Dual mechanism for catecholamine secretion in the dogfish shark Squalus acanthias

1983 ◽  
Vol 244 (5) ◽  
pp. R641-R645
Author(s):  
D. F. Opdyke ◽  
J. Bullock ◽  
N. E. Keller ◽  
K. Holmes
Keyword(s):  
Ganglion Cells ◽  
Pressor Response ◽  
Plasma Catecholamines ◽  
Squalus Acanthias ◽  
Catecholamine Secretion ◽  
Plasma Catecholamine ◽  
Pressor Responses ◽  
Dogfish Shark ◽  
Plasma Catecholamine Concentrations ◽  
Dual Mechanism

Both 1,1-dimethyl-4-phenylpiperazinium iodide, a ganglionic stimulating drug (DMPP), and potassium ion (K+) cause a pressor response when injected into Squalus acanthias, an elasmobranch. The pressor responses are due to increased secretion of epinephrine and norepinephrine. The pressor response to DMPP can be blocked by prior infusion of hexamethonium, a ganglionic blocking drug. However, ganglionic blockade does not inhibit the pressor response to K+. Plasma catecholamine concentrations do not increase significantly in response to challenge with DMPP after hexamethonium infusion, but exceedingly high levels of plasma catecholamines quickly appear after K+ injection following hexamethonium infusion. It is concluded that there are at least two mechanisms controlling catecholamine secretion in the dogfish, one of which involves the ganglion cells that are intimately associated with chromaffin cells in the chromophil bodies that are so characteristic of this species and elasmobranchs in general.

Angiotensin II-mediated catecholamine release during the pressor response in rats

1994 ◽  
Vol 142 (1) ◽  
pp. 19-28 ◽  
Author(s):  
D G Butler ◽  
D A Butt ◽  
D Puskas ◽  
G Y Oudit
Keyword(s):  
Angiotensin Ii ◽  
Pressor Response ◽  
Plasma Renin ◽  
Sympathetic Nerves ◽  
Catecholamine Release ◽  
Plasma Catecholamine ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Pressor Responses ◽  
Plasma Catecholamine Concentrations

Abstract Angiotensin II (ANG II)-mediated catecholamine release and its possible contribution to the pressor response was assessed in baroreceptor-denervated rats. Neonatal male Sprague-Dawley rats were injected with the sympatholytic drug, guanethidine monosulphate (50 mg/kg s.c., 6 days/week) for 40 days. Plasma catecholamine concentrations were measured using a 3H-radioenzymatic assay as follows: (a) before and 30 s after the injection of saline or ANG II (79·3 pmol/kg i.v.), at the peak of the pressor response, then 50 s and 80 s thereafter, in guanethidine-treated (GUAN) and saline-injected (SHAM) rats, and (b) before and after adrenalectomy (ADX), following the same time-sequence for ANG II as in (a). Peak pressor responses to graded doses of ANG II (6·6, 26·4, 53·0 and 79·3 pmol/kg i.v.) were measured in GUAN+ADX and ADX rats. Destruction of peripheral sympathetic nerves was confirmed by measurements of plasma noradrenaline (NA), adrenaline (AD) and dopamine (DA) concentrations and by changes in pressor responses and heart rates following i.v. doses of tyramine. ANG II induced significantly (P<0·05) greater pressor responses in GUAN+ADX rats than in ADX rats, especially after the 53·0 and 79·3 pmol/kg doses. Plasma AD concentrations increased within seconds after the pressor response to ANG II in both GUAN and SHAM rats but there was no change in plasma NA or DA concentrations (P<0·05). ANG-II-mediated AD release from the adrenal medulla may contribute to the overall pressor action of the peptide. The vasculature became more sensitive to ANG II at a time when NA and DA depletion occurred following sympathectomy and/or adrenalectomy. This heightened sensitivity to ANG II was not due to a decrease in circulating ANG II in sympathectomized rats because even though plasma renin activity fell from 6·54 ±0·52 to 3·77 ±0·26 ng ANG I/ml per h it remained within the normal range. Journal of Endocrinology (1994) 142, 19–28

Abstract 57: Therapeutic Effects of Small Molecule Gβγ Inhibition in Pressure Overload Heart Failure

