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PubMed1989

Calcitonin and CGRP block bombesin- and substance P-induced increases in airway tone.

Calcitonin gene-related peptide (CGRP) and calcitonin (C) are two peptides that are cocontained and probably coreleased with the potent bronchocontrictors, bombesin (B) and substance P (SP), within the lung. Although CGRP and C have a wide intrapulmonary distribution, their actions have not been well defined. By the use of a computerized lung mechanics analyzer, changes in response to 10-min infusions of these agents were measured in spontaneously breathing, anesthetized guinea pigs. Infusion of 0.3 nmol.kg-1.min-1 CGRP and 2 nmol.kg-1.min-1 C caused little change in lung mechanics. Infusion of 0.06 nmol.kg-1.min-1 B and 0.3 nmol.kg-1.min-1 SP caused a marked increase in inspiratory, expiratory, and total pulmonary resistance (RT), from base-line values (P less than 0.02), with a maximal effect at 10 min postinfusion (PI) [RT = 326 +/- 20% (SE) (B), 490 +/- 73% (SP)]. Coinfusion of C or CGRP with B or SP at the above concentrations caused a marked reduction in SP - [RT = 189 +/- 28% (C), 142 +/- 16% (CGRP) at 10 min PI] and B - [RT = 157 +/- 18% (C), 158 +/- 10% (CGRP) at 10 min PI] induced changes in resistance (P less than 0.015). The mode of action of C and CGRP is unknown, but these peptides may antagonize the effects of B and SP via autonomic pathways by interfering with B- or SP-induced changes in intracellular calcium concentrations or by increasing intracellular cAMP levels by binding to specific cellular receptors linked to adenylate cyclase.

Airway Resistance↗
PubMed1992

Long-term control of arterial blood pressure.

Two concepts for the long-term regulation of arterial pressure were considered in this review, the neural control hypothesis and the volume regulation hypothesis. The role of the nervous system and fluid volume regulation are intertwined in a way that has made it difficult to experimentally evaluate their separate contributions in the long-term regulation of arterial pressure. Nevertheless, from a substantial body of work related to the neural control of cardiovascular function, it appears that the ability of the nervous system to control arterial pressure is limited to the detection and correction of rapid short-term changes of arterial pressure. A long and exhaustive search has yet yielded no new neural mechanisms beyond the classic sinoaortic baroreceptors that can detect changes of arterial pressure. The baroreceptor mechanisms are of great importance for the moment-to-moment stabilization of arterial pressure, but because they do not possess sufficient strength and because they reset in time to the prevailing level of arterial pressure, they cannot provide a sustained negative feedback signal to provide long-term regulation of arterial pressure in face of sustained stimuli. This is not to say that the nervous system cannot affect the long-term level of arterial pressure. A distinction is made here between the many factors that can influence the long-term level of pressure and those that actually serve to detect changes of pressure and serve to maintain the level of pressure within a narrow range over the period of our adult lifetime. In this sense, there is evidence that in genetically susceptible individuals, environmental stresses can influence the long-term level of arterial pressure via the central and peripheral neural autonomic pathways. It is inappropriate, however, to view the nervous system as a long-term controller of arterial pressure because there is yet no evidence that the CNS can detect changes of arterial pressure nor changes in total body sodium and water content over sustained periods whereby it could provide an adequate long-term normalization of such error signals. In contrast, evidence has grown in support of the renal pressure-diuresis volume regulation hypothesis for the long-term control of arterial pressure over the past decade. An enhanced understanding of the mechanisms of pressure diuresis-natriuresis coupled with studies exploring how changes of vascular volume can influence vascular smooth muscle tone provide a compelling basis for this hypothesis of long-term arterial pressure regulation. This overall concept is represented and summarized in Figure 12.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2006

Multiple acquired renal carcinoma tumor capabilities abolished upon silencing of ADAM17.

Malignancy is a manifestation of acquired defects in regulatory circuits that direct normal cell proliferation and homeostasis. Most of these circuits operate through cell autonomous pathways, whereas others potentially involve the neighboring microenvironment. We report that the metalloprotease ADAM17 plays a pivotal role in several acquired tumor cell capabilities by mediating the availability of soluble transforming growth factor-alpha, an epidermal growth factor receptor (EGFR) ligand, and thus the establishment of a key autocrine signaling pathway. Silencing of ADAM17 in human renal carcinoma cell lines corrects critical features associated with cancer cells, including growth autonomy, tumor inflammation, and tissue invasion. Highly malignant renal carcinoma cancer cells fail to form in vivo tumors in the absence of ADAM17, confirming the essential function of this molecule in tumorigenesis. These data show that ligand shedding is a crucial step in endogenous EGFR activation and endorse prospective therapeutic strategies targeting ADAM17 in human cancer.

