Effect of Renal Beta- and Alpha-Adrenergic Stimulation on Proximal Sodium Reabsorption in Dogs

1972 ◽  
Vol 43 (4) ◽  
pp. 569-576 ◽  
Author(s):  
L. M. Blendis ◽  
R. B. Auld ◽  
E. A. Alexander ◽  
N. G. Levinsky
Keyword(s):  
Beta Blockade ◽  
Sodium Reabsorption ◽  
Adrenergic Stimulation ◽  
Urine Sodium ◽  
Beta Adrenergic ◽  
Acid Clearance ◽  
Urine Sodium Excretion ◽  
Clearance Studies ◽  
Single Nephron ◽  
Alpha Blockade

1. Micropuncture studies were performed in dogs to evaluate more directly the suggestion from clearance experiments that alpha-adrenergic stimulation enhances and beta-adrenergic stimulation depresses proximal sodium reabsorption. Experiments were performed during unilateral renal artery infusion of the appropriate drugs in the doses used in previous clearance studies. 2. To study pure beta stimulation, collections were made during alpha blockade with phenoxybenzamine and re-collections during the addition of beta stimulation with isoproterenol. No significant changes were noted in the ratio of inulin concentrations in tubular fluid and plasma (TF/P)In (1·49 ± 0·04 to 1·52 ± 0·05), absolute sodium reabsorption (23 ± 1 to 23 ± 3 nl/min), single nephron glomerular filtration rate (SNGFR) (75 ± 7 to 76 ± 15 nl/min) and the ratio of SNGFR to inulin clearance (SNGFR/CIn) × (106), (2·95 ± 0·4 to 2·65 ± 0·4). 3. To study pure alpha-adrenergic stimulation, collections were made during beta blockade with propranolol and again during the addition of alpha-adrenergic stimulation with nor-adrenaline. There were no significant changes in (TF/P)In (1·50 ± 0·09 to 1·42 ± 0·04), absolute sodium reabsorption (25 ± 7 to 17 ± 4 nl/min), SNGFR (68 ± 13 to 58 ± 10 nl/min) or SNGFR/CIn(× 106) (2·76 ± 0·6 to 2·51 ± 0·5). 4. CIn increased slightly after beta but not after alpha stimulations. p-Aminohippuric acid clearance (CPAH) and urine sodium excretion (UNaV) were not significantly different in either set of studies. 5. We conclude that neither alpha not beta adrenergic stimulation has a significant effect on proximal sodium reabsorption when infused in doses that do not alter renal haemodynamics.

Enhanced beta-adrenergic-receptor responsiveness in hypoxic neonatal pulmonary circulation

1981 ◽  
Vol 240 (5) ◽  
pp. H697-H703 ◽  
Author(s):  
J. E. Lock ◽  
P. M. Olley ◽  
F. Coceani
Keyword(s):  
Pulmonary Circulation ◽  
Beta Blockade ◽  
Base Line ◽  
Pulmonary Resistance ◽  
Beta Adrenergic ◽  
Beta Receptor ◽  
Adrenergic Activity ◽  
Alpha Blockade ◽  
Alveolar Hypoxia ◽  
Constrictor Response

The influence of alveolar hypoxia on pulmonary vascular adrenergic receptors was studied in conscious newborn lambs. In control animals, pulmonary vessels were directly constricted by epinephrine and norepinephrine, but were unaffected by isoproterenol. Pulmonary resistance (PVR) was also unaffected by propranolol, thus implying minimal beta-receptor activity under normoxic conditions. Hypoxia raised PVR but also modified the pulmonary vascular responses to catecholamines: isoproterenol became a dilator, whereas the constrictor effects of epinephrine and norepinephrine were abolished. Although beta-blockade did not alter base-line PVR, propranolol increased the constrictor response to hypoxia, implying that hypoxia increases beta-adrenergic activity or reactivity in the pulmonary circulation. Consistent with this hypothesis are the following: 1) in alpha-blocked lambs, epinephrine was without local effects during normoxia, but caused vasodilation during hypoxia; 2) the absent constrictor response to epinephrine during hypoxia is fully restored by propranolol; and 3) although alpha-blockade blunts the hypoxic constrictor response, the full response is restored when beta-blockade is added. These results indicate that the hypoxic constrictor response is partially opposed by increased beta-mediated vasodilation. These enhanced beta-receptor effects are due, at least in part, to increased beta-receptor reactivity of unknown mechanism.

The relationship between some beta-adrenergic mediated responses and plasma concentrations of adrenaline and cyclic AMP in man

1990 ◽  
Vol 122 (1) ◽  
pp. 115-120 ◽  
Author(s):  
E. K. Philipsen ◽  
J. Myhre ◽  
S. Larsen ◽  
M. Damkjær Nielsen ◽  
J. J. Holst ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Plasma Concentrations ◽  
Beta Agonist ◽  
Beta Blockade ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Plasma Adrenaline ◽  
Beta Adrenoceptor ◽  
Adrenaline Infusion ◽  
The Relationship

Abstract To test the hypothesis that increments in plasma cyclic AMP during beta-adrenergic stimulation reflect integrated second messenger function of the tissues activated by the angonist, graded adrenaline infusion resulting in plasma adrenaline concentrations within the physiological range was performed in 8 healthy subjects with and without concomitant beta-adrenoceptor blockade by iv propranolol. A significant correlation was found between increments in plasma adrenaline and plasma cyclic AMP in the experiments without beta-blockade; during concomitant beta-blockade the increase in plasma cyclic AMP concentrations at low adrenaline infusion rates was prevented, whereas a small increase in cyclic AMP was found at high adrenaline infusion rates, probably owing to incomplete beta-receptor blockade. Likewise, the adrenaline-induced increments in blood substrates (glucose, lactate, glycerol and betahydroxy butyric acid) were significantly reduced but not completely prevented by beta-blockade. We conclude that an altered relationship between beta-agonist concentrations and plasma cyclic AMP may provide evidence for the existence of differences in beta-adrenergic sensitivity in man.

