Cardiac effects of injections of epinephrine into the spinal intermediolateral column

1993 ◽  
Vol 265 (2) ◽  
pp. H633-H641 ◽  
Author(s):  
V. K. Malhotra ◽  
A. Kachroo ◽  
H. N. Sapru
Keyword(s):  
Adrenergic Receptors ◽  
Cardiovascular Responses ◽  
Spinal Level ◽  
Cardiac Effects ◽  
Alpha Adrenergic Receptors ◽  
Small Doses ◽  
The Right ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Stimulation Of

Small doses of epinephrine (0.008, 0.05, and 0.1 pmol, i.e., 20-nl volumes of 0.40, 2.5, and 5 microM solutions) produced a dose-dependent increase in heart rate when micro-injected into the right intermediolateral column (IML) at T2 spinal level. These effects were mediated via alpha 1-adrenergic receptors because prazosin blocked them. The presence of alpha 1-adrenergic receptors at this site was confirmed by microinjections of phenylephrine (a specific agonist for these receptors); phenylephrine elicited tachycardia. Larger doses of epinephrine (320, 2,000, and 3,200 pmol, i.e., 20-nl volumes of 16, 100, and 160 mM solutions) caused bradycardia when microinjected into the IML. These effects were mediated via alpha 2-adrenergic receptors because idazoxan blocked them. The presence of alpha 2-adrenergic receptors at this site was confirmed by microinjections of clonidine (a specific agonist for these receptors); clonidine elicited bradycardia. Injections of the vehicle (20 nl of normal saline containing 0.3% ascorbic acid, pH 7.4) did not evoke a response. Epinephrine, prazosin, or idazoxan did not alter the responses to L-glutamate. None of the doses of epinephrine elicited any response when injected intravenously. The aforementioned results provide pharmacological evidence for the presence of alpha 1- and alpha 2-adrenergic receptors in the IML at T2. Thus a basis is provided for investigating the role, if any, of alpha-adrenergic receptors in the IML in mediating cardiovascular responses elicited by the stimulation of different brain stem areas.

Alpha 1b-adrenoceptor-mediated stimulation of Na-K pump current in adult rat ventricular myocytes

1993 ◽  
Vol 264 (4) ◽  
pp. H1315-H1318 ◽  
Author(s):  
A. P. Williamson ◽  
R. H. Kennedy ◽  
E. Seifen ◽  
J. P. Lindemann ◽  
J. R. Stimers
Keyword(s):  
Adrenergic Receptors ◽  
Ventricular Myocytes ◽  
Pump Current ◽  
Peak Effect ◽  
Patch Clamp Technique ◽  
Rat Ventricular Myocytes ◽  
Adult Rat ◽  
Whole Cell Patch Clamp ◽  
Dose Dependent ◽  
Stimulation Of

The purpose of this study was to determine if myocardial alpha 1a-and/or alpha 1b-adrenoceptors are involved in the increase in Na-K pump current (Ip) elicited by alpha 1-adrenergic agonists. Single rat ventricular myocytes were isolated by enzymatic disaggregation. The whole cell patch-clamp technique was used to examine dose-dependent effects of phenylephrine (PE) on holding current (Ih) and to determine whether observed actions were mediated via alpha 1a-or alpha 1b-adrenergic receptors. To minimize the contribution of transsar-colemmal currents other than Ip to Ih, membrane voltage was held constant -40 mV, and cells were maintained in a Ca-free perfusate containing 1 mM Ba and 0.1 mM Cd. All experiments were conducted in the presence of 3 microM nadolol. PE elicited dose-dependent increases in Ih, with a peak effect of 0.57 +/- 0.03 pA/pF observed at 30 microM. The response to PE was dose dependently inhibited by prazosin and chloroethylclonidine and was totally eliminated by 1 mM ouabain. When used at doses selective for the alpha 1a-subtype, WB4101 failed to significantly antagonize the action of PE. These data suggest that the observed alpha 1-adrenoceptor-mediated increase in Ih in isolated rat ventricular myocytes is the result of an increase in Ip effected via stimulation of alpha 1b-adrenergic receptors.

Stimulation of acetylcholine release in myenteric plexus by calcitonin gene-related peptide

1990 ◽  
Vol 259 (6) ◽  
pp. G934-G939 ◽  
Author(s):  
M. W. Mulholland ◽  
S. Jaffer
Keyword(s):  
Myenteric Plexus ◽  
Acetylcholine Release ◽  
Calcitonin Gene Related Peptide ◽  
Ach Release ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Dependent Mechanism ◽  
Stimulation Of

The effects of calcitonin gene-related peptide (CGRP) on acetylcholine (ACh) release from myenteric plexus neurons in primary culture were investigated. CGRP (10(-12) to 10(-6) M) produced a dose-dependent increase in [3H]ACh release. The ACh release caused by CGRP was significantly inhibited (74 +/- 24%) by preincubation with dideoxyadenosine but was increased more than threefold by preincubation with theophylline. Incubation of myenteric plexus neurons with CGRP (10(-8) M) in the presence of diltiazem (10(-5) M) or in a calcium-free medium markedly reduced [3H]ACh release. CGRP potentiated [3H]ACh release stimulated by potassium or substance P but not by cholecystokinin octapeptide or forskolin. The results demonstrate that CGRP cause release of ACh from guinea pig myenteric plexus neurons and suggest that the peptide acts through an adenosine 3',5'-cyclic monophosphate-dependent mechanism that involves neuronal calcium channels.