ADAM Proteins↗
PubMed1997

Vasopressin acts in the subfornical organ to decrease blood pressure.

In addition to its traditional role as a circulating vasoactive peptide, vasopressin (VP) has been shown to play significant roles in central cardiovascular processing. The recent description of VP receptors within the subfornical organ (SFO) has suggested this circumventricular organ (CVO) as a potential locus for feedback actions of circulating VP on the brain. The well-established anatomical connections between SFO and hypothalamic autonomic control centers provide further arguments in support of such a view. This study was undertaken to determine the physiological consequences of activation of VP receptors within the SFO of urethane anesthetized rats. Microinjection (0.5 microliter) of 5 pmol VP into SFO resulted in significant decreases in blood pressure (BP, mean AUC -638.3 +/- 110.3 mm Hg.s, p < 0.01, n = 13) without a change in heart rate (HR, mean AUC 7.9 +/- 14.0 beats, p > 0.05, n = 12), effects which were repeatable. These depressor effects were specific to microinjection locations within this CVO as similar VP microinjections into non-SFO tissue were without effect on BP (mean AUC 245.4 +/- 111.5 mm Hg.s, p > 0.05, n = 10), or HR (mean AUC 1.8 +/- 3.1 beats, p > 0.05, n = 9). In contrast to the former depressor effects, VP microinjection (5 pmol in 0.5 microliter) into the third ventricle produced large increases in BP (mean AUC 1,461.8 +/- 368.97 mm Hg.s, p < 0.05, n = 6) again with no change in HR (mean AUC 1.4 +/- 5.96 beats, p > 0.05, n = 6). The hypotensive effects observed in response to VP microinjection into SFO were abolished by systemic treatment with a V1 receptor antagonist (mean AUC 89.5 +/- 67.7 mm Hg.s, p > 0.05) compared to BP response before V1 receptor blockade (mean AUC -605.9 +/- 119.8 mm Hg.s, n = 4). These results suggest that the SFO may be an essential structure in the feedback control loop through which circulating VP influences descending autonomic pathways involved in cardiovascular control.

Animals↗
PubMed1994

Hemodynamic effects elicited by stimulation of the nucleus tractus solitarii.

Microinjection of the excitatory amino acid L-glutamate into the nucleus tractus solitarii (NTS) elicits decreases in arterial pressure and heart rate. In the present study, we sought to determine the regional hemodynamic effects that were correlated with changes in arterial pressure and heart rate produced by stimulation of the NTS. In anesthetized rats, blood flow in the renal (RBF), superior mesenteric (MBF), and hindquarter (HBF) vascular beds was measured by pulsed Doppler flowmeters. Relative vascular resistances (RVR, MVR, and HVR) were calculated by dividing mean arterial pressure (mm Hg) by the Doppler shift (kHz). Microinjection of L-glutamate into the NTS caused rapid, transient, dose-related decreases in mean arterial pressure and heart rate. MVR and RVR were minimally changed immediately after injections, but both demonstrated delayed dilatation. In contrast, HVR fell immediately but demonstrated delayed constriction. Identical changes occurred in intact rats and in those with interruption of the baroreflex by sinoaortic denervation. Ganglionic blockade with hexamethonium abolished virtually all L-glutamate-induced responses. This study suggests that NTS neurons exert differential effects on renal, mesenteric, and hindquarter vascular beds and that glutamate-induced regional hemodynamic changes are mediated predominantly through autonomic pathways.

Animals↗
PubMedDate not supplied

Paradoxical dilation of the large cerebral arteries in hypocapnia in man.

By grouping patients who had carotid angiograms under unusually carefully monitored conditions it has been shown that hypocapnia is associated with vasodilation at low blood pressure but not at high blood pressure. The mechanism is discussed in general terms and it is suggested that the hypocapnic vasodilation may be a response to cerebral hypoxia and may be transmitted via an intracerebral autonomic pathway. Clinical and angiographical diagnoses are given for 50 patients.

Adult↗
PubMed2003

Evidence for cell autonomous AP1 function in regulation of Drosophila motor-neuron plasticity.

