A pharmacological analysis of the adrenergic and cholinergic mechanisms regulating branchial vascular resistance in the rainbow trout (Salmo gairdneri)

1975 ◽  
Vol 53 (11) ◽  
pp. 1569-1577 ◽  
Author(s):  
Chris M. Wood
Keyword(s):  
Blood Pressure ◽  
Rainbow Trout ◽  
Vascular Resistance ◽  
Cholinergic Receptors ◽  
Salmo Gairdneri ◽  
Constant Flow ◽  
Adrenergic Stimulation ◽  
Cholinergic Mechanisms ◽  
Coronary Vasculature ◽  
Pharmacological Analysis

The adrenergic and cholinergic mechanisms regulating branchial vascular resistance in the trout have been studied using a whole gill preparation perfused at constant flow under approximately normal afferent and efferent levels of blood pressure. The receptors have been pharmacologically characterized by agonist potency comparisons within individual preparations and by the use of specific antagonists. The predominant response to adrenergic stimulation is vasodilation mediated by β-receptors, but a more rapid vasoconstriction mediated by α-receptors may also occur. The β-adrenoreceptors appear to be of the β1, variety, as in the homologous coronary vasculature of mammals. The cholinergic receptors of the gills are purely muscarinic in nature and mediate vasoconstriction. The possible functions of the mechanisms are discussed.

The influence of temperature and anaemia on the adrenergic and cholinergic mechanisms controlling heart rate in the rainbow trout

1979 ◽  
Vol 57 (12) ◽  
pp. 2440-2447 ◽  
Author(s):  
Chris M. Wood ◽  
Patricia Pieprzak ◽  
J. N. Trott
Keyword(s):  
Heart Rate ◽  
Rainbow Trout ◽  
Relative Effect ◽  
Salmo Gairdneri ◽  
Resting Heart Rate ◽  
Adrenergic Stimulation ◽  
Cholinergic Mechanisms ◽  
Cholinergic Mechanism ◽  
Cholinergic Tone ◽  
C 30

The capacity for cardioacceleration by adrenergic and cholinergic mechanisms was studied in resting rainbow trout, Salmo gairdneri, at 5, 12, and 20 °C. The trout were fitted with chronic dorsal aortic catheters for heart rate and blood pressure measurements. At all three temperatures, muscarinic cholinergic blockade with atropine caused substantial tachycardia, thereby indicating the presence of cholinergic vagal tone in resting animals. The relative effect of atropine was significantly greater at 5 °C (+53% of resting heart rate) than at 12 and 20 °C (≈ +30%). Maximal adrenergic stimulation (via adrenaline) after atropine caused a small further cardioacceleration at all temperatures. The adrenaline effect increased significantly from +8% (of resting heart rate) at 5 °C to +15% at 20 °C. The findings provide qualified support for the hypothesis that a reduction in vagal cholinergic activity is relatively more important in tachycardia at low temperature, and that adrenergic stimulation is relatively more important at high temperature, although the cardioacceleratory capacity of the cholinergic mechanism remains dominant throughout. The increase in heart rate accompanying experimental anaemia (haematocrit ≤ 6%) at all three temperatures was almost entirely due to a removal of vagal cholinergic tone; the contribution of adrenergic mechanisms, if any, was small.

Changes in Blood Pressure in the Rainbow Trout During Hypoxia

1967 ◽  
Vol 46 (2) ◽  
pp. 297-305 ◽  
Author(s):  
G. F. HOLETON ◽  
D. J. RANDALL
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Rainbow Trout ◽  
Vascular Resistance ◽  
Ventral Aorta

1. Methods for cannulating the ventral aorta of the trout, which permit the measurement of blood pressure in the unanaesthetized, unrestrained, intact fish are described. 2. Rate and amplitude of breathing and blood pressure in the dorsal and ventral aortae increase during hypoxia. These changes are associated with a marked bradycardia. 3. There are increases in vascular resistance to blood flow in both respiratory and systemic circulations during hypoxia. 4. Post hypoxia is associated with large increases in ventral aortic and dorsal aortic pressures.

Effects of gastric distension on the cardiovascular system in rainbow trout (Oncorhynchus mykiss)

2008 ◽  
Vol 294 (5) ◽  
pp. R1648-R1656 ◽  
Author(s):  
Henrik Seth ◽  
Erik Sandblom ◽  
Susanne Holmgren ◽  
Michael Axelsson
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Rainbow Trout ◽  
Gastrointestinal Tract ◽  
Arterial Pressure ◽  
Oncorhynchus Mykiss ◽  
Vascular Resistance ◽  
Stomach Wall ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Chemical Stimuli

