Streptozotocin-induced diabetes in rats causes neuronal deficits in tyrosine hydroxylase and 5-hydroxytryptamine specific to mesenteric perivascular sympathetic nerves and without loss of nerve fibers

1991 ◽  
Vol 113 (1) ◽  
pp. 53-62 ◽  
Author(s):  
G.J.M. Webster ◽  
E.W.A. Petch ◽  
T. Cowen
1982 ◽  
Vol 243 (2) ◽  
pp. H175-H180 ◽  
Author(s):  
P. G. Schmid ◽  
D. D. Lund ◽  
J. A. Davis ◽  
C. A. Whiteis ◽  
R. K. Bhatnagar ◽  
...  

Selective pressure overload of the right ventricle in guinea pigs resulted in early and sustained reductions in tyrosine hydroxylase and dopamine-beta-hydroxylase activities in the right ventricle. No changes in tyrosine hydroxylase activity were detected in stellate ganglia sinoatrial (SA) nodal region, atrioventricular (AV) nodal region, or left ventricle. Reductions in tyrosine hydroxylase activity in stressed right ventricle were similar regardless of duration of pulmonary artery constriction, extent of hypertrophy, presence or absence of hepatic congestion, and preservation or depletion of catecholamines. The changes may represent localized loss of sympathetic nerve fibers; factors involved directly in the process of pressure-overload-induced hypertrophy may be responsible. However, sympathetic nerves remaining in hypertrophied ventricle respond normally to cold-induced sympathetic activation. The reduction in tyrosine hydroxylase activity and the maintenance of norepinephrine turnover in residual innervation to hypertrophied right ventricle support the concept that sympathetic neural regulation of hypertrophied cardiac tissue is altered but not lost.


2021 ◽  
Vol 22 (15) ◽  
pp. 8222
Author(s):  
Dmitry Otlyga ◽  
Ekaterina Tsvetkova ◽  
Olga Junemann ◽  
Sergey Saveliev

The evolutionary and ontogenetic development of the carotid body is still understudied. Research aimed at studying the comparative morphology of the organ at different periods in the individual development of various animal species should play a crucial role in understanding the physiology of the carotid body. However, despite more than two centuries of study, the human carotid body remains poorly understood. There are many knowledge gaps in particular related to the antenatal development of this structure. The aim of our work is to study the morphological and immunohistochemical characteristics of the human carotid body in the antenatal and postnatal periods of development. We investigated the human carotid bodies from 1 embryo, 20 fetuses and 13 adults of different ages using samples obtained at autopsy. Immunohistochemistry revealed expression of βIII-tubulin and tyrosine hydroxylase in the type I cells and nerve fibers at all periods of ontogenesis; synaptophysin and PGP9.5 in the type I cells in some of the antenatal cases and all of the postnatal cases; 200 kDa neurofilaments in nerve fibers in some of the antenatal cases and all of the postnatal cases; and GFAP and S100 in the type II cells and Schwann cells in some of the antenatal cases and all of the postnatal cases. A high level of tyrosine hydroxylase in the type I cells was a distinctive feature of the antenatal carotid bodies. On the contrary, in the type I cells of adults, the expression of tyrosine hydroxylase was significantly lower. Our data suggest that the human carotid body may perform an endocrine function in the antenatal period, while in the postnatal period of development, it loses this function and becomes a chemosensory organ.


1977 ◽  
Vol 233 (5) ◽  
pp. H535-H540
Author(s):  
L. S. D'Agrosa

The effects of ventrolateral and ventromedial cardiac nerve (left sympathetics) stimulation on cardiac force, on rate, and on arrhythmogenic responses were characterized and quantitated. The stimulation of left sympathetic nerves produced augmentation in cardiac contraction in 45% of the experiments, an augmentation of both a cardiac rate and force in 47%, and in cardioacceleration alone in 8%. Two characteristic patterns of arrhythmogenic responses were elicited from stimulations of 100 sympathetic nerves. The two types of neurally induced arrhythmias were atrioventricular junctional or ventricular in origin. The onset and duration of the arrhythmias were quantitated. Both types of neurally induced arrhythmias were prevented either by blocking the beta receptors with propranolol or by preventing the neural release of norepinephrine with bretylium tosylate. The neurally induced arrhythmias were probably the result of enhanced automaticity in the atrioventricular junction area and in the ventricles produced by stimulating the sympathetic nerve fibers. This report thus implicates the ventromedial cardiac nerve in the genesis of cardiac arrhythmias.


2021 ◽  
Vol 27 ◽  
Author(s):  
Sergey V. Dindyaev ◽  
Narasimha M Beeraka ◽  
Denis V. Kasatkin ◽  
Elizaveta V. Mikhaylenko ◽  
Siva G. Somasundaram ◽  
...  