Effects of beta-adrenergic receptor blockade on glycogenolysis during exercise

1982 ◽  
Vol 53 (3) ◽  
pp. 549-554 ◽  
Author(s):  
A. C. Juhlin-Dannfelt ◽  
S. E. Terblanche ◽  
R. D. Fell ◽  
J. C. Young ◽  
J. O. Holloszy
Keyword(s):  
Skeletal Muscle ◽  
Adrenergic Receptor ◽  
Beta Blockade ◽  
Receptor Blockade ◽  
Adrenergic Stimulation ◽  
Glycogen Depletion ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic ◽  
Adrenergic Receptor Blockade ◽  
Exogenous Substrates

The purpose of this study was to determine whether beta-adrenergic receptor blockade inhibits glycogen utilization in rats during exercise. Propranolol (1 mg/kg body wt) completely blocked the glycogenolytic effect of a large dose of epinephrine given by injection but did not prevent glycogen breakdown in skeletal muscle or liver during a bout of treadmill exercise. On the contrary, exercise resulted in greater glycogen depletion in plantaris muscles of beta-blocked rats than in those of control rats, probably as a result of decreased availability of fatty acids. Increasing the availability of exogenous substrates slowed the rate of skeletal muscle glycogen depletion during exercise. However, even with increased availability of exogenous substrates, beta-blockade did not result in reduced utilization of skeletal muscle or liver glycogen. In contrast to its effect on skeletal muscle, beta-blockade markedly reduced glycogen depletion in the heart during exercise. We conclude that beta-adrenergic stimulation is of major importance in mediating glycogenolysis in the heart but is not necessary for glycogenolysis in skeletal muscle or liver during prolonged exercise.

Physiological insulin action is opposed by beta-adrenergic mechanisms in dogs

1988 ◽  
Vol 255 (1) ◽  
pp. E33-E40 ◽  
Author(s):  
G. A. Werther ◽  
S. Joffe ◽  
R. Artal ◽  
M. A. Sperling
Keyword(s):  
Insulin Infusion ◽  
Glucose Production ◽  
Beta Blockade ◽  
Base Line ◽  
Adrenergic Blockade ◽  
Hormonal Changes ◽  
Beta Adrenergic ◽  
Adrenergic Mechanisms ◽  
Alpha Blockade

To investigate the possible role of adrenergic mechanisms in modulating glucose homeostasis during physiological insulin changes, we studied the effects of alpha-, beta-, or combined alpha- and beta-adrenergic blockade on glucose production (Ra) and utilization (Rd) via isotope ([3-(3)H]glucose) dilution during nonstressful, nonhypoglycemic conditions in response to physiological insulin changes in conscious dogs. Without adrenergic blockade, infusion of insulin at 0.275 mU.kg-1.min-1 (control) caused glucose to fall from 92 +/- 4 to 82 +/- 4 mg/dl over 30 min, because of transient fall in Ra from 2.8 +/- 0.4 to 2.3 +/- 0.3 mg.kg-1.min-1, which recovered to base line by 30 min. There was a later rise in Rd to 3.9 +/- 0.4 mg.kg-1.min-1 at 45 min, but no counter-regulatory hormonal changes (glucagon, cortisol, epinephrine, and norepinephrine) to account for these findings in glucose kinetics. alpha-Blockade alone led to an initial rise in base-line insulin and consequent fall in glucose, associated with a transient fall in Ra but no change in Rd; infusion of insulin led to a further small fall in glucose, with no change in Ra, but with a rise at 30 min in Rd similar to controls. beta-Blockade alone led to an initial fall in insulin and modest rise in glucose; insulin infusion led to a greater rate of fall in glucose than in controls (from 112 +/- 6 to 78 +/- 7 mg/dl over 30 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic mechanisms in canine gastric circulation

1975 ◽  
Vol 229 (4) ◽  
pp. 977-982 ◽  
Author(s):  
MJ Zinner ◽  
JC Kerr ◽  
DG Reynolds
Keyword(s):  
Left Gastric Artery ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Gastric Circulation ◽  
Flow Through ◽  
The Right

The effects of adrenergic stimulation and blockade on the gastric circulation were studied in anesthetized dogs. Blood flow through the right and left gastric artery was measured electromagnetically. Norepinephrine and isoproterenol were injected intra-arterially and intravenously before and after alpha- and beta-adrenergic blockade. Isoproterenol caused vasodilation of both right and left gastric circulations and this effect was attenuated by beta blockade. Epinephrine and norepinephrine induced constriction followed by dilation in both circulations. The constrictor components were attenuated or abolished by alpha-adrenergic blockade and the dilator components were attenuated by beta-adrenergic blockade. The right and left gastric vascular beds demonstrated quantitatively different responses to the same dose of each adrenergic amine. The left gastric circulation had a greater vasodilator response than did the right gastric circulation. These data support the classical concepts that epinephrine and norepinephrine are "mixed" adrenergic agonists and isoproterenol is a "pure" beta-adrenerigic agonist. The data further suggest that there is a differential in beta-adrenergic receptor distribution with the left gastric vasculature demonstrating greater dilator responses than the right.

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