Gene expression of tyrosine hydroxylase and neuropeptide Y in prevertebral ganglia of renal hypertensive rats

1991 ◽  
Vol 261 (6) ◽  
pp. R1455-R1460
Author(s):  
T. L. Krukoff ◽  
Y. Zheng
Keyword(s):  
Gene Expression ◽  
Tyrosine Hydroxylase ◽  
Neuropeptide Y ◽  
Adrenal Glands ◽  
Renal Hypertension ◽  
Male Rats ◽  
Mrna Levels ◽  
Hypertensive Rats ◽  
Prevertebral Ganglia ◽  
Th Mrna

The gene expression of tyrosine hydroxylase (TH) and neuropeptide Y (NPY) was studied in prevertebral ganglia and adrenal glands of adult male rats during the development of renal hypertension (removal of 1 kidney/constriction of other kidney). Only tissues from rats with arterial pressures significantly elevated by day 3 were compared with those from controls. At 4 or 5 days after renal surgery, superior cervical ganglia, celiac-mesenteric plexus, adrenal glands, and stellate ganglia were surgically removed from nonfixed rats for Northern blot analysis or from perfusion-fixed rats for in situ hybridization. In all tissues, levels of TH mRNA were decreased in hypertensive rats; cells with decreased levels were scattered throughout each tissue. In contrast, levels of NPY mRNA were unchanged in hypertensive rats compared with controls. Changes in TH mRNA levels suggest that the developing phase of renal hypertension is associated with a decrease in sympathetic outflow to the periphery. In contrast, the failure of NPY mRNA levels to change suggests a different regulatory mechanism for NPY expression or a different role for NPY in sympathetic neurotransmission.

Role of Neuropeptide Y in the Regulation of Tyrosine Hydroxylase Gene Expression in Rat Adrenal Glands

1995 ◽  
Vol 61 (1) ◽  
pp. 85-88 ◽  
Author(s):  
Min Hong ◽  
Songyun Li ◽  
Alain Fournier ◽  
Serge St.-Pierre ◽  
Georges Pelletier
Keyword(s):  
Gene Expression ◽  
Tyrosine Hydroxylase ◽  
Neuropeptide Y ◽  
Adrenal Glands ◽  
Tyrosine Hydroxylase Gene ◽  
Hydroxylase Gene

scholarly journals Differential regulation of catecholamine synthesis and transport in rat adrenal medulla by fluoxetine treatment

2015 ◽  
Vol 87 (1) ◽  
pp. 343-350 ◽  
Author(s):  
NATASA SPASOJEVIC ◽  
PREDRAG JOVANOVIC ◽  
SLADJANA DRONJAK
Keyword(s):  
Gene Expression ◽  
Tyrosine Hydroxylase ◽  
Adrenal Medulla ◽  
Norepinephrine Transporter ◽  
Male Rats ◽  
Mild Stress ◽  
Mrna Levels ◽  
Catecholamine Synthesis ◽  
Fluoxetine Treatment ◽  
Chronic Fluoxetine

We have recently shown that chronic fluoxetine treatment acted significantly increasing plasma norepinephrine and epinephrine concentrations both in control and chronically stressed adult male rats. However, possible effects of fluoxetine on catecholamine synthesis and re-uptake in adrenal medulla have been largely unknown. In the present study the effects of chronic fluoxetine treatment on tyrosine hydroxylase, a rate-limiting enzyme in catecholamine synthesis, as well as a norepinephrine transporter and vesicular monoamine transporter 2 gene expressions in adrenal medulla of animals exposed to chronic unpredictable mild stress (CUMS) for 4 weeks, were investigated. Gene expression analyses were performed using a real-time quantitative reverse transcription-PCR. Chronically stressed animals had increased tyrosine hydroxylase mRNA levels and decreased expression of both transporters. Fluoxetine increased tyrosine hydroxylase and decreased norepinephrine transporter gene expression in both unstressed and CUMS rats. These findings suggest that chronic fluoxetine treatment increased plasma catecholamine levels by affecting opposing changes in catecholamine synthesis and uptake.