Background: Biogenic amines (BAs) secreted by the sympathetic neural apparatus of rat uterus is reported to be conducive to the uterine functional activity during postpartum involution; the imbalance in BAs ratio could confer postpartum reproductive disorders including improper postpartum involution. Objective: The changes in density of uterine sympathetic nerves implicated in the pathology of endometriosis, adenomyosis, and delayed uterine involution. The present study is aimed to ascertain ‘serotonin’ and ‘catecholamine’ concentrations in mesenteric mast cells (MCs), and structural elements of nerve fibers across the perivascular plexuses (PPs) and single sympathetic nerve terminals (SST). Methods: Furthermore, the density of their spatial distribution (SDP and SDT) in the uterine body, cervix, and mesometrium was determined during postpartum involution. Tissue specimens of postpartum uterus were obtained from 55 nulliparous female Wistar outbred strain rats, which were grouped according to the days after parturition at the time of sacrifice. The nerve fibers of PP and SST exhibited emerald green fluorescence, which was detected by glyoxylic acid fluorescence technique; the fluorescence invoked by BAs was identified by microspectrofluorimetry. Results: Concentrations of BAs were extensive in the varicosities of PP and SST on the 10th day. However, the highest BA concentrations were found in structural elements of PP in the uterine mesometrium in the initial days of postpartum. In mesenteric MC, serotonin and catecholamines were at the highest concentration on 10th day postpartum. Histamines peaked on the 6th day. Conclusion: SDP and SDT were increased significantly in all structural elements of uterine nerve fibers in the uterine body and cervix compared to SDP in mesentery. Considering that catecholamines and serotonin are antagonists in many aspects of their biological action, the ratio of BAs should be well-balanced to maintain anabolic-catabolic equilibrium in the rat uterus.


1998 ◽  
Vol 274 (3) ◽  
pp. R626-R634 ◽  
Author(s):  
Graeme Eisenhofer ◽  
Bengt Rundqvist ◽  
Peter Friberg

This study assessed whether the mechanisms regulating cardiac norepinephrine (NE) synthesis with changes in NE release are influenced by functions of sympathetic nerves affecting transmitter turnover independently of transmitter release. Differences in arterial and coronary venous plasma concentrations of NE and its metabolites and of dihydroxyphenylalanine (DOPA), the immediate product of tyrosine hydroxylase (TH), were examined before and during cycling exercise. Relative increases during exercise in cardiac tyrosine hydroxylation (as reflected by the %increase in cardiac DOPA spillover) matched closely corresponding increases in NE turnover, but were much lower than increases in NE release. The much larger relative increases in release than turnover of NE were largely attributable to the extensive contribution to transmitter turnover from intraneuronal metabolism of NE leaking from storage vesicles. This contribution remains unchanged during sympathetic activation so that the relative increase in NE turnover is much smaller than that in exocytotic release of NE. To replenish the NE lost from stores during sympathetic activation, TH activity need increase only in proportion to the smaller increase in turnover rather than the larger relative increase in release. The ability to “gear down” increases in tyrosine hydroxylation relative to increases in NE release provides sympathetic nerves the capacity for a more extended range of sustainable release rates than otherwise possible.


1997 ◽  
Vol 273 (6) ◽  
pp. E1194-E1202 ◽  
Author(s):  
Thomas O. Mundinger ◽  
C. Bruce Verchere ◽  
Denis G. Baskin ◽  
Michael R. Boyle ◽  
Stephan Kowalyk ◽  
...  

Stimulation of canine hepatic nerves releases the neuropeptide galanin from the liver; therefore, galanin may be a sympathetic neurotransmitter in the dog liver. To test this hypothesis, we used immunocytochemistry to determine if galanin is localized in hepatic sympathetic nerves and we used hepatic sympathetic denervation to verify such localization. Liver sections from dogs were immunostained for both galanin and the sympathetic enzyme marker tyrosine hydroxylase (TH). Galanin-like immunoreactivity (GALIR) was colocalized with TH in many axons of nerve trunks as well as individual nerve fibers located both in the stroma of hepatic blood vessels and in the liver parenchyma. Neither galanin- nor TH-positive cell bodies were observed. Intraportal 6-hydroxydopamine (6-OHDA) infusion, a treatment that selectively destroys hepatic adrenergic nerve terminals, abolished the GALIR staining in parenchymal neurons but only moderately diminished the GALIR staining in the nerve fibers around blood vessels. To confirm that 6-OHDA pretreatment proportionally depleted galanin and norepinephrine in the liver, we measured both the liver content and the hepatic nerve-stimulated spillover of galanin and norepinephrine from the liver. Pretreatment with 6-OHDA reduced the content and spillover of both galanin and norepinephrine by >90%. Together, these results indicate that galanin in dog liver is primarily colocalized with norepinephrine in sympathetic nerves and may therefore function as a hepatic sympathetic neurotransmitter.


1992 ◽  
Vol 249 (1) ◽  
Author(s):  
T. Uno ◽  
Y. Hisa ◽  
Y. Murakami ◽  
H. Okamura ◽  
Y. Ibata

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