scholarly journals Haemodynamic effects of secretory agents on the isolated elasmobranch rectal gland

1983 ◽  
Vol 103 (1) ◽  
pp. 193-204 ◽  
Author(s):  
T. J. Shuttleworth
Keyword(s):  
Cyclic Amp ◽  
Adrenergic Receptors ◽  
Rectal Gland ◽  
Secretory Cells ◽  
Vascular Effects ◽  
Alpha Adrenergic Receptors ◽  
Perfusion Flow ◽  
Flow Through ◽  
Ribose Moiety

Perfusion flow rate in the isolated elasmobranch rectal gland, perfused at in vivo pressures, was measured in Scyliorhinus canicula L. and Squalus acanthias L. Flow through the secretory parenchyma of the gland was reduced in the presence of concentrations of catecholamines in the physiological range, an effect mediated via alpha-adrenergic receptors within the gland vasculature. Flow through the non-secretory vascular shunts of the rectal gland was unaffected. The vasoconstriction induced by noradrenaline was blocked by the addition of cyclic AMP + theophylline or adenosine at concentrations known to stimulate secretion by the gland. In Squalus, a similar effect was seen with the secretagogue vasoactive intestinal peptide, but this agent had no effect in the glands of Scyliorhinus. Experiments indicate that the blockage of the noradrenaline effect by the secretory agents does not involve any stimulation of vasodilatory beta-adrenergic receptors and, furthermore, that the vasomotor effects of these agents appear to be entirely independent of their actions on the secretory cells. Evidence is presented indicating that the vasomotor action of adenosine may be mediated via receptors specific for the ribose moiety of the nucleoside (Ra receptors) activating adenylate cyclase, and that this may, in turn, explain the observed effects of the addition of exogenous cyclic AMP. The significance of the observed vascular effects in the overall control of secretion rate by the gland in vivo is discussed.

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)

A PERFUSED TELEOSTEAN GILL PREPARATION: VASCULAR ACTIONS OF NEUROHYPOPHYSIAL HORMONES AND CATECHOLAMINES

1971 ◽  
Vol 51 (4) ◽  
pp. 621-635 ◽  
Author(s):  
J. C. RANKIN ◽  
J. MAETZ
Keyword(s):  
Adrenergic Receptors ◽  
Ringer Solution ◽  
Arginine Vasotocin ◽  
Millipore Filter ◽  
Flow Rates ◽  
Alternative Pathways ◽  
Neurohypophysial Hormones ◽  
Flow Through ◽  
Β Adrenergic Receptors

SUMMARY When isolated eel gills were perfused under conditions resembling, as closely as possible, those found in vivo and under constant pressure, neurohypophysial hormones decreased and catecholamines increased the rate of flow of perfusate, the latter response being mediated by β-adrenergic receptors. When the Ringer solution was not filtered before use, flow rates rapidly declined and 10−5 m-adrenaline or noradrenaline was required to maintain constant flow. Under these conditions, 10−14 m-isotocin or 10−13 m-arginine vasotocin (AVT) produced vasoconstriction. When the Ringer solution was filtered through a 0·22 μm Millipore filter before use, constant high flow rates could be maintained in the absence of catecholamines. Noradrenaline increased the flow rate at concentrations of down to 10−9 mol/l, adrenaline being slightly less active when filtered Ringer solution was used. However, the sensitivity to neurohypophysial hormones was considerably reduced, 10−11 to 10−10 m-isotocin and 5 × 10−11 to 5 × 10−10 m-AVT being the lowest concentrations producing vasoconstriction. No difference in sensitivity to neurohypophysial hormones or catecholamines was observed between gills from seawater adapted or freshwater adapted gills. The results are discussed in relation to the alternative pathways of blood flow through the gills.

scholarly journals Mechanism and control of hyperosmotic NaCl-rich secretion by the rectal gland of Squalus acanthias

1983 ◽  
Vol 106 (1) ◽  
pp. 25-41 ◽  
Author(s):  
F. H. Epstein ◽  
J. S. Stoff ◽  
P. Silva
Keyword(s):  
Cyclic Amp ◽  
Chloride Secretion ◽  
Squalus Acanthias ◽  
Rectal Gland ◽  
Energetic Efficiency ◽  
Secondary Active Transport ◽  
Transport Pathway ◽  
Rectal Glands ◽  
And Control

Secretion of chloride from blood to lumen is accomplished in the rectal gland of elasmobranchs by a process of secondary active transport involving the co-transport of Cl- with Na+ across the basolateral membranes of rectal gland cells. Energy is provided by ATP via membrane Na-K-ATPase, which establishes an electrochemical gradient favouring Na+ influx into the cell. The involvement of K+ in the co-transport mechanism, so as to provide a ratio of 1 Na+:1 K+:2 Cl- entering the cell, would increase the energetic efficiency of the process, and is consistent with the Cl/O2 ration of 27–30 observed in secreting rectal glands. Secretion is stimulated by cyclic AMP (cAMP) and by vasoactive intestinal peptide (VIP) and adenosine, which activate adenylate cyclase. Activation of the gland in vivo probably occurs via VIP-secreting nerves as well as circulating agents; it is inhibited by somatostatin. Cyclic AMP probably stimulates chloride secretion by at least three mechanisms: (1) increasing chloride conductance across the luminal cell membrane, (2) enhancing the co-transport pathway for transmembrane movements of Na+, K+ and Cl- and (3) activating Na-K-ATPase.