Alteration of Atrial Natriuretic Peptide and Brain Natriuretic Peptide Gene Expression Associated with Progression and Regression of Cardiac Hypertrophy in Renovascular Hypertensive Rats

1996 ◽  
Vol 90 (3) ◽  
pp. 197-204 ◽  
Author(s):  
Hideo Kawakami ◽  
Hideki Okayama ◽  
Mareomi Hamada ◽  
Kunio Hiwada
Keyword(s):  
Gene Expression ◽  
Atrial Natriuretic Peptide ◽  
Cardiac Hypertrophy ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Mrna Levels ◽  
Hypertensive Rats ◽  
Regression Of Cardiac Hypertrophy ◽  
Peptide Gene ◽  
Atrial Natriuretic

1. We assessed the changes of atrial natriuretic peptide and brain natriuretic peptide gene expression associated with progression and regression of cardiac hypertrophy in renovascular hypertensive rats (RHR). 2. Two-kidney, one-clip hypertensive rats (6-week-old male Wistar) were made and studied 6 (RHR-1) and 10 weeks (RHR-2) after the procedure. Regression of cardiac hypertrophy was induced by nephrectomy at 6 weeks after constriction, and the nephrectomized rats were maintained further for 4 weeks (nephrectomized rat: NEP). Sham operation was performed, and the rats were studied after 6 (Sham-1) and 10 weeks (Sham-2). Atrial natriuretic peptide and brain natriuretic peptide gene expression in the left ventricle was analysed by Northern blotting. 3. Plasma atrial natriuretic peptide and brain natriuretic peptide were significantly higher in RHR-1 and RHR-2 than in Sham-1, Sham-2 and NEP. Atrial natriuretic peptide and brain natriuretic peptide mRNA levels in RHR-1 were approximately 7.2-fold and 1.8-fold higher than those in Sham-1, respectively, and the corresponding levels in RHR-2 were 13.0-fold and 2.4-fold higher than those in Sham-2, respectively. Atrial natriuretic peptide and brain natriuretic peptide mRNA levels of NEP were normalized. Levels of atrial natriuretic peptide and brain natriuretic peptide mRNA were well correlated positively with left ventricular weight/body weight ratios. There was a significant positive correlation between the levels of atrial natriuretic peptide and brain natriuretic peptide mRNA (r = 0.86, P<0.01). 4. We conclude that the expression of atrial natriuretic peptide and brain natriuretic peptide genes is regulated in accordance with the degree of myocardial hypertrophy and that the augmented expression of these two natriuretic peptides may play an important role in the maintenance of cardiovascular haemodynamics in renovascular hypertension.

Differing temporal roles of Ca2+ and cAMP in nicotine-elicited elevation of tyrosine hydroxylase mRNA

1999 ◽  
Vol 276 (1) ◽  
pp. C54-C65 ◽  
Author(s):  
Volodia D. Gueorguiev ◽  
Richard J. Zeman ◽  
Bhargava Hiremagalur ◽  
Ana Menezes ◽  
Esther L. Sabban
Keyword(s):  
Gene Expression ◽  
Tyrosine Hydroxylase ◽  
Camp Response Element Binding ◽  
Second Phase ◽  
Channel Blockers ◽  
Nicotine Treatment ◽  
Transient Rise ◽  
Element Binding Protein ◽  
Intracellular Ca ◽  
Th Mrna

The involvement of cAMP- and Ca2+-mediated pathways in the activation of tyrosine hydroxylase (TH) gene expression by nicotine was examined in PC-12 cells. Extracellular Ca2+ and elevations in intracellular Ca2+ concentration ([Ca2+]i) were required for nicotine to increase TH mRNA. The nicotine-elicited rapid rise in [Ca2+]iwas inhibited by blockers of either L-type or N-type, and to a lesser extent P/Q-, but not T-type, voltage-gated Ca2+ channels. With continual nicotine treatment, [Ca2+]ireturned to basal levels within 3–4 min. After a lag of ∼5–10 min, there was a smaller elevation in [Ca2+]ithat persisted for 6 h and displayed different responsiveness to Ca2+ channel blockers. This second phase of elevated [Ca2+]iwas blocked by an inhibitor of store-operated Ca2+ channels, consistent with the observed generation of inositol trisphosphate. 1,2-Bis(2-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid-AM (BAPTA-AM), when added before or 2 h after nicotine, prevented elevation of TH mRNA. Nicotine treatment significantly raised cAMP levels. Addition of the adenylyl cyclase inhibitor 2′,5′-dideoxyadenosine (DDA) prevented the nicotine-elicited phosphorylation of cAMP response element binding protein. DDA also blocked the elevation of TH mRNA only when added after the initial transient rise in [Ca2+]iand not after 1 h. This study reveals that several temporal phases are involved in the induction of TH gene expression by nicotine, each of them with differing requirements for Ca2+ and cAMP.

