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.

Cardiovascular responses in vivo to angiotensin II and the peptide antagonist saralasin in rainbow trout Oncorhynchus mykiss.

1998 ◽  
Vol 201 (2) ◽  
pp. 267-272 ◽  
Author(s):  
J Fuentes ◽  
F B Eddy
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Rainbow Trout ◽  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Cardiovascular Responses ◽  
Hypotensive Effect ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Aortic Blood Pressure

The effects of [Asn1,Val5]-angiotensin II (AngII) and [Sar1,Val5, Ala8]-angiotensin II (saralasin) on dorsal aortic blood pressure, pulse pressure and heart rate were examined in rainbow trout in vivo. AngII when administered as a single dose of 25 microg kg-1 induced a biphasic response in blood pressure, with a significant hypertensive response during the initial 10 min, followed by a significant hypotension of 70-75 % compared with the initial blood pressure after 50 min and continuing until approximately 80 min post-injection. The co-administration of AngII (25 microg kg-1) and saralasin (50 microg kg-1) resulted in the same hypertensive response during the initial phase, but abolished the hypotensive effect of AngII. Heart rate was significantly increased in response to AngII, but the administration of AngII and saralasin together attenuated the increase by approximately 44 %. Stimulation of the endogenous renin-angiotensin system using a vasodilator, sodium nitroprusside, significantly increased drinking rate in rainbow trout fry, a response inhibited by saralasin, indicating a role for AngII-induced hypotension in drinking. For the first time, a decrease in blood pressure in response to AngII in vivo has been demonstrated in fish, and this is discussed in relation to homeostasis of blood pressure and a possible role in the control of drinking.

Control of Blood Pressure and the Distribution of Blood Flow

1991 ◽  
Vol 7 (S1) ◽  
pp. 79-84 ◽  
Author(s):  
Hans T. Versmold
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Systemic Blood Pressure ◽  
Adrenergic Innervation ◽  
Systemic Blood ◽  
Low Cardiac Output ◽  
Neurohumoral Control ◽  
The Brain

Systemic blood pressure (BP) is the product of cardiac output and total peripheral resistance. Cardiac output is controlled by the heart rate, myocardial contractility, preload, and afterload. Vascular resistance (vascular hindrance × viscosity) is under local autoregulation and general neurohumoral control through sympathetic adrenergic innervation and circulating catecholamines. Sympathetic innovation predominates in organs receivingflowin excess of their metabolic demands (skin, splanchnic organs, kidney), while innervation is poor and autoregulation predominates in the brain and heart. The distribution of blood flow depends on the relative resistances of the organ circulations. During stress (hypoxia, low cardiac output), a raise in adrenergic tone and in circulating catecholamines leads to preferential vasoconstriction in highly innervated organs, so that blood flow is directed to the brain and heart. Catecholamines also control the levels of the vasoconstrictors renin, angiotensin II, and vasopressin. These general principles also apply to the neonate.

Changes in Blood Pressure, Heart Rate and Breathing Rate During Moderate Swimming Activity in Rainbow Trout

1967 ◽  
Vol 46 (2) ◽  
pp. 307-315 ◽  
Author(s):  
E. DON STEVENS ◽  
D. J. RANDALL
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Rainbow Trout ◽  
Venous Blood ◽  
The Body ◽  
Swimming Activity ◽  
Breathing Rate ◽  
Blood Pressures ◽  
Ventral Aorta ◽  
Pressure Changes

1. Changes in blood pressure in the dorsal aorta, ventral aorta and subintestinal vein, as well as changes in heart rate and breathing rate during moderate swimming activity in the rainbow trout are reported. 2. Blood pressures both afferent and efferent to the gills increased during swimming and then returned to normal levels within 30 min. after exercise. 3. Venous blood pressure was characterized by periodic increases during swimming. The pressure changes were not in phase with the body movements. 4. Although total venous return to the heart increased during swimming, a decreased blood flow was recorded in the subintestinal vein. 5. Heart rate and breathing rate increased during swimming and then decreased when swimming ceased. 6. Some possible mechanisms regulating heart and breathing rates are discussed.

