ROLE OF SYMPATHETIC NERVES IN THE METABOLISM OF EXOGENOUS NORADRENALINE IN RABBIT GINGIVAL TISSUE AND EAR ARTERY

1986 ◽  
Vol 64 (6) ◽  
pp. 505-516 ◽  
Author(s):  
I Parker ◽  
DAS Parker ◽  
IS Lande ◽  
JA Thompson ◽  
C Proctor ◽  
...  
Keyword(s):  
Sympathetic Nerves ◽  
Gingival Tissue ◽  
Ear Artery

Peripheral muscarinic control of norepinephrine release in the cardiovascular system

1980 ◽  
Vol 239 (6) ◽  
pp. H713-H720 ◽  
Author(s):  
E. Muscholl
Keyword(s):  
Physiological Role ◽  
Sympathetic Nerves ◽  
Adrenergic Nerve ◽  
Sequence Of Events ◽  
Adrenergic Response ◽  
Adrenergic Nerve Terminals ◽  
Muscarinic Cholinergic ◽  
Related Compounds ◽  
Stimulation Of

Activation of muscarinic cholinergic receptors located at the terminal adrenergic nerve fiber inhibits the process of exocytotic norepinephrine (NE) release. This neuromodulatory effect of acetylcholine and related compounds has been discovered as a pharmacological phenomenon. Subsequently, evidence for a physiological role of the presynaptic muscarinic inhibition was obtained on organs known to be innervated by the autonomic ground plexus (Hillarp, Acta. Physiol. Scand. 46, Suppl. 157: 1-68, 1959) in which terminal adrenergic and cholinergic axons run side by side. Thus, in the heart electrical vagal stimulation inhibits the release of NE evoked by stimulation of sympathetic nerves, and this is reflected by a corresponding decrease in the postsynaptic adrenergic response. On the other hand, muscarinic antagonists such as atropine enhance the NE release evoked by field stimulation of tissues innervated by the autonomic ground plexus. The presynaptic muscarine receptor of adrenergic nerve terminals probably restricts the influx of calcium ions that triggers the release of NE. However, the sequence of events between recognition of the muscarinic compound by the receptor and the process of exocytosis still remains to be clarified.

Role of Cardiac Sympathetic Nerves in the Genesis of Myocardial Ischemia Distal to Coronary Stenoses

1985 ◽  
Vol 7 ◽  
pp. S13-S18 ◽  
Author(s):  
Gerd Heusch ◽  
Andreas Deussen ◽  
Jochen Schipke ◽  
Holger Vogelsang ◽  
Vera Hoffmann ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Sympathetic Nerves ◽  
Coronary Stenoses

scholarly journals Role of Cathepsin S in Periodontal Inflammation and Infection

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
S. Memmert ◽  
A. Damanaki ◽  
A. V. B. Nogueira ◽  
S. Eick ◽  
M. Nokhbehsaim ◽  
...  
Keyword(s):  
Periodontal Diseases ◽  
Interleukin 1 ◽  
Critical Role ◽  
Gingival Tissue ◽  
Cathepsin S ◽  
Protein Levels ◽  
Periodontal Inflammation

Cathepsin S is a cysteine protease and regulator of autophagy with possible involvement in periodontitis. The objective of this study was to investigate whether cathepsin S is involved in the pathogenesis of periodontal diseases. Human periodontal fibroblasts were cultured under inflammatory and infectious conditions elicited by interleukin-1β and Fusobacterium nucleatum, respectively. An array-based approach was used to analyze differential expression of autophagy-associated genes. Cathepsin S was upregulated most strongly and thus further studied in vitro at gene and protein levels. In vivo, gingival tissue biopsies from rats with ligature-induced periodontitis and from periodontitis patients were also analyzed at transcriptional and protein levels. Multiple gene expression changes due to interleukin-1β and F. nucleatum were observed in vitro. Both stimulants caused a significant cathepsin S upregulation. A significantly elevated cathepsin S expression in gingival biopsies from rats with experimental periodontitis was found in vivo, as compared to that from control. Gingival biopsies from periodontitis patients showed a significantly higher cathepsin S expression than those from healthy gingiva. Our findings provide original evidence that cathepsin S is increased in periodontal cells and tissues under inflammatory and infectious conditions, suggesting a critical role of this autophagy-associated molecule in the pathogenesis of periodontitis.