BACKGROUND: The transcription factor AP1 mediates long-term plasticity in vertebrate and invertebrate central nervous systems. Recent studies of activity-induced synaptic change indicate that AP1 can function upstream of CREB to regulate both CREB-dependent enhancement of synaptic strength as well as CREB-independent increase in bouton number at the Drosophila neuromuscular junction (NMJ). However, it is not clear from this study if AP1 functions autonomously in motor neurons to directly modulate plasticity. RESULTS: Here, we show that Fos and Jun, the two components of AP1, are abundantly expressed in motor neurons. We further combine immunohistochemical and electrophysiological analyses with use of a collection of enhancers that tightly restrict AP1 transgene expression within the nervous system to show that AP1 induction or inhibition in, but not outside of, motor neurons is necessary and sufficient for its modulation of NMJ size and strength. CONCLUSION: By arguing against the possibility that AP1 effects at the NMJ occur via a polysynaptic mechanism, these observations support a model in which AP1 directly modulates NMJ plasticity processes through a cell autonomous pathway in the motor neuron. The approach described here may serve as a useful experimental paradigm for analyzing cell autonomy of genes found to influence structure and function of Drosophila motor neurons.

Animals↗
PubMed2005

An allelic series reveals essential roles for FY in plant development in addition to flowering-time control.

The autonomous pathway functions to promote flowering in Arabidopsis by limiting the accumulation of the floral repressor FLOWERING LOCUS C (FLC). Within this pathway FCA is a plant-specific, nuclear RNA-binding protein, which interacts with FY, a highly conserved eukaryotic polyadenylation factor. FCA and FY function to control polyadenylation site choice during processing of the FCA transcript. Null mutations in the yeast FY homologue Pfs2p are lethal. This raises the question as to whether these essential RNA processing functions are conserved in plants. Characterisation of an allelic series of fy mutations reveals that null alleles are embryo lethal. Furthermore, silencing of FY, but not FCA, is deleterious to growth in Nicotiana. The late-flowering fy alleles are hypomorphic and indicate a requirement for both intact FY WD repeats and the C-terminal domain in repression of FLC. The FY C-terminal domain binds FCA and in vitro assays demonstrate a requirement for both C-terminal FY-PPLPP repeats during this interaction. The expression domain of FY supports its roles in essential and flowering-time functions. Hence, FY may mediate both regulated and constitutive RNA 3'-end processing.

Alleles↗
PubMed1999

Role of the angiotensin II type-2 receptor in the mouse central nervous system.

There are two known major angiotensin II receptor subtypes, type 1 (AT1) and type 2 (AT2), both of which are present in the brain. AT1 and AT2 receptors occur in characteristic distributions that are highly correlated with the distribution of angiotensin II-like immunoreactivity in nerve terminals. Acting through the AT1 receptor in the central nervous system, angiotensin II has effects on fluid and electrolyte homeostasis, neuroendocrine systems, autonomic pathways regulating cardiovascular function and behavior. While the role of the AT2 receptor in the brain is less well understood, recent knockout studies point to their involvement in behavioral and cardiovascular functions. We discuss here evidence regarding the function of the AT2 receptor in the brain, determined using mice lacking the AT2 receptor.

Angiotensin II↗
PubMed2004

Differentiation of autonomic reflex control begins with cellular mechanisms at the first synapse within the nucleus tractus solitarius.

Visceral afferents send information via cranial nerves to the nucleus tractus solitarius (NTS). The NTS is the initial step of information processing that culminates in homeostatic reflex responses. Recent evidence suggests that strong afferent synaptic responses in the NTS are most often modulated by depression and this forms a basic principle of central integration of these autonomic pathways. The visceral afferent synapse is uncommonly powerful at the NTS with large unitary response amplitudes and depression rather than facilitation at moderate to high frequencies of activation. Substantial signal depression occurs through multiple mechanisms at this very first brainstem synapse onto second order NTS neurons. This review highlights new approaches to the study of these basic processes featuring patch clamp recordings in NTS brain slices and optical techniques with fluorescent tracers. The vanilloid receptor agonist, capsaicin, distinguishes two classes of second order neurons (capsaicin sensitive or capsaicin resistant) that appear to reflect unmyelinated and myelinated afferent pathways. The differences in cellular properties of these two classes of NTS neurons indicate clear functional differentiation at both the pre- and postsynaptic portions of these first synapses. By virtue of their position at the earliest stage of these pathways, such mechanistic differences probably impart important differentiation in the performance over the entire reflex pathways.

Baroreflex↗
PubMedDate not supplied

Coordination of sympathetic and respiratory systems: neurophysiological experiments.

