Central and peripheral adrenergic modulation of carotid sinus-induced renin release

1982 ◽  
Vol 242 (3) ◽  
pp. R318-R325 ◽  
Author(s):  
H. D. Schultz ◽  
J. E. Zehr ◽  
A. Livnat
Keyword(s):  
Adrenergic Receptors ◽  
Carotid Sinus ◽  
Renin Release ◽  
Beta Adrenergic ◽  
Alpha Adrenergic Receptors ◽  
Systemic Pressure ◽  
Carotid Sinus Baroreflex ◽  
Adrenergic Blocker ◽  
Reflex Arc ◽  
Anesthetized Dogs

To study central and peripheral mechanisms that regulate the level of circulating renin during activation of the carotid sinus baroreflex, both carotid sinuses were isolated and perfused at constant flow in chloralase-anesthetized dogs. Sinus pressure was controlled by an adjustable reservoir while systemic pressure was stabilized using an external chamber. Arterial renin activity, measured by radioimmunoassay, was increased during sinus hypotension only if systemic pressure was held constant. The renin response was eliminated by either sinus or renal denervation. Administration of propranolol (iv) or phentolamine directly into the renal artery totally blocked the increase in renin during activation of the reflex. Perfusion of a beta-adrenergic blocker (propranolol) or an alpha-adrenergic blocker (phentolamine) through the third and fourth cerebroventricles had no effect on the increase in renin during sinus hypotension, whereas centrally administered clonidine, and alpha-agonist, blocked the response. We conclude that the sinus reflex arc affecting renin release involves not only activation of peripheral alpha- and beta-adrenergic receptors in the kidney but also inhibition of central alpha-adrenergic receptors. No evidence for central beta-involvement was found.

scholarly journals Autoradiographic visualization of beta-adrenergic receptors in normal and denervated skeletal muscle.

1979 ◽  
Vol 27 (10) ◽  
pp. 1308-1311 ◽  
Author(s):  
B Lavenstein ◽  
W K Engel ◽  
N B Reddy ◽  
S Carroll
Keyword(s):  
Skeletal Muscle ◽  
Blood Vessels ◽  
Adrenergic Receptors ◽  
Cellular Localization ◽  
Muscle Fibers ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Adrenergic Blocker

Autoradiographic localization of beta-adrenergic receptors in rat skeletal muscle in vivo was achieved utilizing [125I]-iodohydroxybenzylpindolol, a potent beta-adrenergic blocker with high affinity and specificity for those receptors. In normal muscle the beta-adrenergic receptors were localized mainly to blood vessels, arterioles greater than venules, with much less concentration of grains over the fascicles of muscle fibers. One week after denervation there was an increase in binding both to blood vessels and muscle fibers, more so in soleus and gactrocnemius than in extensor digitorum longus. While these results parallel in vitro biochemical studies, they dictate caution when inferring cellular localization of beta-adrenergic receptors (and other molecules) solely on the basis of biochemical techniques applied to subcellular fractions of whole-organ homogenates.

Modification of cardiac adrenergic receptors by oxygen free radicals

1991 ◽  
Vol 260 (3) ◽  
pp. H821-H826 ◽  
Author(s):  
M. Kaneko ◽  
D. C. Chapman ◽  
P. K. Ganguly ◽  
R. E. Beamish ◽  
N. S. Dhalla
Keyword(s):  
Free Radicals ◽  
Xanthine Oxidase ◽  
Binding Sites ◽  
Adrenergic Receptors ◽  
Oxygen Free Radicals ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Alpha Adrenergic Receptors ◽  
Cgp 12177 ◽  
Number Of Binding Sites

To examine the effects of oxygen free radicals on alpha- and beta-adrenergic receptors, rat heart crude membranes were incubated with xanthine plus xanthine oxidase, H2O2, or H2O2 plus Fe2+. The assay of beta-adrenergic receptors involving [3H]dihydroalprenolol (DHA) binding revealed that the maximal number of binding sites (Bmax) and dissociation constant (Kd) were increased by xanthine plus xanthine oxidase. H2O2 increased the Kd value for [3H]DHA binding. When a hydrophilic ligand, [3H]CGP-12177, was used for the beta-adrenergic receptor assay, an increase in Kd value without any changes in Bmax value was evident on treating the membranes with xanthine plus xanthine oxidase. The assay of alpha-adrenergic receptors involving [3H]prazosin binding showed a decrease in the number of binding sites and an increase in Kd value only after a prolonged period of incubation. Both H2O2 and H2O2 plus Fe2+ increased the Kd value for [3H]prazosin without changes in Bmax. Changes in both alpha- and beta-adrenergic receptors similar to those with crude membranes were also seen by employing the purified heart sarcolemmal membranes. These data indicate that adrenergic receptors in the sarcolemmal membranes are modified by oxygen free radicals.