Characterization of baroreflex impairment in conscious dogs with pacing-induced heart failure

1993 ◽  
Vol 265 (5) ◽  
pp. R1132-R1140 ◽  
Author(s):  
N. B. Olivier ◽  
R. B. Stephenson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Open Loop ◽  
Ventricular Pacing ◽  
Baroreflex Control ◽  
Rapid Ventricular Pacing ◽  
Reflex Control

Open-loop baroreflex responses were evaluated in eight conscious dogs before and during congestive heart failure to determine the effects of failure on baroreflex control of blood pressure, heart rate, cardiac output, and total peripheral resistance. Heart failure was induced by rapid ventricular pacing. Baroreflex function was determined by calculation of the range and gain of the open-loop stimulus-response relationships for the effect of carotid sinus pressure on blood pressure, heart rate, cardiac output, and total peripheral resistance. The range and gain of blood pressure responses were substantially reduced as early as 3 days after induction of heart failure (161 +/- 6 to 99 +/- 8 mmHg and -2.7 +/- 0.3 to -1.5 +/- 0.1, respectively) and remained depressed for the 21 days of heart failure. This depression in baroreflex control of blood pressure was associated with similar depressions in reflex range and gain for heart rate (125 +/- 9 to 78 +/- 11 beats/min and -2.05 +/- 0.2 to -1.16 +/- 0.2 beats/min, respectively) and cardiac output (1.74 +/- 0.2 to 0.46 +/- 0.2 l/min and -0.81 +/- 0.02 to -0.027 +/- 0.008 l/min, respectively). The group-averaged range and gain for reflex control of vascular resistance were not altered by heart failure. In three dogs, discontinuation of rapid ventricular pacing led to resolution of heart failure within 7 days and partial restoration of the range and gain of reflex control of blood pressure. We conclude that heart failure reversibly depresses baroreflex control of blood pressure principally through a concurrent reduction in reflex control of cardiac output, whereas reflex control of vascular resistance is not consistently affected.

scholarly journals Cardiovascular changes during daily torpor in the laboratory mouse

2009 ◽  
Vol 297 (3) ◽  
pp. R769-R774 ◽  
Author(s):  
Steven J. Swoap ◽  
Margaret J. Gutilla
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Core Body Temperature ◽  
Laboratory Mouse ◽  
Caloric Intake ◽  
Peripheral Resistance ◽  
Cardiovascular Changes ◽  
Blood Pressures ◽  
Core Body ◽  
Insight Into

The laboratory mouse is a facultative daily heterotherm in that it experiences bouts of torpor under caloric restriction. Mice are the most frequently studied laboratory mammal, and often, genetically modified mice are used to investigate many physiological functions related to weight loss and caloric intake. As such, research documenting the cardiovascular changes during fasting-induced torpor in mice is warranted. In the current study, C57BL/6 mice were implanted either with EKG/temperature telemeters or blood pressure telemeters. Upon fasting and exposure to an ambient temperature (Ta) of 19°C, mice entered torpor bouts as assessed by core body temperature (Tb). Core Tb fell from 36.6 ± 0.2°C to a minimum of 25.9 ± 0.9°C during the fast, with a concomitant fall in heart rate from 607 ± 12 beats per minute (bpm) to a minimum of 158 ± 20 bpm. Below a core Tb of 31°C, heart rate fell exponentially with Tb, and the Q10 was 2.61 ± 0.18. Further, mice implanted with blood pressure telemeters exhibited similar heart rate and activity profiles as those implanted with EKG/temperature telemeters, and the fall in heart rate and core Tb during entrance into torpor was paralleled by a fall in blood pressure. The minimum systolic, mean, and diastolic blood pressures of torpid mice were 62.3 ± 10.2, 51.9 ± 9.2, 41.0 ± 7.5 mmHg, respectively. Torpid mice had a significantly lower heart rate (25–35%) than when euthermic at mean arterial pressures from 75 to 100 mmHg, suggesting that total peripheral resistance is elevated during torpor. These data provide new and significant insight into the cardiovascular adjustments that occur in torpid mice.

scholarly journals Changes in Respiratory Rate, Blood Pressure and Heart Rate Variability in Rabbits during Orthostasis

2006 ◽  
Vol 75 (1) ◽  
pp. 3-12 ◽  
Author(s):  
J. Mokrý ◽  
T. Remeňová ◽  
K. Javorka
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Respiratory Rate ◽  
Supine Position ◽  
Spectral Power ◽  
Systemic Blood Pressure ◽  
Microcomputer System ◽  
Systemic Blood ◽  
Frequency Bands

The purpose of the study was to evaluate the changes of respiratory rate, systemic blood pressure and heart rate variability parameters (HRV) during orthostasis in anaesthetized rabbits. Furthermore, these changes were influenced by affecting the renin-angiotensin-aldosterone (RAA) system and autonomic nervous system (ANS) to study the mechanisms participating in activity of spectral frequency bands of HRV in rabbits. Ten adult rabbits (Chinchilla) were anaesthetized by ketamine and flunitrazepam. The systemic blood pressure, tidal volume and respiratory rate were measured. HRV was evaluated by microcomputer system VariaPulse TF3E. The R-R intervals were derived from the electrocardiogram signal from subcutaneous needle electrodes. The evaluation of HRV in very low (VLF; 0.01-0.05 Hz), low (LF; 0.05-0.15 Hz) and high frequency bands (HF; 0.15-2.0 Hz) was made and parameters of frequency and time analysis were calculated. The measurements were made in horizontal (supine) position, in orthostasis (the angle of 60 °) and again in supine position before and after enalapril (0.5 mg/kg b.w.), metipranolol (0.2 mg/kg b.w.), and after subsequent bilateral cervical vagotomy. The orthostasis in anaesthetized rabbits is accompanied by depression of respiratory rate reversed only by vagotomy. Furthermore, decrease of systemic blood pressure, unchanged heart rate and increased characteristics of heart rate variability were found, with predominant increase of spectral power in LF and VLF bands. This elevation can be eliminated only by complete blockade of ANS. Although the participation of ANS or RAA system in modification of individual HRV frequency bands is not as specific as in humans, we confirmed the participation of RAA system in determination of the VLF band.