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.

scholarly journals Effects of verapamil on lipolysis due to dibutyryl cyclic AMP

1984 ◽  
Vol 220 (1) ◽  
pp. 321-324 ◽  
Author(s):  
H Goko ◽  
S Takashima ◽  
S Shimizu ◽  
S Kagawa ◽  
A Matsuoka
Keyword(s):  
Cyclic Amp ◽  
Adrenergic Receptors ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Dibutyryl Cyclic Amp ◽  
Alpha Adrenergic Receptors ◽  
Biphasic Effect ◽  
Adrenergic Antagonists ◽  
Dose Dependent ◽  
Isolated Rat

The effects of verapamil, a calcium antagonist, on lipolysis in isolated rat adipocytes were studied. Verapamil (100 microM) potentiated lipolysis due to dibutyryl cyclic AMP (Bt2cAMP) at submaximal concentrations, with or without extracellular Ca2+. Lipolysis due to 0.5 mM-Bt2cAMP was potentiated by verapamil in a dose-dependent manner up to 200 microM, whereas at concentrations higher than 100 microM the stimulatory effect of verapamil was progressively diminished with or without extracellular Ca2+. Verapamil showed only an inhibitory effect on lipolysis due to adrenaline (0.1-10 microM) or 3-isobutyl-1-methylxanthine (IBMX; 25-200 microM). The stimulatory effect of verapamil on lipolysis due to Bt2cAMP was not blocked by alpha-adrenergic antagonists. These results suggest (i) that verapamil has a biphasic effect on lipolysis due to Bt2cAMP and only an inhibitory effect on that due to adrenaline or IBMX, and (ii) that extracellular Ca2+ or alpha-adrenergic receptors are not involved in the action of verapamil.

Responsiveness of superficial hand veins to adrenergic stimuli in patients with cystic fibrosis

1989 ◽  
Vol 76 (3) ◽  
pp. 283-287 ◽  
Author(s):  
Hans-Georg Eichler ◽  
Irmgard Eichler ◽  
Norman Lewiston ◽  
Terrence F. Blaschke ◽  
Brian B. Hoffman
Keyword(s):  
Cystic Fibrosis ◽  
Cyclic Amp ◽  
Geometric Mean ◽  
Clinical Score ◽  
Secretory Cells ◽  
Adrenergic Stimulation ◽  
Dorsal Hand Vein ◽  
Severity Of The Disease ◽  
And Control

1. The basic biochemical defect of cystic fibrosis (CF) remains undetermined, but impaired function of the β-adrenoceptor-mediated adenosine 3′:5′-cyclic monophosphate (cyclic AMP)-dependent regulatory pathway in secretory cells is likely to be involved in the pathophysiology of the disease. 2. We have compared responsiveness to β-adrenergic stimulation in vivo by infusing isoprenaline locally into peripheral veins of CF patients and control subjects; the dorsal hand vein technique was used to measure the vascular response to isoprenaline. 3. CF patients required significantly higher doses of isoprenaline for half-maximal dilatation of the preconstricted veins (ED50) than controls (geometric mean: 44.5 ng/min in CF patients compared with 14.8 ng/min in controls; P < 0.05). Maximal venodilatation was 74 ± 30% of baseline in CF patients compared with 94 ± 50% in controls (NS between groups). 4. The clinical score of CF patients was uncorrelated with the ED50 of isoprenaline. Thus the decreased β-adrenergic responsiveness does not seem to be related to the severity of the disease. 5. Our results indicate a defect in the cyclic-AMP-dependent pathway in vascular smooth muscle cells of CF patients. Whether this is associated with the CF gene defect itself requires further study.

An in Vivo Evaluation of Alpha Adrenergic Receptors in Canine Prostate

1989 ◽  
Vol 141 (5) ◽  
pp. 1230-1233 ◽  
Author(s):  
William J. Somers ◽  
Diane felsen ◽  
Ting-Chao Chou ◽  
Donald N. Marion ◽  
Chris E. Chernesky ◽  
...  
Keyword(s):  
Adrenergic Receptors ◽  
In Vivo Evaluation ◽  
Alpha Adrenergic Receptors
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