Adrenergic Stimulation of Regional Plasminogen Activator Release in Rabbits

1992 ◽  
Vol 68 (05) ◽  
pp. 545-549 ◽  
Author(s):  
W L Chandler ◽  
S C Loo ◽  
D Mornin
Keyword(s):  
Lower Extremity ◽  
Plasminogen Activator ◽  
Beta Blocker ◽  
Time Course ◽  
Vascular System ◽  
Adrenergic Stimulation ◽  
Epinephrine Administration ◽  
Adrenergic Antagonist ◽  
Vascular Beds ◽  
Stimulation Of

SummaryThe purpose of this study was to determine whether different regions of the rabbit vascular system show variations in the rate of plasminogen activator (PA) secretion. To start, we evaluated the time course, dose response and adrenergic specificity of PA release. Infusion of 1 µg/kg of epinephrine stimulated a 116 ± 60% (SD) increase in PA activity that peaked 30 to 60 s after epinephrine administration. Infusion of 1 µg/kg of norepinephrine, isoproterenol and phenylephrine had no effect on PA activity. Pretreatment with phentolamine, an alpha adrenergic antagonist, blocked the release of PA by epinephrine while pretreatment with the beta blocker propranolol had no effect. This suggests that PA release in the rabbit was mediated by some form of alpha receptor.Significant arterio-venous differences in basal PA activity were found across the pulmonary and splanchnic vascular beds but not the lower extremity/pelvic bed. After stimulation with epinephrine, PA activity increased 46% across the splanchnic bed while no change was seen across the lower extremity/pelvic bed. We conclude that several vascular beds contribute to circulating PA activity in the rabbit, and that these beds secrete PA at different rates under both basal and stimulated conditions.

scholarly journals Stimulation of phosphoinositide metabolism in hamster brown adipocytes exposed to α1-adrenergic agents and its inhibition with phorbol esters

1986 ◽  
Vol 236 (3) ◽  
pp. 757-764 ◽  
Author(s):  
R J Schimmel ◽  
D Dzierzanowski ◽  
M E Elliott ◽  
T W Honeyman
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Time Course ◽  
Early Event ◽  
Phosphoinositide Metabolism ◽  
Adrenergic Stimulation ◽  
Brown Adipocytes ◽  
Adrenergic Agents ◽  
Kinase C ◽  
Stimulation Of

The present experiments were undertaken to investigate the role of the phosphoinositides phosphatidylinositol 4-phosphate (PtdIns-4-P) and phosphatidylinositol 4,5-biphosphate (PtdIns-4,5-P2) in the alpha 1-adrenergic stimulation of respiration in isolated hamster brown adipocytes. Exposure of isolated brown adipocytes to the alpha-adrenergic-receptor agonist phenylephrine provoked a breakdown of 30-50% of the PtdIns-4-P and PtdIns-4,5-P2 after prelabelling of the cells with [32P]Pi. Coincident with the breakdown of phosphoinositides was an accumulation of labelled phosphatidic acid, which continued for the duration of the cell incubation. The time course of phosphoinositide breakdown was defined more precisely by pulse-chase experiments. Under these conditions, phenylephrine caused radioactivity in phosphatidylinositol, PtdIns-4-P and PtdIns-4,5-P2 to fall by more than 50% within 30 s and to remain at the depressed value for the duration of the incubation (10 min). This phospholipid response to alpha-adrenergic stimulation was blocked by exposure of the cells to phorbol 12-myristate 13-acetate (PMA); likewise phenylephrine stimulation of respiration was prevented by PMA. beta-Adrenergic stimulation of respiration and inhibition of respiration by 2-chloroadenosine and insulin were, however, unaffected by treatment with PMA. On the assumption that PMA is acting in these cells as an activator of protein kinase C, these results suggest the selective interruption of alpha-adrenergic actions in brown adipocytes by activated protein kinase C. These findings suggest that breakdown of phosphoinositides is an early event in alpha-adrenergic stimulation of brown adipocytes which may be important for the subsequent stimulation of respiration. The results from the pulse-chase studies also suggest, however, that phenylephrine-stimulated breakdown of inositol phospholipids is a short-lived event which does not appear to persist for the entire period of exposure to the alpha 1-adrenergic ligand.