When animals feed, blood flow to the gastrointestinal tract increases to ensure an adequate oxygen supply to the gastrointestinal tissue and an effective absorption of nutrients. In mammals, this increase depends on the chemical properties of the food, as well as, to some extent, on the mechanical distension of the stomach wall. By using an inflatable nitrile balloon positioned in the stomach, we investigated the cardiovascular responses to mechanical stretch of the stomach wall in rainbow trout ( Oncorhynchus mykiss). Distension with a volume equivalent to a meal of 2% of the body mass increased dorsal aortic blood pressure by up to 29%, and central venous blood pressure increased transiently nearly fivefold. The increase in arterial pressure was mediated by an increased vascular resistance of both the systemic and the intestinal circulation. Cardiac output, heart rate, and stroke volume (SV) did not change, and only transient changes in gut blood flow were observed. The increase in arterial pressure was abolished by the α-adrenergic antagonist prazosin, indicating an active adrenergic vasoconstriction, whereas the venous pressor response could be the consequence of a passive increase in intraperitoneal pressure. Our results show that mechanical distension of the stomach causes an instantaneous increase in general vascular resistance, which may facilitate a redistribution of blood to the gastrointestinal tract when chemical stimuli from a meal induce vasodilation in the gut circulation. The normal postprandial increase in gut blood flow in teleosts is, therefore, most likely partly dependent on mechanical stimuli, as well as on chemical stimuli.

DORSAL AORTIC BLOOD PRESSURES RECORDED FROM THE RAINBOW TROUT (SALMO GAIRDNERI)

1965 ◽  
Vol 43 (5) ◽  
pp. 863-872 ◽  
Author(s):  
D. J. Randall ◽  
L. S. Smith ◽  
J. R. Brett
Keyword(s):  
Blood Pressure ◽  
Oxygen Consumption ◽  
Rainbow Trout ◽  
Systolic Blood Pressure ◽  
Salmo Gairdneri ◽  
Free Swimming ◽  
Aortic Blood ◽  
Cannulation Technique ◽  
Blood Pressures

Dorsal aortic blood pressures were recorded from unanesthetized, free-swimming intact fish by a previously described cannulation technique. Some cardiovascular and breathing changes during recovery from the operation and anesthesia are reported. Dorsal aortic systolic blood pressures of 38.7 ± 2.9 mm Hg were recorded from unrestrained intact trout (Salmo gairdneri). A limited study indicated that there were no variations in dorsal aortic systolic blood pressure with changes in oxygen consumption in quiescent fish.

Neural regulation of blood pressure in rainbow trout (Salmo gairdneri)

1978 ◽  
Vol 56 (8) ◽  
pp. 1678-1683 ◽  
Author(s):  
D. G. Smith
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Rainbow Trout ◽  
Peripheral Resistance ◽  
Systemic Blood Pressure ◽  
Salmo Gairdneri ◽  
Exercise Tachycardia ◽  
Aortic Blood Pressure ◽  
And Control ◽  
Selective Increase

Mean dorsal aortic blood pressure (Pda) and heart rate were measured in free-swimming rainbow trout (Salmo gairdneri). The fish were swum in a water tunnel at 0.5 body lengths/s (control) and were exercised at 45-min intervals by a 5-min period of rapid swimming at 2 body lengths/s.Control Pda was 4.0 ± 0.11 kPa and control heart rate was 56 ± 2.1 beats/min. During rapid swimming Pda and heart rate increased by 15 and 13% respectively. α-Receptor blockade with phentolamine (2 mg/kg) or adrenergic transmitter release blockade with bretylium (10 mg/kg) prevented the exercise hypertension and converted it to a decrease of 5% (phentolamine) or 18% (bretylium). Exercise tachycardia was reduced slightly by each compound. Phentolamine decreased the control Pda by 5%. Acute bretylium treatment increased Pda by 39% but Pda in fish treated chronically with bretylium was 30% below control and decreased by a further 6% during rapid swimming. The acute effects of these and other antihypertensive compounds are discussed. It is concluded that systemic blood pressure in trout is controlled by tonically active adrenergic nerves acting on systemic vessels via α-adrenoreceptors. These nerves produce a selective increase in peripheral resistance during rapid swimming.

The control of blood pressure during external hypercapnia in the rainbow trout (Oncorhynchus mykiss)

1999 ◽  
Vol 202 (16) ◽  
pp. 2177-2190 ◽  
Author(s):  
S.F. Perry ◽  
R. Fritsche ◽  
T.M. Hoagland ◽  
D.W. Duff ◽  
K.R. Olson
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Central Venous ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Blood Pressures