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Fadia A Kamal ◽  
Alan V Smrcka ◽  
Burns C Blaxall
Keyword(s):  
Heart Failure ◽  
Small Molecule ◽  
Interstitial Fibrosis ◽  
Plasma Catecholamines ◽  
Pressure Overload ◽  
Plasma Catecholamine ◽  
Therapeutic Effects ◽  
Mrna Levels ◽  
Group V ◽  
Plasma Catecholamine Concentrations

Heart failure (HF) is a progressive disease with rapidly increasing rates of morbidity and mortality; it is the leading cause of death worldwide. Elevated sympathetic nervous system activity, a salient feature of HF progression, leads to pathologic attenuation and desensitization of β-adrenergic receptors (β-ARs) due in part to Gβγ-mediated signaling. We recently reported that novel small molecule Gβγ inhibitors selectively block specific Gβγ signals and halt HF progression in pharmacologic and transgenic mouse models of HF. We assessed the hypothesis that the Gβγ inhibitor Gallein could be salutary in treating pre-existing HF in a clinically relevant model. We utilized the pressure-overload HF model of mouse transverse aortic constriction (TAC). Four weeks post-TAC, mice received daily IP injections of vehicle (PBS; group V) or Gallein (10mg/Kg/day; group G) for eight weeks. Gallein treatment improved survival (7 of 9 mice survived vs. 5 of 9 mice in group V) and cardiac function (%EF 75.2 ± 7.5 vs 35.6 ± 17.2 in group V, +dP/dt (mmHg/sec) 7022 ± 485.3 vs. 3584 ± 598.6 in group V), -dP/dt (mmHg/sec) -5826 ± 910.7 vs. -3260 ± 62.3 in group V, LVEDP (mmHg) 11.5 ± 3.7 vs. 29.45 ± 3.6 in group V). In addition, gallein reduced cardiac hypertrophy (HW/BW (mg/g) 5.8 ± 0.3 vs. 8.8 ± 1.1 in group V) and plasma catecholamine concentrations (adrenaline (ng/ml) 1.3 ± 0.3 vs. 6.6 ± 2.8 in group V, noradrenaline (ng/ml) 3.6 ± 0.6 vs. 15.1 ± 3.6 in group V). Reduction of interstitial fibrosis as well as mRNA levels of α-SMA, TNF-α, and IL-6 was observed in the hearts of Gallein treated animals (59.7 ± 14.1%, 43.8 ± 9.3% and 28.5 ± 3.5% relative to group V, respectively). On the molecular level, Gallein treated mice showed less GRK2 and PI3Kγ membrane recruitment, and less Akt activation (42.9 ± 7.1%, 66.7 ± 13.3% and 46.2 ± 7.7% relative to group V, respectively) in myocardial lysates. In conclusion , these data suggest a possible therapeutic role for small molecule Gβγ inhibition in halting the progression of HF, potentially via inhibition of the Gβγ-GRK2-PI3Kγ-Akt pathway. The combined effect of halting HF progression and reducing plasma catecholamines suggests a possible systemic role for small molecule Gβγ inhibition in both the heart and the adrenal gland.

Sample preparation with ion-exchange resin before liquid-chromatographic determination of plasma catecholamines.

1983 ◽  
Vol 29 (7) ◽  
pp. 1426-1428 ◽  
Author(s):  
K N Frayn ◽  
P F Maycock
Keyword(s):  
Cation Exchange ◽  
High Performance ◽  
Exchange Resin ◽  
Plasma Catecholamines ◽  
Cation Exchange Resin ◽  
Chromatographic Determination ◽  
Ion Exchange Resin ◽  
Plasma Catecholamine ◽  
Plasma Catecholamine Concentrations ◽  
Liquid Chromatographic

Abstract Estimation of plasma catecholamine concentrations by "high-performance" liquid chromatography, although increasingly used, still presents difficulties. We describe a method for clean-up of plasma samples on cation-exchange resin before they are extracted with alumina. This procedure eliminates many of the interfering compounds often present in plasma extracts prepared with the alumina treatment alone. The method can be adapted to use commercially available disposable cation-exchange columns.