Cerebral venous outflow in the dog; influence of adrenergic and cholinergic substances

1959 ◽  
Vol 197 (6) ◽  
pp. 1183-1190 ◽  
Author(s):  
Claude McClure ◽  
Harold D. Green
Keyword(s):  
Jugular Vein ◽  
Venous Blood ◽  
Jugular Bulb ◽  
Metabolic Effects ◽  
Lateral Sinus ◽  
Adrenergic Stimulation ◽  
Venous Outflow ◽  
Jugular Veins ◽  
Vascular Beds ◽  
Stimulation Of

In the intact dog, jugular vein outflow markedly decreased during adrenergic stimulation. After occlusion of both jugular bulbs and both vertebral venous sinuses with celloidin and ligation of all collateral communications along the jugular veins, in the orbit and underlying masseter muscle, lateral sinus outflow was not appreciably influenced by intra-arterial injections of 50 µg of epinephrine or arterenol, or by stimulation of the headward end of the severed vasosympathetic trunk, but intra-arterial injections of methacholine caused a weak vasodilator response. It was concluded that, in the dog, prominent communications exist between intra- and extracranial venous structures. Apparent vasoconstrictor responses are due to a reduced contribution to the jugular bulb from extracranial structures and/or to a deflection of some of the cerebral venous blood into channels other than the jugular bulb, as a result of vasoconstriction in the extracranial beds. Vasoconstrictor and cerebral metabolic effects reported in man, using the nitrous oxide technique, might be due similarly to varying contamination of the internal jugular vein blood by blood draining from adrenergically reactive facial vascular beds.

Reduction of cerebrovascular reactivity during hypercapnia

1982 ◽  
Vol 242 (5) ◽  
pp. R441-R446 ◽  
Author(s):  
A. L. Lopez de Pablo ◽  
M. C. Gonzalez ◽  
G. Dieguez ◽  
B. Gomez ◽  
S. Lluch
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebrovascular Reactivity ◽  
Cerebral Vessels ◽  
Maxillary Artery ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Cervical Sympathetic ◽  
Vascular Beds ◽  
Stimulation Of

The effects on cerebral blood flow of alpha- or beta-adrenergic receptor stimulation of cerebral vessels were examined in 13 unanesthetized goats before and during hypercapnia produced by inhalation of 10% CO2 in air. This procedure increased the PCO2 from 34 to 52 and was accompanied by a fall in pH from 7.39 to 7.26. Electrical stimulation of the cervical sympathetic nerve and injections of norepinephrine and tyramine into the internal maxillary artery produced reductions in cerebral blood flow that were abolished or reduced in hypercapnia. The increase in cerebral blood flow in response to beta-adrenergic stimulation with isoproterenol was also reduced. Hypercapnia caused a similar depression of the constrictor and dilatory effects of the nonadrenergic drugs vasopressin and diazoxide. The results show a decreased response of cerebral vessels to adrenergic and nonadrenergic stimuli in hypercapnia. The findings do not suggest any difference between the refractoriness of cerebral vessels in hypercapnia and that described in other vascular beds.

Adrenergic stimulation of tissue-type plasminogen activator release in a model of vascular perfusion in rats

1993 ◽  
Vol 70 ◽  
pp. S77
Author(s):  
Licia Iacoviello ◽  
Amalia De Curtis ◽  
Maria Cristina D'Adamo ◽  
Wlodzimierz Buczko ◽  
Maria Benedetta Donati
Keyword(s):  
Plasminogen Activator ◽  
Tissue Type ◽  
Adrenergic Stimulation ◽  
Vascular Perfusion ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Stimulation Of

Alpha 2-receptors mediate catecholamine-stimulated acid secretion in Amphiuma jejunum

1988 ◽  
Vol 255 (5) ◽  
pp. G640-G646
Author(s):  
C. F. Hinton ◽  
J. F. White
Keyword(s):  
Acid Secretion ◽  
Basolateral Membrane ◽  
Adrenergic Agonists ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Ussing Chambers ◽  
Adrenergic Antagonist ◽  
Half Maximal Effective Concentration ◽  
Uk 14,304 ◽  
Stimulation Of