Renal denervation alters cardiovascular and endocrine responses to hemorrhage in conscious newborn lambs

1998 ◽  
Vol 275 (1) ◽  
pp. H285-H291 ◽  
Author(s):  
Francine G. Smith ◽  
Isam Abu-Amarah
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Renal Denervation ◽  
Plasma Renin ◽  
Sympathetic Nerves ◽  
Renal Nerves ◽  
Elevated Plasma ◽  
Baseline Levels ◽  
Renal Sympathetic

To investigate the role of renal sympathetic nerves in modulating cardiovascular and endocrine responses to hemorrhage early in life, we carried out three experiments in conscious, chronically instrumented lambs with intact renal nerves (intact; n = 8) and with bilateral renal denervation (denervated; n = 5). Measurements were made 1 h before and 1 h after 0, 10, and 20% hemorrhage. Blood pressure decreased transiently after 20% hemorrhage in intact lambs and returned to control levels. In denervated lambs, however, blood pressure remained decreased after 60 min. After 20% hemorrhage, heart rate increased from 170 ± 16 to 207 ± 18 beats/min in intact lambs but not in denervated lambs, in which basal heart rates were already elevated to 202 ± 21 beats/min. Despite an elevated plasma renin activity (PRA) measured in denervated (12.0 ± 6.4 ng ANG I ⋅ ml−1 ⋅ h−1) compared with intact lambs (4.0 ± 1.1 ng ANG I ⋅ ml−1 ⋅ h−1), the increase in PRA in response to 20% hemorrhage was similar in both groups. Plasma levels of arginine vasopressin increased from 11 ± 8 to 197 ± 246 pg/ml after 20% hemorrhage in intact lambs but remained unaltered in denervated lambs from baseline levels of 15 ± 10 pg/ml. These observations provide evidence that in the newborn, renal sympathetic nerves modulate cardiovascular and endocrine responses to hemorrhage.

scholarly journals Laporan Kasus: Manifestasi Oral Penderita Hipertensi berupa Ginggival Enlargement

2020 ◽  
Vol 17 (2) ◽  
pp. 54
Author(s):  
Anindita L. ◽  
Aris Aji K. ◽  
Arcadia Sulistijo J.
Keyword(s):  
Case Reports ◽  
Gingival Tissue ◽  
High Dose ◽  
Gingival Inflammation ◽  
Gingival Enlargement ◽  
History Of ◽  
Root Planning ◽  
Pro Inflammatory Cytokines

Hypertension presents an increase in blood pressure following the oral manifestations, such as gingival enlargement. A 42-year-old woman came to the General Sudirman University Dental and Oral Hospital complaining of enlarged front gums seven years ago. The patient had a history of hypertension and regularly consumed drugs, amlodipine 5 mg. Extraoral examination revealed no lymphadenopathy and no swelling of the head and neck area. Intraoral examination revealed a gingival enlargement involving the papilla to the gingival margin present on the entire upper and lower labial gingival surface. The patient's diagnosis was gingival enlargement caused by gingival enlargement due to the use of amlodipine. Gingival enlargement has been noted with long-term or high-dose amlodipine use. The mechanism of amlodipine in causing gingival enlargement is through the role of fibroblasts with abnormal susceptibility to the drug, resulting in increased levels of protein synthesis, especially collagen. The role of pro-inflammatory cytokines occurs through an increase in interleukin-1β (IL-1β) and IL-6 in the inflamed gingival tissue due to the gingival fibrogenic response to drugs. Therapies were DHE and scaling and root planning as phase I in periodontal treatment. Plaque elimination is vital to reduce gingival inflammation that may occur. Substitution of the drug amlodipine may be needed if there is no improvement. Based on case reports, hypertension patients who took amlodipine could have gingival enlargement. The therapy given was plaque elimination in the form of DHE and Scaling and regular check-ups with the dentist.