Pentobarbital effects on plasma catecholamines: temperature, heart rate, and blood pressure

1985 ◽  
Vol 248 (1) ◽  
pp. E95-E100 ◽  
Author(s):  
D. Baum ◽  
J. B. Halter ◽  
G. J. Taborsky ◽  
D. Porte
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Animal Models ◽  
Sympathetic Nervous System ◽  
Rectal Temperature ◽  
Plasma Catecholamines ◽  
Plasma Catecholamine ◽  
Sympathetic Nervous ◽  
Plasma Catecholamine Concentrations

The effects of intravenous pentobarbital were studied in dogs. Plasma pentobarbital concentrations were inversely related to epinephrine and norepinephrine concentrations. Plasma catecholamines appeared fully suppressed at pentobarbital levels greater than 25-30 micrograms/ml. Furthermore, pentobarbital levels were negatively related to rectal temperature, heart rate, and mean blood pressure. The methods of pentobarbital administration influenced plasma pentobarbital as well as epinephrine and norepinephrine levels, temperature, heart rate, and blood pressure. These observations suggest the possibility that pentobarbital inhibits the sympathetic nervous system, which in turn may affect temperature, heart rate, and blood pressure. Because pentobarbital anesthesia affects plasma catecholamine concentrations, the regimen used in animal models requires consideration when interpreting data potentially influenced by the sympathetic nervous system.

Systemic arterial pressor responses induced by potassium in dogfish, Squalus acanthias

1981 ◽  
Vol 241 (3) ◽  
pp. R228-R232
Author(s):  
D. F. Opdyke ◽  
R. G. Carroll ◽  
N. E. Keller
Keyword(s):  
Pressor Response ◽  
Muscle Tension ◽  
Plasma Catecholamines ◽  
Blocking Agent ◽  
Adrenergic Stimulation ◽  
Direct Exposure ◽  
Pressor Responses ◽  
Before And After ◽  
K Concentration

Intravascular injection of small doses of potassium (0.025-0.5 meq) into dogfish results in dose-related dorsal aortic pressor responses. The responses are blocked by phentolamine, an alpha-adrenergic blocking agent. Assays of plasma catecholamines before and after injection of potassium (K+) showed that plasma levels of epinephrine (E) and norepinephrine (NE) had increased significantly (E, 314%; NE, 233%) 1 min after injection. The pressor responses were initiated 40-90 s after K+ injection at which time plasma E and NE levels were already significantly elevated. Experiments on isolated dogfish arterial strips showed that phentolamine cannot block the increase in vascular smooth muscle tension that occurs after direct exposure to small increases (0.003 meq/ml) in K+ concentration. Because phentolamine effectively blocks the pressor response to even higher doses of K+ in vivo, it is thought that, in addition to any direct vasoconstrictor effect or K+, the adrenergic stimulation provided by catecholamine release is required to produce the observed pressor response.

Lack of Nonshivering Thermogenesis in Infants Anesthetized with Fentanyl and Propofol 

1997 ◽  
Vol 86 (4) ◽  
pp. 772-777 ◽  
Author(s):  
Olga Plattner ◽  
Margot Semsroth ◽  
Daniel I. Sessler ◽  
Angelika Papousek ◽  
Christoph Klasen ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Metabolic Rate ◽  
Core Temperature ◽  
Plasma Catecholamines ◽  
Skin Surface ◽  
Infants And Children ◽  
Plasma Catecholamine ◽  
Nonshivering Thermogenesis ◽  
Arterial Blood ◽  
Plasma Catecholamine Concentrations

