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 Autonomic Regulation of Splanchnic Circulation

1991 ◽  
Vol 5 (4) ◽  
pp. 147-153 ◽  
Author(s):  
Kathleen A Fraser ◽  
Samuel S Lee
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Adrenergic Receptors ◽  
Splanchnic Circulation ◽  
Autonomic Nervous ◽  
Vascular Reserve ◽  
Afferent Nerves ◽  
Primary Afferent Nerves ◽  
Stimulation Of

The role of the autonomic nervous system in circulatory regulation of the splanchnic organs (stomach, small intestine, colon, liver, pancreas and spleen) is reviewed. In general, the sympathetic nervous system is primarily involved in vasoconstriction, while the parasympathetic contributes to vasodilation. Vasoconstriction in the splanchnic circulation appears to be mediated by alpha-2 receptors and vasodilation by activation of primary afferent nerves with subsequent release of vasodilatory peptides, or by stimulation of beta-adrenergic receptors. As well, an important function of the autonomic nervous system is to provide a mechanism by which splanchnic vascular reserve can be mobilized during stress to maintain overall cardiovascular homeostasis.

Vasodilator responses to ATP and UTP are not dependent on nitric oxide release, K+ATP channel activation, or the release of vasodilator prostaglandins in the hindlimb vascular bed of the cat

2000 ◽  
Vol 78 (8) ◽  
pp. 612-621 ◽  
Author(s):  
Hunter C Champion ◽  
Philip J Kadowitz
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Phosphodiesterase Inhibitor ◽  
Inhibitory Effect ◽  
Cyclooxygenase Inhibitors ◽  
Adrenergic System ◽  
Camp Phosphodiesterase ◽  
Nitric Oxide Release ◽  
Vascular Bed ◽  
Adrenergic Nervous System

The effects of the purinergic agonists, ATP, ATPγS, UTP, and 2-Met-Thio AP, were investigated in the hindlimb vascular bed of the cat. Under constant-flow conditions, injections of the purinergic agonists into the perfusion circuit elicited dose-related decreases in perfusion pressure. The order of potency was 2-Met-Thio ATP > ATPγS > ATP > UTP. In contrast, injections of GTPγS, cAMP, UDP, and UMP had no effect. Vasodilator responses to ATP, ATPγS, UTP, and 2-Met-Thio ATP were increased in duration by the cAMP phosphodiesterase inhibitor rolipram, whereas the cGMP phosphodiesterase inhibitor zaprinast had no effect. Responses to the purinergic agonists were not altered by nitric oxide synthase inhibitors, K+ATP channel antagonists, cyclooxygenase inhibitors, or agents that interfere with the actions of the adrenergic nervous system. These data suggest that ATP, ATPγS, UTP, and 2-Met-Thio ATP dilate the hindlimb vascular bed by a direct cAMP-dependent mechanism, and that the release of nitric oxide, vasodilator prostaglandins, K+ATP channel opening, or an inhibitory effect on the adrenergic nervous system play little, if any, role in mediating or modulating responses to the purinergic agonists in the hindlimb circulation of the cat.Key words: purinergic agonists, P2 purinergic receptors, cAMP-dependent vasodilator activity, adrenergic system, nitric oxide prostaglandins.

Role of autonomic nervous system controlling surface tension in fetal rabbit lungs

1977 ◽  
Vol 43 (6) ◽  
pp. 1039-1045 ◽  
Author(s):  
A. J. Corbet ◽  
P. Flax ◽  
A. J. Rudolph
Keyword(s):  
Nervous System ◽  
Adrenergic Receptors ◽  
Static Pressure ◽  
Parasympathetic Nervous System ◽  
Uterine Wall ◽  
System A ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Stimulation Of

After the maternal abdomen was opened under methoxyflurane anesthesia, fetal rabbits of 27.5 days gestation were given injections through the intact uterine wall of saline, pilocarpine, isoxsuprine, muscarine, phenylephrine, atropine, phenoxybenzamine, or propranolo, alone or in appropriate combinations. Fetal rabbits were delivered by hysterotomy and killed without breathing 2.5 h later. Static pressure-volume curves with air showed improved retention on deflation in fetal rabbits that had injections of pilocarpine, or isoxsuprine, but not of muscarine or phenylephrine. The effect of pilocarpine on the pressure-volume curve was blocked by atropine, phenoxybenzamine, and propranolol, and the effect of isoxsuprine was blocked by propranolol but not phenoxybenzamine. The data suggest that pilocarpine produces secretion of surfactant into lung air spaces by exciting the sympathetic nervous system, a known function of pilocarpine, rather than the parasympathetic nervous system. This may result in stimulation of the same beta-adrenergic receptors affected by isoxsuprine which is also thought to stimulate surfactant secretion.