Hyperinsulinemia in rats with hypothalamic obesity: effects of autonomic drugs and glucose

1983 ◽  
Vol 245 (3) ◽  
pp. R372-R378 ◽  
Author(s):  
S. Inoue ◽  
Y. S. Mullen ◽  
G. A. Bray
Keyword(s):  
Adrenergic Receptors ◽  
Serum Insulin ◽  
The Other ◽  
Glucose Stimulation ◽  
Hypothalamic Obesity ◽  
Insulin Levels ◽  
Alpha Adrenergic Receptors ◽  
Beta Receptors ◽  
Increased Sensitivity ◽  
Stimulation Of

The present study examined the effects of autonomic drugs and glucose on the insulin and glucose concentrations of sham-operated rats and of rats with ventromedial hypothalamic (VMH) lesions and obesity. In the basal condition both epinephrine and atropine significantly decreased serum insulin levels in VMH-lesioned but not sham-operated rats. During glucose stimulation of insulin secretion in VMH-lesioned rats, epinephrine inhibited the increase of insulin by 83% and atropine inhibited it by 42%; whereas in sham-operated rats, epinephrine inhibited it by 70% and atropine inhibited it by 34%. Epinephrine with atropine completely blocked the increase of insulin in response to glucose in both VMH-lesioned and sham-operated rats. In the basal condition, epinephrine together with propranolol significantly decreased serum insulin levels in VMH-lesioned but not sham-operated rats. Epinephrine with phentolamine, on the other hand, markedly increased insulin in the VMH-lesioned rats and to a lesser degree in the sham-operated rats. During glucose stimulation epinephrine with propranolol inhibited the increase of insulin in both groups. Epinephrine with phentolamine or isoproterenol markedly increased serum insulin in VMH-lesioned rats. These results suggest that stimulation of the vagus nerve and increased sensitivity of the beta-receptors on the beta-cells of the islet contribute to the development of hyperinsulinemia. The sympathetic contribution may also be through suppression of alpha-adrenergic receptors.

Role of central and peripheral chemoreceptors in diving responses of ducks

1982 ◽  
Vol 243 (5) ◽  
pp. R537-R545 ◽  
Author(s):  
D. R. Jones ◽  
W. K. Milsom ◽  
G. R. Gabbott
Keyword(s):  
Carotid Body ◽  
Significant Contribution ◽  
Cardiovascular Responses ◽  
Peripheral Circulation ◽  
Blood Gas ◽  
Peripheral Chemoreceptors ◽  
Central Chemoreceptors ◽  
The Right ◽  
Stimulation Of

Using techniques of vascular isolation and subsequent perfusion we have investigated the effects of altering blood gas tensions, in the cerebral and carotid body circulations, on some cardiovascular responses to diving in unanesthetized ducks. After denervating the right carotid body, perfusion of the innervated left carotid body with hyperoxic blood significantly reduced diving bradycardia and reduced the increase in hindlimb vascular resistance (HLVR) in 1-min dives compared with dives in which the innervated carotid body was autoperfused. Denervation of systemic arterial baroreceptors reduced the fall in heart rate (HR) and increased the rise in HLVR in all dives. Cross-perfusion of the head, from a donor with blood of normal blood gas tensions, did not significantly affect HR or HLVR in 2-min dives compared with dives in which the head was autoperfused. however, cross-perfusing the cerebral circulation with blood of elevated PaCO2 caused significantly greater increases in HLVR than when high PaCO2 only affected the peripheral circulation. We conclude that peripheral chemoreceptors cause virtually all the bradycardia in the later stages of a dive but only about one-half the increase in HLVR, a significant contribution comes from the stimulation of central chemoreceptors with blood of high PaCO2.

Stimulation of HCO3- transport in isolated proximal bullfrog duodenum by prostaglandins

1980 ◽  
Vol 239 (3) ◽  
pp. G198-G203 ◽  
Author(s):  
G. Flemstrom
Keyword(s):  
Electrical Potential ◽  
Potential Difference ◽  
Electrical Potential Difference ◽  
Morphological Examination ◽  
Minimal Concentration ◽  
Dependent Transport ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Stimulation Of

An in vitro preparation of proximal duodenum from the bullfrog transported alkali into the luminal solution (approximately 1 mueq x h-1 x cm-2) and generated a transepithelial electrical potential difference (5-10 mV, lumen negative). Transport was inhibited by 2,4-dinitrophenol (10(-5) M), CN- (5 X 10(-3) M), indomethacin (5 X 10(-5) M), and acetazolamide (5 X 10(-3) M) indicating that metabolism is required. Both alkali transport and the electrical potential difference showed a dose-dependent increase on administration of the prostaglandins E2, 16,16-dimethyl E2, and F2 alpha. The minimal concentration stimulating transport was lower with the E-type prostaglandins (10(-8) M than with F2 alpha (10(-6) M), and the former also produced greater maximal responses. In addition to metabolic-dependent transport of alkali, there was passive transmucosal migration of HCO3-, amounting to approximately 40% of basal (unstimulated) transport and sensitive to variation of the transmucosal hydrostatic pressure. Morphological examination showed that the preparation is devoid of Brunner glands. Stimulation of duodenal epithelial HCO3- transport by prostaglandins may contribute to their previously demonstrated ability to prevent duodenal ulceration.