Adult freshwater rainbow trout (Oncorhynchus mykiss) were exposed acutely (approximately 20 min) in a stepwise manner to increasing levels of environmental carbon dioxide ranging between 1.7 and 9.0 mmHg (0.23-1.2 kPa). Experiments were performed to examine, for the first time, the influence of hypercapnic acidosis on aspects of cardiovascular physiology including blood pressure, cardiac output and vascular resistance. Fish displayed dose (water CO(2) partial pressure) -dependent increases in ventral aortic (13–39 %) and dorsal aortic (17–54 %) blood pressures that reflected marked increases in systemic vascular resistance (16–78 %); branchial vascular resistance was unaffected by hypercapnia. At the highest level of hypercapnia (9.0 mmHg), central venous pressure was significantly elevated by 54 %. Although cardiac output remained constant, heart rate was significantly lowered by 4–7 beats min(−)(1) at the two highest levels of hypercapnia. To determine whether the cardiovascular responses to hypercapnia were being blunted by the stepwise increase in external P(CO2), a separate group of fish was exposed directly to a single step of hypercapnia (water P(CO2) 8.0 mmHg). The cardiovascular responses were similar to those exhibited by the more gradually exposed fish except that central venous pressure did not increase and the extent of the bradycardia was greater (13 beats min(−)(1)). After confirming the effectiveness of yohimbine in blocking the vasoconstrictory (α)-adrenoreceptors of the systemic vasculature, this antagonist was used as a tool to assess the importance of (α)-adrenoreceptor stimulation in promoting the cardiovascular responses during hypercapnia. Prior treatment of fish with yohimbine prevented the increased blood pressures and systemic vascular resistance during hypercapnia but did not influence the CO(2)-induced bradycardia. Plasma levels of catecholamines did not change during hypercapnia, and therefore the stimulation of the systemic (α)-adrenoreceptors presumably reflected increased sympathetic nerve activity. To determine whether the cardiovascular changes elicited by hypercapnia were related to acidosis-induced hypoxaemia, fish were exposed to hypoxia in a stepwise manner (water P(O2) 65–151 mmHg). The cardiovascular responses to hypoxia were markedly different from those to hypercapnia and consisted of pronounced increases in systemic and branchial vascular resistance, but only at the most severe level of hypoxia; ventral and dorsal aortic pressures were unaffected. The differences between the responses to hypercapnia and hypoxia, coupled with the smaller reductions in blood oxygen content during hypercapnia, support the hypothesis that the cardiovascular responses to CO(2) are direct and are unrelated to hypoxaemia.

Disturbances in Haematology, Fluid Volume Distribution and Circulatory Function Associated with Low Environmental pH in the Rainbow Trout, Salmo Gairdneri

1982 ◽  
Vol 99 (1) ◽  
pp. 397-415 ◽  
Author(s):  
C. LOUISE MILLIGAN ◽  
CHRIS M. WOOD
Keyword(s):  
Blood Pressure ◽  
Rainbow Trout ◽  
Low Ph ◽  
Body Water ◽  
Salmo Gairdneri ◽  
Volume Distribution ◽  
Plasma Ions ◽  
Arterial Blood ◽  
Intracellular Compartments ◽  
Total Body

Exposure of adult rainbow trout to low pH (4.0–4.5) for 3 days resulted in progressive increases in heart rate, mean arterial blood pressure and haematocrit. The haematocrit increase resulted from erythrocyte swelling, a reduction in plasma volume and a mobilization of erythrocytes from the spleen. Erythrocyte swelling probably resulted from plasma acidosis and a reduction in plasma ions (McDonald & Wood, 1981). There was an associated redistribution of body water from extracellular to intracellular compartments, but maintenance of total body water content. Erythrocyte mobilization was reflected in an increase in reticulocyte and erythrocyte counts, and a depletion of splenic blood reserves. Haemoconcentration caused large increases in blood viscosity, which contributed to the rise in blood pressure. Pharmacological analysis revealed an adrenergic component to the cardiovascular disturbance. These events are thought to play a key role in the toxic syndrome.

CARDIOVASCULAR RESPONSES TO SCYLIORHININ I AND II IN THE RAINBOW TROUT, ONCORHYNCHUS MYKISS, IN VIVO AND IN VITRO

1994 ◽  
Vol 191 (1) ◽  
pp. 155-166 ◽  
Author(s):  
J Kagstrom ◽  
M Axelsson ◽  
S Holmgren
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Cardiovascular Responses ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Initial Decrease

Changes in cardiac output, heart rate, dorsal aortic blood pressure and coeliac artery blood flow were measured in unrestrained rainbow trout, Oncorhynchus mykiss, following injections of the elasmobranch tachykinins scyliorhinin I and II. The resistance in the coeliac vascular bed and the total systemic vasculature were calculated from blood pressure and flow. In addition, isolated tails were perfused to investigate the effect of the peptides on the somatic vasculature. Scyliorhinin I (SCY I) produced a biphasic change in the coeliac vascular resistance: an initial decrease was followed by an increase. The decrease in coeliac vascular resistance was accompanied by a decrease in the total systemic vascular resistance, leading to an increased cardiac output. The ensuing increase in coeliac vascular resistance caused a slight increase in blood pressure. In the perfused tail, SCY I produced a marked increase in the somatic vascular resistance. Scyliorhinin II (SCY II) decreased the systemic vascular resistance, causing an increase in cardiac output. SCY II also caused a late increase in the coeliac vascular resistance, which led to hypertension and bradycardia. In vitro, SCY II produced a biphasic response in which an initial decrease in the somatic resistance was followed by a larger increase. The results demonstrate that exogenous SCY I and II are vasoactive peptides that act by different mechanisms in the rainbow trout cardiovascular system. Their actions also differ from the actions of substance P previously observed in the cod, Gadus morhua, and possibly involve a neural reflex.

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