Abstract 16763: Unchanged Central Aortic Blood Pressure and Increased Myocardial Perfusion in Patients With Stable Coronary Artery Disease Receiving Ivabradine

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Bernard I. Levy ◽  
Jean-Guillaume Dillinger ◽  
Patrick Henry ◽  
Damien Logeart ◽  
Stephane Manzo Silberman ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Myocardial Perfusion ◽  
Beta Blocker ◽  
Central Blood Pressure ◽  
Pronounced Increase ◽  
Aortic Blood ◽  
Perfusion Time ◽  
Aortic Blood Pressure ◽  
Central Aortic Blood Pressure

Background: Treatment of hypertensive patients with beta-blockers reduces heart rate (HR) and increases central blood pressure, implying that the decrease in HR could explain reported increases in cardiovascular risk with beta-blocker. This analysis from a randomized, double-blind study explores whether HR reduction with the I f inhibitor ivabradine had an impact on central blood pressure and coronary perfusion. Methods and results: We included 12 normotensive patients with stable CAD, HR ≥70 bpm (sinus rhythm), and stable background beta-blocker therapy. Patients received ivabradine 7.5 mg bid or matched placebo for two 3-week periods with a crossover design and evaluation by aplanation tonometry. Treatment with ivabradine was associated with a significant reduction in resting HR after 3 weeks versus no change with placebo (-15.8±7.7 versus +0.3±5.8 bpm, p=0.0010). There was no relevant between-group difference in change in central aortic SBP (-4.0±9.6 versus +2.4±12.0 mm Hg, p=0.13) or augmentation index (-0.8±10.0% versus +0.3±7.6%, p=0.87). Treatment with ivabradine was associated with prolongation of diastolic perfusion time by 41% from baseline to 3 weeks (+215.6±105.3 versus -3.0±55.8 ms with placebo, p=0.0005) (Figure) and with a pronounced increase in an index of myocardial viability (Buckberg index, +39.3±27.6% versus -2.5±13.5% with placebo, p=0.0015). There were no safety issues during the study. Conclusion: Heart rate reduction with ivabradine does not modify central aortic blood pressure and is associated with a marked prolongation of diastolic perfusion time and an improvement in myocardial perfusion.

Pet CO2 inversely affects MSNA response to orthostatic stress

2001 ◽  
Vol 281 (3) ◽  
pp. H1040-H1046 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Debbie D. O'Leary ◽  
Richard L. Hughson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Orthostatic Intolerance ◽  
Muscle Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Burst Frequency ◽  
Head Up Tilt ◽  
End Tidal ◽  
Combined Data

Arterial hypocapnia has been associated with orthostatic intolerance. Therefore, we tested the hypothesis that hypocapnia may be detrimental to increases in muscle sympathetic nerve activity (MSNA) and total peripheral resistance (TPR) during head-up tilt (HUT). Ventilation was increased ∼1.5 times above baseline for each of three conditions, whereas end-tidal Pco 2 (Pet CO2 ) was clamped at normocapnic (Normo), hypercapnic (Hyper; +5 mmHg relative to Normo), and hypocapnic (Hypo; −5 mmHg relative to Normo) conditions. MSNA (microneurography), heart rate, blood pressure (BP, Finapres), and cardiac output (Q, Doppler) were measured continuously during supine rest and 45° HUT. The increase in heart rate when changing from supine to HUT ( P < 0.001) was not different across Pet CO2 conditions. MSNA burst frequency increased similarly with HUT in all conditions ( P < 0.05). However, total MSNA and the increase in total amplitude relative to baseline (%ΔMSNA) increased more when changing to HUT during Hypo compared with Hyper ( P < 0.05). Both BP and Q were higher during Hyper than both Normo and Hypo (main effect; P < 0.05). Therefore, the MSNA response to HUT varied inversely with levels of Pet CO2 . The combined data suggest that augmented cardiac output with hypercapnia sustained blood pressure during HUT leading to a diminished sympathetic response.

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