Many sympathetic neurons exhibit respiratory rhythmicity in their activity which is due to a central coupling between respiratory neurons and neurons of autonomic pathways. The presence or absence and the pattern of this respiratory modulation depend on the function of sympathetic neurons and on the way by which both systems are coupled. In the cat, neurons supplying resistance vessels such as muscle vasoconstrictor and visceral vasoconstrictor neurons are activated during inspiration and suppressed during postinspiration. In contrast, most cutaneous vasoconstrictor neurons show no respiratory modulation in their activity, some are inhibited during inspiration and activated during expiration, and others exhibit a weak peak during inspiration. Sudomotor neurons are preferentially active during postinspiration and "inspiratory-type" neurons only during inspiration. In addition to the central coupling between presympathetic and respiratory neurons, cardiovascular afferents, notably the arterial baroreceptors, contribute an important peripheral reflex component of respiratory modulation, but only in neurons of muscle and visceral vasoconstrictor pathways.

Animals↗
PubMed1999

Distribution of NADPH-d and nNOS-IR in the thoracolumbar and sacrococcygeal spinal cord of the guinea pig.

The distribution of NADPH-d staining and neuronal nitric oxide synthase (nNOS)-immunoreactivity in the spinal cord of the guinea pig was studied to evaluate the potential role of nitric oxide in lumbosacral afferent and spinal autonomic pathways and to compare the distribution of these two markers to that observed in other species. NADPH-d staining and nNOS-immunoreactivity were present in neurons and fibers in the superficial dorsal horn, dorsal commissure and in neurons around the central canal in all levels of the spinal cord examined. Sympathetic preganglionic neurons in the thoracic and rostral lumbar segments identified by choline acetyl transferase (ChAT) immunoreactivity exhibited prominent NADPH-d staining and nNOS-immunoreactivity; whereas the ChAT-immunoreactive parasympathetic preganglionic neurons in the sacral segments were not stained. The most prominent NADPH-d staining in the sacral segments occurred in fibers extending from Lissauer's tract through laminae I along the lateral edge of the dorsal horn to the region of the sacral parasympathetic nucleus (lateral collateral pathway of Lissauer). These fibers were prominent in the S1-S3 segments but not in adjacent (L5-L7 and Cx1) or thoracolumbar segments. These NADPH-d fibers were, for the most part, not nNOS-immunoreactive, but did overlap with a prominent fiber bundle containing vasoactive intestinal polypeptide immunoreactivity in the sacral spinal cord. These results indicate that nitric oxide may function as a transmitter in thoracolumbar sympathetic preganglionic neurons, but not in sacral parasympathetic preganglionic neurons. Although the functional significance of the NADPH-d positive, nNOS-negative fiber bundle on the lateral edge of the sacral dorsal horn remains to be determined, this fiber tract may represent, in part, visceral afferent projections to the sacral parasympathetic nucleus.

Journal Article↗
PubMed2001

Disorders of the pupil.

The pupil is one objective marker of vision and autonomic pathways. A good understanding of its anatomy and careful examination techniques are the essential tools for proper clinical diagnosis of pupillary disorders.

Diagnostic Techniques, Ophthalmological↗
PubMedDate not supplied

[Gastroesophageal reflux: a pulmonologist's viewpoint].

Gastroesophageal reflux (GER) is a common situation that can express with digestive, extra-digestive, respiratory or otolaryngologic symptoms. Some chronic pulmonary disorders include in their setting GER as well. This review will address pathogenesis, clinical signs, complications and treatment of GER with a special focus towards the pulmonologist field. GER is a physiological post-prandial phenomenon of limited duration. It is induced by transient lower esophageal sphincter relaxation (tLESR) or by factors that impede LES function by reducing its tone or disrupting its contractions. Extra-digestive symptoms are caused by vagal stimulation through common autonomic pathways to the esophagus and bronchi. This reflex is triggered by gastric acid stimulation of esophageal receptors and by acid micro-aspirations into the airways. The responsibility of GER towards respiratory symptoms is often difficult to attest despite thorough investigations. Results of one to three-month treatment trial with proton pump inhibitors can be of value. Gastroesophageal assessment is mandatory as pulmonary manifestations might indicate disease severity.

Esophagogastric Junction↗
PubMed2003

[Central nervous control of erection].

