scholarly journals Haemodynamic effects of adrenaline on the isolated, perfused head of the dogfish ‘pup’ (Squalus acanthias)

1983 ◽  
Vol 105 (1) ◽  
pp. 363-371
Author(s):  
D. H. Evans ◽  
J. B. Claiborne
Keyword(s):  
Flow Pattern ◽  
Adrenergic Receptors ◽  
Haemodynamic Effects ◽  
Squalus Acanthias ◽  
Dorsal Aorta ◽  
Beta Adrenergic Receptors ◽  
Alpha Adrenergic Receptors ◽  
Constant Rate ◽  
Branchial Epithelium

The isolated, perfused head of the dogfish ‘pup’ (Squalus acanthias) maintained pressure:flow relationships near to those described for the in vivo adult for at least 3 h when perfused at a constant rate. The addition of 3% polyvinylpyrrolidone reversibly increased branchial resistance, and the postbranchial outflow (arterial + venous) equalled the inflow. 10(−5) M adrenaline reversibly reduced gill resistance (in some cases after a transient increase in resistance) and stimulated perfusate outflow from the dorsal aorta, at the expense of flow from the cephalic and branchial venous system. Phentolamine did not alter the effect of adrenaline on pressure and flow pattern; addition of propranolol inhibited both adrenaline effects and resulted in a slight increase in afferent pressure, indicating that alpha-adrenergic receptors are present, but that the dominant haemodynamic effects are mediated via beta-adrenergic receptors. The isolated, perfused ‘pup’ head may provide a vehicle for investigation of transport phenomena in the elasmobranch branchial epithelium.

Contraction of dog trachealis muscle in vivo: role of alpha-adrenergic receptors

1980 ◽  
Vol 48 (2) ◽  
pp. 329-336 ◽  
Author(s):  
W. H. Beinfield ◽  
J. Seifter
Keyword(s):  
Adrenergic Receptors ◽  
Beta Blockers ◽  
Systemic Arterial Pressure ◽  
Alpha Adrenergic Receptors ◽  
Bilateral Vagotomy ◽  
Cervical Trachea ◽  
Spontaneously Breathing ◽  
Trachealis Muscle

Contraction, relaxation, and longitudinal tension were recorded by isometric strain gauge arches attached to cervical tracheal muscle (CTM) in 60 spontaneously breathing dogs anesthetized with pentobarbital. Intravenous norepinephrine (NE) (3 X 10(-9), 6 X 10(-9), 1.2 X 10(-8), and 2.4 x 10(-8) mol/kg) increased spontaneous mechanical activities (SMA) and caused dose related contraction of CTM in all dogs even though there was no pretreatment with beta-blockers. These activities were first potentiated by propranolol and then prevented by phentolamine. NE briefly decreased SMA and induced CTM relaxation prior to the onset of contraction in one-third of dogs. Propranolol prevented this initial relaxation. CTM responses induced by NE were 1) not significantly altered by atropine, tripelennamine, bilateral vagotomy, curarization, and complete tracheal transection below transducer sites; 2) unrelated to passive constriction of cervical trachea associated with airway elongation; and 3) independent of reflexes initiated by elevations of systemic arterial pressure. The moles per kilogram doses of acetylcholine were found to exceed those of NE when their intravenous administration caused equal CTM contractions in the same dog. These findings are consistent with the existence of alpha-adrenergic receptors in CTM.

Endogenous vasoconstrictor tone in intestine of normal and portal hypertensive rats

1993 ◽  
Vol 264 (1) ◽  
pp. H171-H177 ◽  
Author(s):  
T. Joh ◽  
D. N. Granger ◽  
J. N. Benoit
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Adrenergic Receptors ◽  
Adrenergic Blockade ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Alpha Adrenergic Receptors ◽  
Control Plasma ◽  
Arteriolar Diameter

The purpose of the present study was to determine the effects of endogenous norepinephrine, vasopressin (AVP), and angiotensin II (ANG II) on normal intestinal microvascular dimensions and to determine whether endogenous vasoconstrictor tone was altered in chronic portal hypertension. The intestine of normal and portal hypertensive rats was prepared for in vivo microscopic observation, and an arteriole (1A, 2A, or 3A) was selected for study. Arteriolar diameter and erythrocyte velocity were continuously monitored and used in the calculation of arteriolar blood flow. Once steady-state conditions were established, specific antagonists to alpha-adrenergic, AVP, or ANG II receptors were applied locally to remove the influences of each of these systems. In normal animals, blockade of alpha-adrenergic receptors produced a 1.3, 1.5, and 14.7% increase in the diameter of 1A, 2A, and 3A, respectively. AVP blockade in normal animals produced an 8.7, 1.6, and 1.5% increase in the diameter of 1A, 2A, and 3A, respectively; ANG II blockade only produced an increase in 3A diameter (5.8%). alpha-Adrenergic blockade produced a smaller increase in portal hypertensive 3A diameter (2.3%) compared with normal rats. AVP and ANG II blockade produced a significantly larger dilation of 3A (AVP, 4.8%) and 1A (ANG II, 3.8%), respectively, compared with control. Plasma AVP and ANG II levels were higher in portal hypertensive (AVP, 9.1 pg/ml; ANG II, 8.6 pg/ml) than in normal rats (AVP, 5.5 pg/ml; ANG II, 6.6 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Paraventricular nucleus modulation of glycemia and insulinemia in freely moving lean rats