Alpha- and beta-adrenergic mechanisms in the control of vascular capacitance by the carotid sinus baroreflex system

1994 ◽  
Vol 267 (1) ◽  
pp. H201-H210 ◽  
Author(s):  
K. Shigemi ◽  
M. J. Brunner ◽  
A. A. Shoukas
Keyword(s):  
Adrenergic Receptor ◽  
Carotid Sinus ◽  
Venous Pressure ◽  
Systemic Circulation ◽  
Adrenergic System ◽  
Beta Adrenergic ◽  
Vascular Volume ◽  
Adrenergic Mechanisms ◽  
Vascular Capacitance ◽  
Carotid Sinus Baroreflex

We examined the active and passive contributions of the alpha- and beta-adrenergic receptor mechanisms to the changes in systemic vascular capacitance caused by the carotid sinus baroreflex system in anesthetized, vagotomized dogs. The carotid sinuses were isolated from the systemic circulation and perfused with controlled pressures. To determine the changes in vascular capacitance, a constant flow, constant venous pressure cardiopulmonary bypass was used. The changes in unstressed vascular volume were calculated when carotid sinus pressure was reduced from 200 to 50 mmHg without any adrenergic receptor antagonist, with either an alpha- (phentolamine) or a beta- (propranolol) antagonist and then with both. The reflex change in unstressed vascular volume in the systemic circulation (22.6 +/- 9.0 ml/kg without any antagonist) was reduced by 72% with phentolamine, by 35% with propranolol, and by 73% with both antagonists. Our results suggest that the alpha-adrenergic mechanisms contribute significantly to active changes in systemic venous capacity. In addition, the beta-adrenergic system has very little effect on active changes in venous vessels but does contribute to the overall capacity changes by dilating the hepatic outflow resistance when the carotid sinus baroreflex system is activated.

Effects of some autonomic drugs on duodenal smooth muscle.

1979 ◽  
Vol 236 (1) ◽  
pp. E33
Author(s):  
S Anuras ◽  
D L Faulk ◽  
J Christensen
Keyword(s):  
Smooth Muscle ◽  
Adrenergic Receptors ◽  
Longitudinal Muscle ◽  
Circular Muscle ◽  
Adrenergic Agonists ◽  
Beta Adrenergic Receptors ◽  
Cholinergic Agonists ◽  
Beta Adrenergic ◽  
Alpha Adrenergic Receptors ◽  
Relative Potencies

Longitudinal muscle strips (LMS) and circular muscle strips (CMS), 2 mm wide and 1.5--2 cm long, from opossum duodenum were exposed to some autonomic agonists. The cholinergic agonists, acetylcholine, carbachol, methacholine, and bethanechol stimulated only tonic contractions in LMS and tonic followed by phasic contractions in CMS. These effects were abolished by atropine 10(-6) M. The ED50S of all cholinergic agonists for LMS were significantly lower than for CMS. Norepinephrine caused initial contraction (abolished by phenoxybenzamine, 10(-4) M), followed by relaxation (abolished by propranolol, 10(-5) M), and isopropylnorepinephrine caused relaxation (abolished by propranolol, 10(-5) M) in both layers. There were no differences in relative potencies for adrenergic agonists between the layers. Tetrodotoxin did not affect the response to adrenergic agonists. Thus, the potency of cholinergic agonists is greater in longitudinal than in circular muscle, and the layers respond differently to cholinergic agonists. The alpha-adrenergic receptors mediate contraction and beta-adrenergic receptors mediate relaxation on the duodenal smooth muscle.

Hormonal regulation of hepatic glycogenolysis in the carp, Cyprinus carpio

1987 ◽  
Vol 252 (4) ◽  
pp. R653-R660 ◽  
Author(s):  
P. A. Janssens ◽  
P. Lowrey
Keyword(s):  
Cyprinus Carpio ◽  
Hormonal Regulation ◽  
Adrenergic Receptors ◽  
Specific Binding ◽  
Arginine Vasotocin ◽  
Dependent Manner ◽  
Beta Adrenergic ◽  
Alpha Adrenergic Receptors ◽  
Adrenergic Antagonist ◽  
Carp Cyprinus Carpio

