Adrenergic Nervous System in Hypertension

2015 ◽  
pp. 145-155
Author(s):  
Vito M. Campese
Keyword(s):  
Nervous System ◽  
Adrenergic Nervous System

Synaptosomal [125I]triiodothyronine after intravenous [125I]thyroxine.

1978 ◽  
Vol 235 (6) ◽  
pp. E638
Author(s):  
M B Dratman ◽  
F L Crutchfield
Keyword(s):  
Nervous System ◽  
Amino Acid ◽  
Male Rats ◽  
Time Interval ◽  
Nerve Terminals ◽  
Brain Uptake ◽  
Uptake Mechanism ◽  
Hormone Administration ◽  
Adrenergic Nervous System ◽  
Brain Cytosol

We administered [125I]thyroxine intravenously to adult male rats and measured uptake and subcellular distribution of the hormone and its metabolites in brain. Fractional brain uptake decreased after a large dose of iodothyronine, providing evidence for saturability of the uptake mechanism. Well-defined patterns of regional and subcellular labeling were noted within 1 h after [125I]thyroxine injection. Radioactivity in synaptosomes was always greater than in any other particle separated per gram of brain, increasing linearly relative to radioactivity in brain cytosol during the 1st h. Although [125I]triiodothyronine derived from [125I]thyroxine was not identified in serum at any time interval, it was measurable in synaptosomes within 20 min and in brain cytosol within 1 h after labeled hormone administration. Concentrations of the radioactive metabolite were twofold greater and ratios of [125I]triiodothyronine to [125I]thyroxine concentration were threefold greater in synaptosomes than in cytosol. Therefore, thyroxine may be converted to triiodothyronine within nerve terminals. Synaptosomal localization of iodothyronines and their metabolites may be relevant to the marked central and peripheral adrenergic nervous system effects of these aromatic amino acid hormones.

Synthesis of high-specific-radioactivity 4- and 6-[18F]fluorometaraminol- PET tracers for the adrenergic nervous system of the heart

2001 ◽  
Vol 9 (3) ◽  
pp. 677-694 ◽  
Author(s):  
Oliver Langer ◽  
Frédéric Dollé ◽  
Héric Valette ◽  
Christer Halldin ◽  
Françoise Vaufrey ◽  
...  
Keyword(s):  
Nervous System ◽  
Specific Radioactivity ◽  
Pet Tracers ◽  
High Specific Radioactivity ◽  
Adrenergic Nervous System

Acute pulmonary hemodynamic effects of intravenous copper sulfate: role of alpha-adrenergic system

1981 ◽  
Vol 51 (5) ◽  
pp. 1204-1213 ◽  
Author(s):  
T. Ahmed ◽  
A. Januszkiewicz ◽  
P. Eyre ◽  
M. J. Robinson ◽  
M. A. Sackner
Keyword(s):  
Nervous System ◽  
Pulmonary Artery ◽  
Vascular Resistance ◽  
Adrenergic Receptor ◽  
Base Line ◽  
Receptor Blockade ◽  
Hemodynamic Effects ◽  
Pulmonary Hemodynamic ◽  
Adrenergic Nervous System ◽  
Conscious Sheep

We investigated the acute pulmonary hemodynamic effects of intravenous copper sulfate (CuSO4) infusion and its mechanism of action in six groups of conscious sheep (total 40). After 300 mg CuSO4 alone, mean pulmonary artery pressure (Ppa) increased from 10.3 to 22.5 Torr and pulmonary artery wedge pressure (Ppaw) from 3.5 to 7.6 Torr, whereas systemic arterial pressure (Psa) increased from 95 to 102 Torr. Cardiac output (Qp) decreased from 4.7 to 3.3 l/min. Pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR) increased to 320 and 160% of base line, respectively. The hemodynamic changes correlated well with serum copper, which increased from a base-line value of 0.12 to 3.5 mg/dl after the CuSO4. Serum dopamine beta-hydroxylase increased from 3.2 U/l before CuSO4 injection to 5.7 after its administration, signifying activation of adrenergic nervous system. H1-histamine receptor blockade with chlorpheniramine failed to prevent the effects of CuSO4. Pretreatment with methysergide, a serotonin antagonist, partially attenuated the effects of CuSO4. Phenoxybenzamine, an alpha-adrenergic receptor blocker, and 6-hydroxydopamine, a catecholamine depleting agent, completely blocked the effects of CuSO4. beta-Adrenergic receptor blockade with propranolol enhanced the effects of CuSO4. We conclude, that, in conscious sheep, acute infusion of CuSO4 caused a marked reversible increase in PVR with a slight transient increase in SVR, and this pulmonary hypertension was produced by stimulation of the alpha-adrenergic nervous system.

Evidence for α-adrenergic receptors mediated TSH release in men

1980 ◽  
Vol 95 (2) ◽  
pp. 172-176 ◽  
Author(s):  
Stefan Zgliczyński ◽  
Marek Kaniewski
Keyword(s):  
Nervous System ◽  
Healthy Volunteers ◽  
Adrenergic Receptors ◽  
Bolus Injection ◽  
Physiological Mechanism ◽  
Adrenergic System ◽  
Trh Stimulation ◽  
Tsh Secretion ◽  
Adrenergic Nervous System

Abstract. In order to elucidate the role of the adrenergic nervous system in the mechanism of TSH release in men the effects of α- and β-receptors blocking agents were studied in 11 healthy volunteers. Phentolamine administetred iv as a bolus injection in a dose of 10 mg, significantly lowered the TSH release in basal condition and in response to TRH stimulation. However, propranolol in a dose of 0.1 mg/kg administered in the same fashion as phentolamine had no effect on the TSH secretion. The results obtained suggest that the α-receptors of the adrenergic system are involved in the physiological mechanism which stimulates TSH release in men.

scholarly journals Modulation of the BP Response to Diet by Genes in the Renin-Angiotensin System and the Adrenergic Nervous System

2011 ◽  
Vol 24 (2) ◽  
pp. 209-217 ◽  
Author(s):  
L. P. Svetkey ◽  
E. L. Harris ◽  
E. Martin ◽  
W. M. Vollmer ◽  
G. T. Meltesen ◽  
...  
Keyword(s):  
Nervous System ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Adrenergic Nervous System
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