathetic and sympathetic nerves were still present.

Origin and distribution of capsaicin-sensitive substance P-immunoreactive nerves in the nasal mucosa.

Neuropeptide Y and sympathetic vascular control in man.

Electrical stimulation of the maxillary branches of the trigeminal nerve induced an increase in vascular permeability to macromolecules and an interstitial edema in the nasal mucosa of the rat, as indicated by extravasation of Evans blue. In animals that had been treated neonatally with capsaicin, the effect of trigemindl nerve stimulation was abolished. Local application of capsaicin or substance P (SP) also induced a significant Evans blue extravasation in the nasal mucosa. In capsaicin-pretreated animals the effect of SP was still present, while the permeability increase induced by capsaicin was abolished. In conclusion, chemogenic irritation of the nasal mucosa by capsaicin induces edema probably via a local axon reflex inducing release of SP. Capsaicin-sensitive SP-containing afferents in the nasal mucosa may also be involved in the pathogenesis of nasal congestion seen in various types of rhinitis.

Increased vascular permeability in rat nasal mucosa induced by substance P and stimulation of capsaicin-sensitive trigeminal neurons.

1. Applications of capsaicin, nicotine and methacholine were made locally onto the nasal mucosa in human controls and patients suffering from hyperreactive nasal disorders. Perception of sensation was registered as a sympton score and secretion quantified. The sensory reaction (irritation - pain) to capsaicin was similar in the three groups studied, i.e. controls, a group of patients with the diagnosis of vasomotor rhinitis and a group of patients with increased nasal secretion as the main symptom of the hyperreactive disorder. Nicotine induced only a mild itching sensation in the three groups. However, capsaicin and nicotine challenge caused a significantly larger secretory response in the last group than in the unselected vasomotor rhinitis group and in the control group. 2. Pretreatment with muscarinic receptor antagonists almost completely abolished the secretory response to both capsaicin and nicotine, and blocked methacholine-induced secretion. Furthermore, pretreatment with a combination of local anaesthetic and vasoconstrictor agent abolished the capsaicin-induced irritation, as well as the capsaicin- and nicotine-induced secretion on both the ipsilateral and the contralateral side. Therefore, no clearcut contribution seems to be exerted by locally released peptides from sensory neurones as direct trigger substances for the secretory response to capsaicin. 3. In conclusion, the nasal secretory response, in man, to both capsaicin and nicotine, seems to be mediated via cholinergic parasympathetic reflexes. In patients with hyperreactive non-allergic disorders of the nasal mucosa with rhinorrhea as the main complaint, the enhanced secretion may be due to a hyperreactive efferent cholinergic mechanism rather than hypersensitive irritant receptors on capsaicin- and nicotine-sensitive sensory neurones.(ABSTRACT TRUNCATED AT 250 WORDS)

/pdf/capsaicin-and-nicotine-sensitive-afferent-neurones-and-nasal-2w4572p9ui.pdf

Capsaicin and nicotine-sensitive afferent neurones and nasal secretion in healthy human volunteers and in patients with vasomotor rhinitis

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-β-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.

A. Änggård

Papers

Origin and distribution of capsaicin-sensitive substance P-immunoreactive nerves in the nasal mucosa.

Neuropeptide Y and sympathetic vascular control in man.

Increased vascular permeability in rat nasal mucosa induced by substance P and stimulation of capsaicin-sensitive trigeminal neurons.

Capsaicin and nicotine-sensitive afferent neurones and nasal secretion in healthy human volunteers and in patients with vasomotor rhinitis

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