Carp (Cyprinus carpio) liver maintained normal glycogen content and enzyme complement for several days in organ culture. Epinephrine-stimulated glycogenolysis, phosphorylase activation, and cyclic AMP (cAMP) accumulation in a concentration-dependent manner with EC50s of 100, 100, and 500 nM, respectively. These actions were blocked by the beta-adrenergic antagonist, propranolol, but not by the alpha-adrenergic antagonist phentolamine. Glycogenolysis and tissue cAMP were uninfluenced by 10(-6) M arginine vasotocin, arginine vasopressin, lysine vasotocin, lysine vasopressin, mesotocin, or oxytocin, but were slightly increased by 10(-5) M isotocin and slightly decreased by 10(-6) M angiotensin II. [125I]-iodocyanopindolol (ICP), a beta-adrenergic ligand, bound to isolated carp liver membranes with a KD of 83 pM. Maximum binding of 45 fmol/mg protein was at 600 pM. Propranolol, isoprenaline, epinephrine, phenylephrine, norepinephrine, and phenoxybenzamine displaced ICP with KDs of 100 nM, 2, 20, 20, 60, and 200 microM, respectively. The alpha-adrenergic antagonists, yohimbine and prazosin, showed no specific binding. These data provide evidence that catecholamines act via beta-adrenergic receptors in carp liver and that alpha-adrenergic receptors are not present. Vasoactive peptides play no significant role in regulation of carp liver glycogenolysis.

Adrenergic and local control of O2 uptake during and after severe hypoxia

1986 ◽  
Vol 61 (5) ◽  
pp. 1920-1927 ◽  
Author(s):  
C. E. King ◽  
S. M. Cain
Keyword(s):  
Adrenergic Receptors ◽  
Regional Distribution ◽  
Severe Hypoxia ◽  
Whole Body ◽  
Beta Adrenergic Receptors ◽  
O2 Uptake ◽  
Beta Adrenergic ◽  
Alpha Adrenergic Receptors ◽  
O2 Delivery ◽  
O2 Deficit

The distribution of whole-body O2 supply during severe hypoxia and recovery and its relation to the regional distribution of O2 deficit and repayment was studied. Mongrel dogs were anesthetized, paralyzed, and ventilated to maintain an end-tidal PCO2 between 35 and 40 Torr. In one group, the alpha- and beta-adrenergic receptors were blocked to eliminate neural and humoral adrenergic influences. In a second group, alpha-adrenergic receptors were stimulated to decrease O2 delivery by excessive vasoconstriction. In a third group, beta-adrenergic receptors were stimulated to increase O2 delivery. Whole-body and hindlimb muscle O2 uptake and vascular responses were measured during normoxic control, 15 or 30 min of severe hypoxia (9% O2 in N2), and 20 or 30 min of normoxic recovery, respectively. The whole-body O2 deficit and excess O2 uptake in recovery were partitioned into muscle and nonmuscle areas. The data showed that neural or humoral influences had little effect on the regional distribution of the total O2 deficit and O2 excess in recovery. The O2 deficit could be decreased somewhat by increasing delivery, but the amount of excess O2 used in recovery was unaffected. This suggested that the excess O2 use in recovery was more a function of an energy deficit during hypoxia and not an O2 deficit.

Norepinephrine and iloprost improve barrier function of human endothelial cell monolayers: role of cAMP

1991 ◽  
Vol 260 (5) ◽  
pp. C1052-C1059 ◽  
Author(s):  
E. G. Langeler ◽  
V. W. van Hinsbergh
Keyword(s):  
Barrier Function ◽  
Adrenergic Receptors ◽  
Cell Periphery ◽  
Camp Concentration ◽  
Passage Rate ◽  
Human Artery ◽  
Beta Adrenergic ◽  
Cell Monolayers ◽  
Alpha Adrenergic Receptors ◽  
Adrenergic Antagonist

The barrier function of human artery endothelial cells was improved by addition of agents that increase the cellular adenosine 3',5'-cyclic monophosphate (cAMP) concentration. Together with a decrease in the passage rate of peroxidase, an increase in the transendothelial electrical resistance was observed. A direct correlation was found between the relative increases in cellular cAMP concentration and the relative decrease in peroxidase passage after incubation of the cells with forskolin (0.25 and 2.5 microM), the beta-adrenergic agonist isoproterenol (10 microM), and the stable prostacyclin analogue iloprost (10 microM). Norepinephrine (10 microM) reduced the peroxidase passage to a much larger extent (40% reduction) than might be expected on the basis of a small increase of cAMP concentration. This small increase in cAMP (44%) was the result of interactions of norepinephrine with beta-adrenergic receptors, which increase cAMP, and alpha-adrenergic receptors, which decrease cAMP. The relatively strong reduction in permeability (also found in the presence of the alpha-adrenergic antagonist phentolamine) suggests that an additional cAMP-independent mechanism underlaid the barrier-improving effect of norepinephrine. A marked elevation of cAMP by forskolin was accompanied by a disappearance of F-actin and myosin from stress fibers. They were found diffusely spread over the cell, and F-actin in the cell periphery became prominently visible.

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