Role of adrenergic nervous system in cigarette smoke-induced bronchoconstriction in guinea pigs

1998 ◽  
Vol 358 (1) ◽  
pp. 49-54 ◽  
Author(s):  
Koichiro Matsumoto ◽  
Hisamichi Aizawa ◽  
Hiromasa Inoue ◽  
Shohei Takata ◽  
Mutsumi Shigyo ◽  
...  
Keyword(s):  
Nervous System ◽  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Adrenergic Nervous System

Interaction of propranolol and phentolamine with ethanol in the rat

1976 ◽  
Vol 54 (4) ◽  
pp. 622-625 ◽  
Author(s):  
D. Frankel ◽  
H. Kalant ◽  
J. M. Khanna ◽  
A. E. LeBlanc
Keyword(s):  
Nervous System ◽  
Dependent Manner ◽  
Low Doses ◽  
Adrenergic Mechanism ◽  
Adrenergic Nervous System ◽  
Ethanol Effect ◽  
Dose Dependent ◽  
Higher Doses

The possible role of the adrenergic nervous system in the intoxicant effects of ethanol was examined in studies of the interaction of propranolol and phentolamine with ethanol. Propranolol tended to increase the effect of lower doses of ethanol in a dose-dependent manner. However, the effect of higher doses of ethanol (over 2.0 g/kg) tended to be diminished by low doses of propranolol, whereas higher doses of propranolol were ineffective or actually increased the ethanol effect. Phentolamine tended to decrease the effect of the lower ethanol doses. These findings are inconsistent with any simple adrenergic mechanism in the mediation of the intoxicant effect of ethanol.

Interaction of renal prostaglandins with the renin-angiotensin and renal adrenergic nervous systems in healthy subjects during dietary changes in sodium intake

1985 ◽  
Vol 68 (4) ◽  
pp. 387-393 ◽  
Author(s):  
Herbert J. Kramer ◽  
Bruno Stinnesbeck ◽  
Georg Klautke ◽  
Jochen Kipnowski ◽  
Dietrich Klingmueller ◽  
...  
Keyword(s):  
Nervous System ◽  
Renal Function ◽  
Urinary Excretion ◽  
Healthy Subjects ◽  
Sodium Intake ◽  
Renin Angiotensin ◽  
Low Sodium ◽  
Renal Prostaglandins ◽  
Adrenergic Nervous System

1. In six healthy subjects the role of renal prostaglandins (PG) in modulating the actions of the renin-angiotensin and renal adrenergic nervous systems on renal function was investigated. 2. During high dietary sodium intake (350 mmol/day) for 4 days no changes in urinary excretion of PGE2, PGF2α, noradrenaline or adrenaline were noted, whereas plasma renin activity (PRA) and urinary aldosterone excretion were suppressed. 3. After 4 days of low sodium intake (35 mmol/day) urinary excretion of PGE2, aldosterone and noradrenaline, as well as PRA, had significantly increased. 4. Inhibition of PG synthesis with indomethacin (2 mg/kg body weight) had no effects on renal function on day 5 of high sodium intake. Despite suppression of PRA and urinary aldosterone, indomethacin significantly reduced p-aminohippurate (PAH) clearance, glomerular filtration rate (GFR) and urinary sodium excretion on day 5 of low sodium intake, when urinary noradrenaline excretion remained high. 5. The results point to the crucial role of the renal adrenergic nervous system in controlling renal vascular resistance and sodium conservation in healthy subjects during low sodium intake, which is unmasked when renal PG synthesis is blocked by indomethacin. Enhanced renal PG synthesis during sodium restriction therefore not only attenuates the vascular and tubular effects of the renin-angiotensin system but, more importantly, also those of the highly stimulated renal adrenergic nervous system.

Sympathetic nervous system and blood pressure maintenance in the Brattleboro DI rat

1986 ◽  
Vol 250 (5) ◽  
pp. R770-R775 ◽  
Author(s):  
J. L. Williams ◽  
M. D. Johnson
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Bolus Injection ◽  
Plasma Concentrations ◽  
Sympathetic Function ◽  
Unstressed State ◽  
Basal Plasma ◽  
Sympathetic Nervous

Experiments were performed to determine the functional role of the sympathetic nervous system (SNS) in blood pressure regulation in Brattleboro diabetes insipidus (DI) rats and to determine the effects of synthetic arginine vasopressin (AVP) on sympathetic function in DI rats. The experiments were conducted in male age-matched Long-Evans (LE) and DI rats in the conscious unstressed state. Mean arterial pressure (MAP) and heart rate were similar in conscious unstressed LE and DI rats, but basal plasma concentrations of norepinephrine (NE) and epinephrine (E) were elevated in DI rats compared with LE rats. An intra-arterial bolus injection of hexamethonium (30 mg/kg) resulted in greater reductions of MAP in DI rats (-62 +/- 5 mmHg) than in LE rats (-42 +/- 7 mmHg; P less than 0.05). Administration of AVP to DI rats by osmotic minipump reduced plasma NE concentration in DI rats to a level not different from that in LE rats, but E concentration remained elevated. AVP administration to DI rats also reduced the hexamethonium-induced fall in MAP in these animals (-47 +/- 7 mmHg) to a level not different from that in LE rats. We conclude that the SNS plays a greater role in blood pressure maintenance in conscious DI rats than in LE rats and that AVP administration can normalize plasma NE concentration and the contribution of the SNS to blood pressure maintenance in these animals.

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