Acute central effects of L-glutamate in pentobarbital-anesthetized dogs

1987 ◽  
Vol 252 (3) ◽  
pp. R594-R598
Author(s):  
J. E. Chelly ◽  
M. F. Doursout ◽  
J. P. Buckley
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Dose Effect ◽  
Central Effects ◽  
Intravenous Injections ◽  
Induced Hypertension ◽  
Anesthetized Dogs ◽  
The Right ◽  
Dose Dependent Increase ◽  
Dose Dependent

Microinjections of L-glutamate (10(-10) to 2 X 10(-8) mol/kg) into the nucleus of tractus solitarii produced a dose-dependent increase in mean arterial pressure and a decrease in heart rate. L-Glutamate-induced hypertension was prevented by spinal transection and pretreatment with atropine (1 mg/kg iv) reversed the bradycardia. L-Glutamate also produced a dose-dependent increase in mean arterial pressure when injected intravenously and into the cisterna magna, but the dose-effect curves were shifted to the right. Finally, pretreatment with hexamethonium (30 mg/kg iv) abolished the hypertension resulting from intravenous injections of L-glutamate. These data demonstrate that the nucleus of tractus solitarii may play a determinant role in the central pressor effects of L-glutamate. In addition, we demonstrated that this hypertension was due to a central sympathetic stimulation and that the autonomic nervous system also mediated the pressor effects of intravenous L-glutamate.

scholarly journals Atypical Gastric Ulcer in an Elderly Cocaine User

2013 ◽  
Vol 2013 ◽  
pp. 1-3
Author(s):  
Vinaya Gaduputi ◽  
Hassan Tariq ◽  
Ariyo Ihimoyan
Keyword(s):  
Gastric Ulcer ◽  
Adrenergic Receptors ◽  
Mesenteric Arteries ◽  
Cocaine User ◽  
Gastrointestinal Manifestations ◽  
Cocaine Use ◽  
Alpha Adrenergic Receptors ◽  
Gastrointestinal Ischemia ◽  
Stimulation Of

Cocaine or Benzoylmethylecgonine is an alkaloid extracted from the leaves of the Erythroxylon plant, which can cause gastrointestinal ischemia from severe arterial vasoconstriction via stimulation of alpha-adrenergic receptors in the gastric and mesenteric arteries. We report this case of a 65-year-old man who presented with a single massive ulcer at the incisura of the stomach as a result of cocaine use. The size and location of this ulcer were atypical and illustrate the potential for serious gastrointestinal manifestations from cocaine use.

Stimulation of lipolysis in rat heart myocytes by isoproterenol

1985 ◽  
Vol 248 (2) ◽  
pp. H208-H216 ◽  
Author(s):  
A. Kryski ◽  
K. A. Kenno ◽  
D. L. Severson
Keyword(s):  
Phosphodiesterase Inhibitor ◽  
Myocardial Cells ◽  
Cyclic Monophosphate ◽  
Rat Hearts ◽  
Triacylglycerol Content ◽  
Rat Heart Myocytes ◽  
Dose Dependent Increase ◽  
Release Of Glycerol ◽  
Dose Dependent ◽  
Stimulation Of

Calcium-tolerant myocytes were isolated from rat hearts. Isoproterenol produced a dose-dependent increase in glycerol output (lipolysis) that could be blocked by propranolol. The presence of glucose in the incubation medium enhanced the release of glycerol from myocytes but had no effect on the decline in triacylglycerol content. No incorporation of radioactivity from [U-14C]glucose into glycerol could be detected. In incubations with isoproterenol, there was a stoichiometric relationship between the glycerol output and the decrease in triacylglycerol levels. The addition of the phosphodiesterase inhibitor 1-methyl-3-isobutylxanthine resulted in an increase in the basal glycerol output and an enhancement of the isoproterenol-stimulated lipolytic rate. Forskolin and 8-(4-chlorophenylthio)adenosine 3',5'-cyclic monophosphate also produced a concentration-dependent stimulation of lipolysis in myocytes. Therefore, lipolysis in isolated myocytes must be regulated by adenosine 3',5'-cyclic monophosphate-dependent mechanisms. These results demonstrate that lipolysis can be observed in myocardial cells and that the lipolytic response to isoproterenol cannot be secondary to a physiological (inotropic) response since these myocyte preparations are quiescent.

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