1989 ◽  
Vol 257 (6) ◽  
pp. R1370-R1376 ◽  
Author(s):  
E. Ionescu ◽  
C. C. Coimbra ◽  
C. D. Walker ◽  
B. Jeanrenaud
Keyword(s):  
Paraventricular Nucleus ◽  
Adrenergic Receptors ◽  
Plasma Insulin ◽  
Zucker Rats ◽  
Sympathetic Outflow ◽  
Beta Adrenergic Receptors ◽  
Glucose Levels ◽  
Alpha Adrenergic Receptors ◽  
Adrenergic Blockers ◽  
Freely Moving

The effect of norepinephrine (NE) injection (40 nmol) into the paraventricular nucleus (PVN) on plasma insulin and glucose levels was studied in freely moving lean Zucker rats bearing chronic right jugular catheters for blood sampling and unilateral intracerebral cannulas placed just above the PVN. Already 2.5 min after NE injection, plasma glucose levels rose significantly, reaching a peak at 10 min poststimulus, whereas the insulin output was strongly inhibited. This NE-induced hyperglycemia was independent of the corticosterone levels. A ganglionic blockade performed by intravenous chlorisondamine (1 mg/kg body wt) reduced by 80% the 4.5-min NE-induced incremental glucose areas. NE-induced hyperglycemia was reduced to a large extent when the PVN alpha-adrenergic receptors were blocked with phentolamine and to a lesser extent when the beta-adrenergic receptors were blocked with propranolol. NE-induced inhibition of insulin output was not affected by these adrenergic blockers. It is concluded that, when administered locally into the PVN, NE can activate the sympathetic outflow expressed by a neurally mediated hyperglycemia through central alpha- and beta-adrenoreceptor and an inhibition of insulin output through other types of receptors and/or mechanisms.

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.

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.

Adrenergic modulation of insulin secretion in vivo dependent on thyroid states.

1978 ◽  
Vol 234 (2) ◽  
pp. E106 ◽  
Author(s):  
F Okajima ◽  
M Ui
Keyword(s):  
Drinking Water ◽  
Insulin Secretion ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Thyroid State ◽  
Adrenergic Modulation ◽  
Adrenergic Agent

Insulin secretory responses via adrenergic mechanisms were studied in vivo with hyperthyroid rats prepared by daily injections with thyroxine and with rats rendered hypothyroid by the addition of methylthiouracil in the drinking water. Isoproterenol, a beta-adrenergic agent, caused hyperinsulinemia in hyperthyroid rats more markedly than in euthyroid rats, but failed to induce hyperinsulinemia in hypothyroid rats. The isoproterenol-induced hyperinsulinemia was abolished by a beta-adrenergic receptor blocker in hyperthyroid as well as in euthyroid rats. The glucose-induced hyperinsulinemia was enhanced in hyperthyroid, was not essentially affected in euthyroid, and was inhibited in hypothyroid rats, by an alpha- and beta-adrenergic agent such as epinephrine. It is concluded that the relative function of alpha- to beta-adrenergic receptors responsible for the pancreatic secretion of insulin is dependent on the thyroid state; beta-adrenergic actions are predominant over alpha-actions in hyperthyroidism and vice versa in hypothyroidism.

Thromboxane A2-Stimulated Human Platelet Aggregation Is Potentiated By Epinephrine Acting VIA Alpha Adrenergic Receptors

1981 ◽  
Author(s):  
G J Johnson ◽  
G H R Rao ◽  
J G White
Keyword(s):  
Platelet Aggregation ◽  
Adrenergic Receptors ◽  
Human Platelet ◽  
Thromboxane A2 ◽  
Human Platelets ◽  
Adrenergic Agents ◽  
Alpha Adrenergic Receptors ◽  
Human Platelet Aggregation ◽  
Induced Aggregation

Epinephrine (E) potentiates arachidonate (A)-induced aggregation of human platelets. A-insensitive dog platelets (AIP), that form thromboxane A2 (T) but do not aggregate when stirred with A alone, aggregate when exposed to E + A. Therefore, we studied the effect of E on T-stimu- lated human platelet aggregation. AIP stirred with A formed T which was confirmed by TLC. 1/100 to 1/200 volume of AIP was removed 30 sec. after A, and transferred to gel- filtered, aspirin-incubated human platelets. Recipient platelet aggregation was proportional to the volume of AIP transferred. The addition of the thromboxane synthetase inhibitor, Azo Analog I, abolished the aggregating activity of AIP. Transfer of an aliquot of AIP that was inadequate to aggregate human gel-filtered, aspirin-incubated platelets resulted in irreversible aggregation in the presence of ≥0.5nM E. E potentiated aggregation when added 3 min. before but not 3 min. after aliquot transfer. T-stimulated aggregation was abolished by the T-antagonist, 13 azapro- stenoic acid (APA), but E added after APA and before T restored aggregation. E potentiation of T-stimulated aggregation was abolished by prior exposure to equimolar yohimbine, dihydroergocryptine and phentolamine, agents that bind to alpha2 adrenergic receptors, but not by prazosin an alpha1 antagonist. Higher concentrations of E reversed the inhibitory effects of the alpha2 adrenergic agents. All of these agents in higher concentrations (1-100μM) also blocked aggregation induced by T alone. Therefore T-induced platelet aggregation is potentiated by E, in concentrations attained in vivo, by a mechanism linked to platelet alpha adrenergic receptors. Platelet alpha2 receptors have a close functional relationship to the postulated T receptor. E may initiate platelet aggregation in vivo when T is formed in quantities inadequate to alone induce aggregation.

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