Background Sweating, vasoconstriction, and shivering have been observed during general anesthesia. Among these, vasoconstriction is especially important because-once triggered-it minimizes further hypothermia. Surprisingly, the core-temperature plateau associated with vasoconstriction appears to preserve core temperature better in infants and children than adults. This observation suggests that vasoconstriction in anesthetized infants may be accompanied by hypermetabolism. Consistent with this theory, unanesthetized infants rely on nonshivering thermogenesis to double heat production when vasoconstriction alone is insufficient. Accordingly, the authors tested the hypothesis that intraoperative core hypothermia triggers nonshivering thermogenesis in infants. Methods With Ethics Committee approval and written parental consent, the authors studied six infants undergoing abdominal surgery. All were aged 1 day to 9 months and weighed 2.4-9 kg. Anesthesia was maintained with propofol and fentanyl. The infants were mechanically ventilated and allowed to cool passively until core (distal esophageal) temperatures reached 34-34.5 degrees C. Oxygen consumption-the authors' index of metabolic rate-was recorded throughout cooling. Because nonshivering thermogenesis triples circulating norepinephrine concentrations, arterial blood was analyzed for plasma catecholamines at approximately 0.5 degree C intervals. Thermoregulatory vasoconstriction was evaluated using forearm-fingertip, skin-surface gradients, with gradients exceeding 4 degrees C, indicating intense vasoconstriction. The patients were subsequently rapidly rewarmed to 37 degrees C. Regression analysis was used to correlate changes in oxygen consumption and plasma catecholamine concentrations with core temperature. Results All patients were vasoconstricted by the time core temperature reached 36 degrees C. Further reduction in core temperature to 34-34.5 degrees C did not increase oxygen consumption. Instead, oxygen consumption decreased linearly. Hypothermia also failed to increase plasma catecholamine concentrations. Conclusions Even at core temperatures approximately 2 degrees C below the vasoconstriction threshold, there was no evidence of nonshivering thermogenesis. This finding is surprising because all other major thermoregulatory responses have been detected during anesthesia. Infants and children thus appear similar to adults in being unable to increase metabolic rate in response to mild intraoperative hypothermia.

Comparison of double- and single-isotope enzymatic derivative methods for measuring catecholamines in human plasma.

1978 ◽  
Vol 24 (4) ◽  
pp. 567-570 ◽  
Author(s):  
M I Evans ◽  
J B Halter ◽  
D Porte
Keyword(s):  
Plasma Catecholamines ◽  
Assay Method ◽  
Plasma Catecholamine ◽  
Isotope Method ◽  
Coefficients Of Variation ◽  
Basal Plasma ◽  
Isotope Technique ◽  
Assay Time ◽  
Plasma Catecholamine Concentrations ◽  
Double Isotope

Abstract We directly compared the reliability of a single-isotope enzymatic derivative technique for measurement of plasma catecholamines with that of the well-established double-isotope method. A significant (p less than 0.001) correlation was observed between measurements (n = 52) in the two assays, both for norepinephrine (r = 0.97) and epinephrine (r = 0.80). Means and coefficients of variation for the two analytes in a pooled specimen of plasma, measured repeatedly during six months, were virtually identical by each assay method. Basal plasma catecholamine concentrations in two different groups of apparently healthy subjects were also similar by each method. Dopamine concentrations in plasma were consistently below the limits measurable by either technique. The single-isotope assay requires half the assay time and 1/200th the sample as the double-isotope method. We conclude that this assay is just as reliable as the double-isotope technique and gives virtually identical values for norepinephrine and epinephrine concentrations in the physiological range.

Autonomic Regulation during Rest and Mental Load in Gilles de la Tourette Syndrome

1998 ◽  
Vol 83 (2) ◽  
pp. 515-529 ◽  
Author(s):  
J. H. M. Tulen ◽  
B. J. M. van de Wetering ◽  
F. Boomsma
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Tourette Syndrome ◽  
Color Word ◽  
Plasma Catecholamines ◽  
Baseline Period ◽  
Plasma Catecholamine ◽  
Cardiovascular Activity ◽  
Mental Load ◽  
Plasma Catecholamine Concentrations

Cardiovascular and catecholaminergic activity during mental load were studied in patients with Tourette syndrome. Patients and controls performed the Color Word Test, preceded by a baseline period, with continuous measurements of heart rate and blood pressure. Blood samples for assay of plasma catecholamine concentrations were obtained before and during the test. The patients showed higher heart rate and blood pressure during baseline than controls, but no differences regarding plasma catecholamines. The tics corresponded with transient increases in heart rate and blood pressure. Spectral analysis of cardiovascular variability during mental load gave only limited evidence of increased sympathetic activity and no alterations in parasympathetic activity in the patients. Therefore, our findings indicate enhanced cardiovascular activity in the patients but not during mental load. The effects of tics on the cardiovascular parameters illustrate the functional complexity of the autonomic nervous system in Tourette syndrome.