scholarly journals Upregulation of Kiss-1 and Gpr54 Genes Expression in Pituitary of Male Rats Following the Central Administration of Neuropeptide Y

2019 ◽  
Vol 4 (4) ◽  
pp. 137-142
Author(s):  
Vahid Azizi ◽  
Shahrbanoo Oryan ◽  
Homayuon Khazali ◽  
Abdolkarim Hosseini
Keyword(s):  
Gene Expression ◽  
Pituitary Gland ◽  
Neuropeptide Y ◽  
Wistar Rats ◽  
Third Ventricle ◽  
Male Rats ◽  
Control Group ◽  
Central Administration ◽  
Reproductive Axis ◽  
Male Wistar Rats

Introduction: The neuropeptide Y (NPY) in the neural circuits of the hypothalamus has a stimulating effect on reproductive activities in mammals. Kisspeptin (KiSS1) is a quintessential neurotransmitter in the reproductive axis which directly stimulates gonadotropin-releasing hormone neurons in the hypothalamus. The distribution of KiSS1 expressing cells in the pituitary was described previously. Despite earlier reports showing the KiSS1 receptor, G-protein coupled receptor 54 (GPR54) expression in the pituitary, the potential physiological roles of kisspeptin at this gland have remained obscure. Accordingly, this study investigated the role of NPY on the relative expression of Kiss1 and Gpr54 genes in the pituitary gland in male Wistar rats. Methods: In general, 20 male Wistar rats weighing 200-250 g in 4 groups (5 in each group) received saline, NPY (2.3 nM), BIBP3226 (NPY receptor antagonist, 7.8 nM), and NPY+ BIBP3226. Then, they received the simultaneous injection of these molecules through the third ventricle of the brain. Finally, the relative mean expressions of Kiss1 and Gpr54 genes in the anterior pituitary were quantitatively analyzed by the real-time polymerase chain reaction. Results: The central injection of NPY increased the relative mean expressions of Kiss1 and Gpr54 genes in the pituitary gland compared to the control group although the injection of BIBP3226 eradicated these effects. However, the gene expression of Gpr54 in the rats receiving NPY coupled with BIBP3226 in hypophysis in comparison to the group receiving only NPY demonstrated a significant reduction (P<0.05). Conclusion: Overall, the central injection of NPY stimulated the gene expression of Kiss1 and Gpr54 in the pituitary gland.

scholarly journals Effects of Insulin Treatment without and with Recurrent Hypoglycemia on Hypoglycemic Counterregulation and Adrenal Catecholamine-Synthesizing Enzymes in Diabetic Rats

Endocrinology ◽  
2006 ◽  
Vol 147 (4) ◽  
pp. 1860-1870 ◽  
Author(s):  
Karen E. Inouye ◽  
Jessica T. Y. Yue ◽  
Owen Chan ◽  
Tony Kim ◽  
Eitan M. Akirav ◽  
...  
Keyword(s):  
Tyrosine Hydroxylase ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
Hyperinsulinemic Hypoglycemia ◽  
Mrna Levels ◽  
Relevant Model ◽  
Counterregulatory Hormones ◽  
Catecholamine Synthesizing Enzymes ◽  
Recurrent Hypoglycemia ◽  
Th Mrna