Nasopharyngeal reflexes: role of brain monoamines in central integration. a review

1988 ◽  
Vol 66 (1) ◽  
pp. 173-181
Author(s):  
Saxon White ◽  
Anthony Quail
Keyword(s):  
Functional Anatomy ◽  
Sympathetic Nerves ◽  
Lung Inflation ◽  
Independent Mechanism ◽  
Vagal Nerves ◽  
Intact Brain ◽  
Output Component ◽  
Trigeminal Nerves ◽  
Arterial Baroreceptor

The nasopharyngeal reflex in the rabbit (respiratory suppression, activation of vagal and sympathetic nerves, and reduction in oxygen usage) is initiated by trigeminal nerves and is enhanced by the arterial baroreceptor and by loss of lung inflation afferent activity. A review of (i) the functional anatomy of central nervous catecholamine and 5-hydroxytryptamine pathways participating in cardiorespiratory regulation, (ii) studies of the reflex in pontine, thalamic, and intact-brain rabbits in which the arterial baroreceptor and lung inflation inputs were manipulated, and (iii) studies of the reflex in rabbits in which central nervous catecholamine and 5-hydroxytryptamine were depleted indicates that the trigeminal nerve can initiate the reflex pattern during maintained ventilation at the ponto-medullo-spinal level through interactions that may include convergence with glossopharyngeal and vagal nerves in the nucleus of the solitary tract. By contrast, loss of lung inflation activity in itself activates vagal and sympathetic pathways through interactions with arterial baroreceptor activity and diencephalic influences. The vagal output component of the reflex is relatively independent of either central nervous monoamine, but the sympathetic vasoconstrictor component appears clearly dependent on central nervous catecholamine and, to a much lesser extent, on 5-hydroxytryptamine. Both monoamines play a role in respiratory suppression. Pentobarbitone blocks centrally the vagal output component of the nasopharyngeal reflex by a monoamine-independent mechanism. The findings provide a framework for testing postulates concerning central nervous catecholamine integration and neurotransmitter control of submergence reflexes in diving species.

scholarly journals Neutrophil Extracellular Traps in Periodontitis

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1494 ◽  
Author(s):  
Antonio Magán-Fernández ◽  
Sarmad Muayad Rasheed Al-Bakri ◽  
Francisco O’Valle ◽  
Cristina Benavides-Reyes ◽  
Francisco Abadía-Molina ◽  
...  
Keyword(s):  
Current Knowledge ◽  
Decisive Role ◽  
Neutrophil Extracellular Traps ◽  
Gingival Tissue ◽  
Multifactorial Disease ◽  
Extracellular Traps ◽  
Wide Range ◽  
Neutrophil Response ◽  
Inflammatory Component

Neutrophils are key cells of the immune system and have a decisive role in fighting foreign pathogens in infectious diseases. Neutrophil extracellular traps (NETs) consist of a mesh of DNA enclosing antimicrobial peptides and histones that are released into extracellular space following neutrophil response to a wide range of stimuli, such as pathogens, host-derived mediators and drugs. Neutrophils can remain functional after NET formation and are important for periodontal homeostasis. Periodontitis is an inflammatory multifactorial disease caused by a dysbiosis state between the gingival microbiome and the immune response of the host. The pathogenesis of periodontitis includes an immune-inflammatory component in which impaired NET formation and/or elimination can be involved, contributing to an exacerbated inflammatory reaction and to the destruction of gingival tissue. In this review, we summarize the current knowledge about the role of NETs in the pathogenesis of periodontitis.

scholarly journals Pro‐contractile role of chloride in arterial smooth muscle: Postnatal decline potentially governed by sympathetic nerves

2019 ◽  
Vol 104 (7) ◽  
pp. 1018-1022 ◽  
Author(s):  
Daria S. Kostyunina ◽  
Dina K. Gaynullina ◽  
Vladimir V. Matchkov ◽  
Olga S. Tarasova
Keyword(s):  
Smooth Muscle ◽  
Sympathetic Nerves ◽  
Arterial Smooth Muscle

Physiology in perspective: The Wisdom of the Body. Neural control of the kidney

2005 ◽  
Vol 289 (3) ◽  
pp. R633-R641 ◽  
Author(s):  
Gerald F. DiBona
Keyword(s):  
Nervous System ◽  
Renal Function ◽  
Autonomic Nervous System ◽  
Neural Control ◽  
Sympathetic Nerves ◽  
The Body ◽  
Regulatory Agencies ◽  
Internal Environment ◽  
Renal Sympathetic

Cannon equated the fluid matrix of the body with Bernard’s concept of the internal environment and emphasized the importance of “the safe-guarding of an effective fluid matrix.” He further emphasized the important role of the autonomic nervous system in the establishment and maintenance of homeostasis in the internal environment. This year’s Cannon Lecture discusses the important role of the renal sympathetic nerves to regulate various aspects of overall renal function and to serve as one of the major “self-regulatory agencies which operate to preserve the constancy of the fluid matrix.”

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