The receptors mediating adrenergic stimulation of acid secretion by Amphiuma jejunum were characterized in this study using alpha- and beta-adrenergic agonists and antagonists. Isolated segments of jejunum were mounted in Ussing chambers and bathed in Cl- -free (SO4(2-] medium. Shortcircuit current (Isc) and acid secretion (JH) were recorded, the latter by measuring the rate of alkalinization of the serosal medium. The beta-adrenergic receptor antagonist, propranolol (10(-4) M), had no effect on the Isc and JH stimulated by norepinephrine (NE). The alpha 2-adrenergic agonists, clonidine and UK-14,304, mimicked the effect of NE, with effective concentrations providing 50% maximal delta Isc of 2.0 X 10(-7) and 9.0 X 10(-8) M, respectively. NE added subsequently produced no greater stimulation. In contrast, the alpha 1-adrenergic agonists, phenylephrine and methoxamine, produced little stimulation of JH and Isc; NE added subsequently stimulated the Isc. The alpha 1-adrenergic antagonist prazosin had no effect on the NE-induced Isc or JH, whereas the alpha 2-adrenergic antagonist yohimbine inhibited the NE-stimulated Isc with a half-maximal effective concentration of 3.5 X 10(-7) M. Yohimbine (10(-4) M) reduced the NE-stimulated Isc by 88%, whereas the spontaneous Isc was reduced by only 12%. These results demonstrate that alpha 2-adrenergic receptors on the basolateral membrane of Amphiuma enterocytes mediate NE-enhanced, but not spontaneous, intestinal acid secretion.

Desmopressin Stimulates Parallel Norepinephrine and Tissue Plasminogen Activator Release in Normal Subjects and Patients with Diabetes Mellitus

1988 ◽  
Vol 59 (02) ◽  
pp. 269-272 ◽  
Author(s):  
M B Grant ◽  
C Guay ◽  
R Lottenberg
Keyword(s):  
Diabetes Mellitus ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Time Course ◽  
Vascular Endothelial Cells ◽  
Normal Subjects ◽  
Plasma Norepinephrine ◽  
Endogenous Catecholamine ◽  
Tissue Plasminogen ◽  
Patients With Diabetes

SummaryDesmopressin acetate administration markedly stimulates release of tissue plasminogen activator (t-PA) from vascular endothelial cells. The mechanism for this effect is unknown. Because infusion of epinephrine has been shown to increase t-PA levels, we examined the role of endogenous catecholamine mediation of t-PA release by desmopressin. Intravenous desmopressin acetate (0.3 μg/kg) was infused over 30 min in 9 controls and 11 subjects with diabetes mellitus, a condition associated with abnormalities of the fibrinolytic system. Plasma was collected in the supine, overnight fasted state at 15 min intervals (0-60 min) for measurement of t-PA activity, t-PA antigen and fractionated catecholamines. t-PA activity peaked at 30-45 min and subsequently decreased. The norepinephrine levels paralleled the t-PA activity. t-PA activity increased 10-fold from 0.14 ± .12 to 1.49 ± 0.79 IU/ml (Mean ± SD) and plasma norepinephrine increased 2- fold from 426 ± 90 to 780 ± 292 pg/ml. However, epinephrine and dopamine levels did not change significantly. The response to desmopressin of control and diabetic subjects was not shown to differ and their data were combined. We conclude that desmopressin increases plasma norepinephrine in addition to t-PA and that the parallel time course of change suggests a possible role for norepinephrine in mediating endothelial cell t-PA release.

Activation of Hageman Factor by α-Adrenergic Stimulation

1970 ◽  
Vol 23 (03) ◽  
pp. 417-422 ◽  
Author(s):  
D. G McKay ◽  
J.-G Latour ◽  
Mary H. Parrish
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Adrenergic Receptor ◽  
Adrenergic Stimulation ◽  
Hageman Factor ◽  
Intravascular Coagulation ◽  
Receptor Sites ◽  
High Doses ◽  
Stimulation Of

SummaryThe infusion of epinephrine in high doses produces disseminated intravascular coagulation by activation of Hageman factor. The effect is blocked by phenoxybenz-amine and is therefore due to stimulation of α-adrenergic receptor sites.

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