Untreated diabetic rats show impaired counterregulation against hypoglycemia. The blunted epinephrine responses are associated with reduced adrenomedullary tyrosine hydroxylase (TH) mRNA levels. Recurrent hypoglycemia further impairs epinephrine counterregulation and is also associated with reduced phenylethanolamine N-methyltransferase mRNA. This study investigated the adaptations underlying impaired counterregulation in insulin-treated diabetic rats, a more clinically relevant model. We studied the effects of insulin treatment on counterregulatory hormones and adrenal catecholamine-synthesizing enzymes and adaptations after recurrent hypoglycemia. Groups included: normal; diabetic, insulin-treated for 3 wk (DI); and insulin-treated diabetic exposed to seven episodes (over 4 d) of hyperinsulinemic-hypoglycemia (DI-hypo) or hyperinsulinemic-hyperglycemia (DI-hyper). DI-hyper rats differentiated the effects of hyperinsulinemia from those of hypoglycemia. On d 5, rats from all groups were assessed for adrenal catecholamine-synthesizing enzyme levels or underwent hypoglycemic clamps to examine counterregulatory responses. Despite insulin treatment, fasting corticosterone levels remained increased, and corticosterone responses to hypoglycemia were impaired in DI rats. However, glucagon, epinephrine, norepinephrine, and ACTH counterregulatory defects were prevented. Recurrent hypoglycemia in DI-hypo rats blunted corticosterone but, surprisingly, not epinephrine responses. Norepinephrine and ACTH responses also were not impaired, whereas glucagon counterregulation was reduced due to repeated hyperinsulinemia. Insulin treatment prevented decreases in basal TH protein and increased PNMT and dopamine β-hydroxylase protein. DI-hypo rats showed increases in TH, PNMT, and dopamine β-hydroxylase. We conclude that insulin treatment of diabetic rats protects against most counterregulatory defects but not elevated fasting corticosterone and decreased corticosterone counterregulation. Protection against epinephrine defects, both without and with antecedent hypoglycemia, is associated with enhancement of adrenal catecholamine-synthesizing enzyme levels.

Elevated tyrosine hydroxylase mRNA levels in medulla oblongata of spontaneously hypertensive rats

1996 ◽  
Vol 36 (1) ◽  
pp. 197-199 ◽  
Author(s):  
Toshio Kumai ◽  
Masami Tanaka ◽  
Minoru Watanabe ◽  
Hironori Nakura ◽  
Tomonori Tateishi ◽  
...  
Keyword(s):  
Tyrosine Hydroxylase ◽  
Medulla Oblongata ◽  
Spontaneously Hypertensive Rats ◽  
Mrna Levels ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Peripheral and Central Catecholaminergic Neurons in Genetic and Experimental Hypertension in Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 377s-380s ◽  
Author(s):  
H. Grobecker ◽  
J. M. Saavedra ◽  
M. F. Roizen ◽  
V. Weise ◽  
I. J. Kopin ◽  
...  
Keyword(s):  
Tyrosine Hydroxylase ◽  
Adrenal Glands ◽  
Experimental Hypertension ◽  
Hypertensive Rats ◽  
Hydroxylase Activity ◽  
Methyl Transferase ◽  
Spontaneously Hypertensive ◽  
Catecholaminergic Neurons ◽  
Wistar Kyoto ◽  
The Brain

1. Activity of peripheral and central catecholaminergic neurons was studied in spontaneously hypertensive rats (SHR) and deoxycorticosterone (DOCA)—salt hypertensive rats. 2. In young SHR (4 weeks) the plasma values of both noradrenaline and dopamine-β-hydroxylase activity were increased compared with those of normotensive rats of the Wistar/Kyoto strain. Total catecholamines (mostly adrenaline) were not significantly different. 3. In the adrenal glands of 2-weeks-old and 4-weeks-old SHR activities of tyrosine hydroxylase, dopamine-β-hydroxylase, phenylethanolamine-N-methyl transferase were decreased, compared to Wistar/Kyoto rats. 4. The adrenaline-forming enzyme was elevated in the A1 and A2 regions of the brain stem of 4-weeks-old SHR and in the A1 region of adult DOCA—salt hypertensive rats. 5. In the adrenal glands of adult DOCA—salt hypertensive rats tyrosine hydroxylase activity was increased. 6. These results implicate peripheral noradrenaline-containing neurons and central adrenaline-containing neurons in the development of genetic and experimental hypertension in rats.

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