Penile erection is caused by a change of the activity of efferent autonomic pathways to the erectile tissues and of somatic pathways to the perineal striated muscles. The sympathic outflow is mainly antierectile, the sacral parasympathic outflow is proerectile and the pudendal outflow, through contraction of the perineal striated muscles, enhances an erection already present. Spinal neurones controlling erection are activated by afferents from the genitals. It is likely that these primary afferents do not directly stimulate the spinal sympathetic, parasympathetic and somatic nuclei, but do through spinal interneurones. This spinal network is able of integrating information from periphery to elicit reflexive erections. It also receives supraspinal descending pathways from pons and hypothalamic nuclei, among the latter, the paraventricular nucleus and the medial preoptic area. These structures are likely involved to regulate penile erection in more integrated and coordinated responses occurring during sexual behavior. By receiving ascending projections from the spinal level which convoy informations from genitals, they could reinforce penile erection. Role of putative neuromediators or regulatory peptides is evoked.

Afferent Pathways↗
PubMed2004

[Cardiovascular risk factors, erection disorders and endothelium dysfunction].

Upon sexual stimulation, penile erection, occurring in response to the activation of pro-erectile autonomic pathways, is greatly dependent on adequate inflow of blood to the erectile tissue and requires coordinated arterial endothelium-dependent vasodilatation and sinusoidal endothelium-dependent corporal smooth muscle relaxation. Nitric oxide (NO) is the principal peripheral pro-erectile neurotransmitter which is released by both non-adrenergic, non-cholinergic neurons and the sinusoidal endothelium to relax corporal smooth muscle through the cGMP pathway. Any factors modifying the basal corporal tone, the arterial inflow of blood to the corpora, the synthesis/release of neurogenic or endothelial NO are prime suspects for being involved in the pathophysiology of erectile dysfunction (ED). In fact, conditions associated with altered endothelial function, such as ageing, hypertension, hypercholesterolemia and diabetes, may, by changing the balance between contractant and relaxant factors, cause circulatory and structural changes in penile tissues, resulting in arterial insufficiency and defect in smooth muscle relaxation and thus, ED. There is increasing evidence to suggest that ED is predominantly a vascular disease and may even be a marker for occult cardiovascular disease. Recent results illustrating the importance of endothelial dysfunction in the pathophysiology of different forms of experimental ED are discussed. These pathways may represent new potential treatment targets.

Animals↗
PubMed2005

The role of bombesin in the mechanism of pituitary hormones release.

OBJECTIVES: Functional studies indicate that bombesin may be involved in many physiological functions, including sensory transmission, the regulation of central autonomic pathways, thermoregulation, secretion of pituitary hormones, gastric and pancreatic secretion, food intake and satiety. MATERIAL AND METHODS: In order to evaluate the role of bombesin in the mechanism of pituitary hormones release the effects of bombesin on rGH, rTSH, rPRL, rFSH and rLH release were investigated in female Wistar-Kyoto rats. In studies 'in vitro' bombesin in a dose of 1nM, 10nM, 100nM was administered to pituitary cell culture. After 60, 120, 240 min. of incubation pituitary hormones were measured. In studies 'in vivo' bombesin was injected intraventricularly (icv) in a dose of 0.5 microg/5 microl aCSF (artificial cerebrospinal fluid) for 5 min. (experiment I). In experiment II bombesin was administered intravenously (iv) in a dose of 10 microg. After 60 min, 120 mins the animals were decapitated and serum rGH, rPRL, rTSH, rLH, rFSH concentrations were measured with RIA methods. RESULTS: Bombesin stimulated rLH, rPRL, rTSH release from cultured pituitary cells. A slight increase of GH was also observed. After intravenous (iv) injection of bombesin an increase in serum rPRL and rGH levels was found. However, the intraventricular (icv) administration of bombesin leads to decrease of serum rGH, rPRL and rTSH concentrations. CONCLUSION: Our studies 'in vitro' and 'in vivo' indicate that bombesin may be involved in the modulation of pituitary hormones release.

Animals↗
PubMed1989

Bombesin-like peptides as growth factors.

Bombesin-like peptides (BN-LP) are involved in the regulation of many important functions, including sensory transmission, regulation of central autonomic pathways, thermoregulation, pituitary, gastric and pancreatic secretion, food intake and satiety. They also stimulate cellular proliferation in a developmental and tissue-specific manner. Their role in pathogenesis appears to be related to their properties as growth factors, especially in the lung, where BN-LP can induce growth of normal and neoplastic epithelial cells. The formulated hypothesis of autocrine control of small cell lung cancer growth by BN-LP will be tested using specific synthetic bombesin antagonists.

Animals↗