Effect of clonidine on the thermic effect of feeding in humans

1988 ◽  
Vol 254 (1) ◽  
pp. R90-R94 ◽  
Author(s):  
R. S. Schwartz ◽  
L. F. Jaeger ◽  
R. C. Veith

Previous studies in humans attempting to assess the role of the sympathetic nervous system (SNS) in the thermic effect of feeding (TEF) have investigated the effect of oral or intravenous propranolol on TEF. This approach is potentially limited, however, because of the direct effects of propranolol on catecholamine and thyroid metabolism. In the present study we chose instead to evaluate the effect of clonidine, a centrally acting alpha 2-adrenergic receptor agonist that inhibits SNS outflow, on TEF and SNS activity as reflected by both plasma catecholamines and norepinephrine (NE) kinetics. The TEF and SNS response to an 800-kcal high-carbohydrate liquid meal (85% carbohydrate, 15% protein) was studied in eight healthy male subjects (27 +/- 6 yr) on two separate occasions with the subjects wearing either a clonidine or placebo skin patch for 48 h prior to study. Clonidine significantly suppressed base-line plasma NE concentration (-46%, P less than 0.01) and NE appearance rate (-47%, P = 0.01) compared with placebo, whereas there was no significant effect on epinephrine concentrations, NE clearance rate, or base-line energy expenditure. The expected increments in plasma NE and NE appearance after a meal were also reduced by 54% (P less than 0.05) and 70% (P less than 0.01) of placebo values, respectively, after clonidine. Associated with this reduced SNS response to the meal was a blunting of the expected TEF by 33% (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Metabolism ◽  
1983 ◽  
Vol 32 (2) ◽  
pp. 114-117 ◽  
Author(s):  
Robert S. Schwartz ◽  
Jeffrey B. Halter ◽  
Edwin L. Bierman

2018 ◽  
Author(s):  
Kirsty Spence ◽  
Steven Hunter ◽  
Campbell Brown ◽  
Paul Thompson ◽  
Karen Mullan ◽  
...  

1980 ◽  
Vol 48 (1) ◽  
pp. 109-113 ◽  
Author(s):  
J. M. Pequignot ◽  
L. Peyrin ◽  
G. Peres

Adrenergic response to exercise and the relationships between plasma catecholamines and blood energetic substrates were studied in sedentary men after 15 h of fasting. Subjects pedaled a bicycle ergometer until exhaustion at a work load approximating 80% maximal oxygen consumption. Working ability was diminished by the fast (P less than 0.025). Resting plasma norepinephrine level was increased by fasting. During exercise plasma epinephrine (E) and norepinephrine (NE) concentrations were more elevated in fasting subjects than in fed subjects. Plasma catecholamine (CA) levels in fasting men correlated with blood glucose, blood lactate, and plasma glycerol concentrations. There was no significative correlation between CA and plasma free fatty acid (FFA) levels. The increased adrenergic activity in fasting subjects correlated with reduced endurance time. This study emphasizes the role of CA release, probably combined with other hormonal factors, in the mobilization of energy substrates during submaximal exercise.


1994 ◽  
Vol 267 (2) ◽  
pp. H751-H756 ◽  
Author(s):  
A. W. Cowley ◽  
E. Szczepanska-Sadowska ◽  
K. Stepniakowski ◽  
D. Mattson

Despite the well-recognized vasoconstrictor and fluid-retaining actions of vasopressin, prolonged administration of arginine vasopressin (AVP) to normal animals or humans fails to produce sustained hypertension. The present study was performed to elucidate the role of the V1 receptor in determining the ability of AVP to produce sustained hypertension. Conscious Sprague-Dawley rats with implanted catheters were infused with the selective V1 agonist, [Phe2,Ile3,Orn8]vasopressin (2 ng.kg-1.min-1), for 14 days in amounts that were acutely nonpressor. Blood pressure (MAP), heart rate (HR), body weight, and water intake (WI) were determined daily. Plasma AVP, plasma catecholamines norepinephrine and epinephrine, plasma osmolality, and electrolyte concentration were determined before and on days 1 and 7 of infusion. MAP increased significantly by 10.4 +/- 4.5 mmHg on day 1 and rose to 22 +/- 5 mmHg above control by day 14 (transient decrease on days 6-9) and then fell to control levels after the infusion was stopped. HR did not change significantly. Plasma AVP immunoreactivity increased from 2.5 +/- 0.3 to 10.9 +/- 2.1 pg/ml, whereas norepinephrine tended to fall only on day 1, with epinephrine only slightly elevated on day 7. No evidence of fluid retention was found, and rats lost sodium only on the first day of V1 agonist infusion. Body weight increased throughout the study but was unrelated to the changes of MAP. We conclude that chronic stimulation of V1 receptors results in sustained hypertension in rats.