Thermogenesis after surgery: effect of perioperative heat conservation and epidural anesthesia

1992 ◽  
Vol 263 (3) ◽  
pp. E441-E447 ◽  
Author(s):  
F. Carli ◽  
J. Webster ◽  
P. Nandi ◽  
I. A. MacDonald ◽  
J. Pearson ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Plasma Catecholamines ◽  
Carbon Dioxide Production ◽  
Plasma Catecholamine ◽  
Colonic Surgery ◽  
Reactive Protein ◽  
Before And After ◽  
Heat Conservation ◽  
Plasma Catecholamine Concentrations ◽  
Protein Response

Body temperature, respiratory gas exchange, and plasma catecholamines were determined before and after surgery in three groups [control (C), warmed (W), and epidural (E) who received local anesthetic at T4-S5 dermatomes during and for 24 h after surgery] of patients undergoing colonic surgery under general anesthesia. At the end of surgery, group W were nursed in an ambient temperature of 28-30 degrees C, whereas the others were at 20-23 degrees C for a period of 24 h. Core (Tc) and dorsal hand temperature decreased during surgery in both C and E (P less than 0.05) but not in W. After surgery, Tc increased similarly in C and E and by a smaller amount in W. Plasma catecholamine concentrations increased significantly in C and W but not in E (P less than 0.001), with the greatest response occurring in C. Postoperative oxygen consumption and carbon dioxide production exceeded preoperative values (P less than 0.01) in C but not in W or E. After surgery, plasma albumin fell and C-reactive protein increased similarly in all three groups. Thus body heat conservation or epidural blockade attenuates or abolishes the rise in plasma catecholamines and oxygen consumption postoperatively but does not prevent the increase in Tc or the acute phase protein response.

Inhibition by BMS 186295, a selective nonpeptide AT1 antagonist, of adrenal catecholamine release induced by angiotensin II in the dog in vivo

1995 ◽  
Vol 73 (4) ◽  
pp. 459-464 ◽  
Author(s):  
Daniel Martineau ◽  
Nobuharu Yamaguchi ◽  
Richard Briand
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Gland ◽  
Catecholamine Release ◽  
Catecholamine Secretion ◽  
Control Group ◽  
Plasma Catecholamine ◽  
Dose Dependency ◽  
At1 Antagonist ◽  
Plasma Catecholamine Concentrations

The aim of the present study was to investigate whether a novel nonpeptide AT1 selective antagonist, BMS 186295 (BMS), can antagonize adrenal catecholamine release induced by local administration of angiotensin II (AII) in anesthetized dogs. Plasma catecholamine concentrations in adrenal venous and aortic blood were determined by an HPLC–electrochemical method. AII was locally administered to the left adrenal gland in the absence and presence of BMS. In the first group (n = 7), local infusion (0.5 mL/min, 1 min) of AII (0.001 – 1.0 μg/mL) resulted in a significant dose-dependent increase in the basal secretion of adrenal catecholamines. Aortic catecholamine levels and mean aortic pressure remained unchanged at all doses tested. In the second group (control, n = 10), four repeated infusions (at intervals of 15 min) of AII at 0.1 μg/mL resulted in significant increases of adrenal catecholamine secretion compared with the baseline. In the third group receiving BMS given locally to the gland (n = 8), the basal adrenal catecholamine secretion was not significantly altered by BMS itself at any dose tested. However, the net catecholamine response to AII (0.1 μg/mL) was significantly and dose dependency attenuated by approximately 40, 60, and 80% in the presence of BMS at doses of 0.1, 1.0, and 10 μg/mL, respectively, compared with the control group. The study indicates that BMS dose dependency blocks AII-induced catecholamine secretion in the dog adrenal gland in vivo.Key words: adrenal gland, angiotensin II, AT1 antagonist, BMS 186295, catecholamine, dog, in vivo.

Sign in / Sign up

Export Citation Format

Share Document