1987 ◽  
Vol 253 (4) ◽  
pp. H909-H918 ◽  
Author(s):  
E. K. Jackson

The purpose of this study was to compare the in vivo role of adenosine as a modulator of noradrenergic neurotransmission in the spontaneously hypertensive rat (SHR) and Wistar-Kyoto control rat (WKY). In the in situ blood-perfused rat mesentery, vascular responses to periarterial (sympathetic) nerve stimulation (PNS) and to exogenous norepinephrine (NE) were enhanced in SHR compared with WKY. In both SHR and WKY, vascular responses to PNS were more sensitive to inhibition by adenosine than were responses to NE. At matched base-line vascular responses, compared with WKY, SHR were less sensitive to the inhibitory effects of adenosine on vascular responses to PNS, but SHR and WKY were equally sensitive with respect to adenosine-induced inhibition of responses to NE. Antagonism of adenosine receptors with 1,3-dipropyl-8-p-sulfophenylxanthine shifted the dose-response curve to exogenous adenosine sixfold to the right yet did not influence vascular responses to PNS or NE in either SHR or WKY. Furthermore, PNS did not alter either arterial or mesenteric venous plasma levels of adenosine in SHR or WKY, and plasma levels of adenosine in both strains were always lower than the calculated threshold level required to attenuate neurotransmission. It is concluded that in vivo 1) exogenous adenosine interferes with noradrenergic neurotransmission in both SHR and WKY; 2) SHR are less sensitive to the inhibitory effects of exogenous adenosine on noradrenergic neurotransmission than are WKY; 3) endogenous adenosine does not play a role in modulating neurotransmission in either strain under the conditions of this study; and 4) enhanced noradrenergic neurotransmission in the SHR is not due to defective modulation of neurotransmission by adenosine.


2017 ◽  
Vol 26 (4) ◽  
pp. 594-595
Author(s):  
Alan R. Saltiel

1981 ◽  
Author(s):  
M Kikuchi ◽  
Y Ikeda ◽  
M Handa ◽  
S Matsuda ◽  
H Muraki ◽  
...  

Microtubules exist in a dynamic equilibrium between polymerized and depolymerized forms in human platelets, playing a major role to maintain the discoid shape of platelets. It has been previously shown that the interaction of aggregating agents with platelets leads to a rapid but transient disassembly of microtubules. ( Steiner and Ikeda, J.Clin. Invest. 63:443,1979 ) In this paper, the role of calcium in the equilibrium between assembled and disassembled microtubules was investigated. The respective pools of soluble and polymerized tubulin were “frozen” by addition of a glycerol-dimethyl sulfoxide-containing medium to platelet rich plasma, preincubated with 2 µM A23187 for various time intervals. The two pools of tubulin were estimated by measuring the colchicine binding activities of total and polymerized tubulin according to the method of Wilson.Resting platelets were found to contain 56.2 ± 2.7 µg tubulin per 109 platelets, of which 56.7 % was in polymerized form. Addition of A23187 to platelet rich plasma produced a transient decrease in the pool of polymerized tubulin within 30 sec., followed by a return to base-line values within 2 min.. TMB-8, a known intracellular calcium antagonist, abolished this transient decrease in polymerized tubulin induced by A23187 in a concentration dependent manner, while indomethacin or acetylsalycylic acid did not.These findings may indicate the important role of intracellular calcium in microtubule assembly-disassembly.


1982 ◽  
Vol 242 (5) ◽  
pp. R528-R532 ◽  
Author(s):  
A. J. Hance ◽  
E. D. Robin ◽  
J. B. Halter ◽  
N. Lewiston ◽  
D. A. Robin ◽  
...  

Plasma epinephrine and norepinephrine concentrations were measured in five harbor seals, Phoca vitulina, during a control period, during a 6-min dive, and during a 30-min postdiving recovery period. Measurements were performed with and without prior glucose administration. Control epinephrine concentrations [189 +/- 118 (SD) pg/ml] and norepinephrine concentrations (340 +/- 191 pg/ml) were similar to resting values in humans. During diving there are dramatic increases in both epinephrine and norepinephrine concentrations, which returned to control values by 30 min of the postdiving recovery period. A similar pattern was found after glucose infusion. The increased catecholamines were not the primary mechanism responsible for arterial constriction during the dive. Persistent diving bradycardia suggests obliteration of the chronotropic effects of catecholamines during the dive. An unchanged stroke volume suggests obliteration of the inotropic effects of catecholamines during the dive. Catecholamines do not appear to be involved in postdiving hyperglycemia and hyperglucogenemia. Neither the regulatory role of increased catecholamines nor the physiological function of increased catecholamines was apparent from the studies. However, dramatic increases in plasma catecholamines during diving appear to be an important component of the hormonal response to prolonged diving in aquatic mammals.


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