Effects of Enkephalins on Arterial Blood Pressure are Reduced by Propranolol

1978 ◽  
Vol 55 (s4) ◽  
pp. 237s-241s ◽  
Author(s):  
W. Simon ◽  
K. Schaz ◽  
U. Ganten ◽  
G. Stock ◽  
K. H. Schlör ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Effects ◽  
Pressure Control ◽  
Methionine Enkephalin ◽  
Leucine Enkephalin ◽  
Arterial Blood ◽  
Wistar Kyoto ◽  
Blood Pressure Responses ◽  
The Brain

1. The cardiovascular effects of enkephalins have been tested in normotensive Wistar—Kyoto rats. Methionine—enkephalin and leucine—enkephalin increased blood pressure and heart rate after infusion into the brain ventricles. 2. After intravenous injection, blood pressure was increased by methionine—enkephalin and leucine—enkephalin, but heart rate was increased by methionine—enkephalin only. 3. Propranolol treatment reduced the increases in blood pressure following intraventricular methionine—enkephalin and leucine—enkephalin, while only the methionine—enkephalin-induced increases in heart rate were reduced by propranolol. 4. Heart rate and blood pressure responses after intravenous administration of methionine— enkephalins and leucine—enkephalin were not affected by propranolol. 5. Since opioid peptides occur in the blood and in regions of the brain involved in blood pressure regulation, the demonstrated cardiovascular effects to intraventricular and intravenous enkephalins support a role of these peptides in central and peripheral mechanisms of blood pressure control.

Increased Pressor Responsiveness to Enkephalin in Spontaneously Hypertensive Rats: The Role of Vasopressin

1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Hypertensive Rats ◽  
Methionine Enkephalin ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.

scholarly journals Cardiovascular effects of lumbar epidural anaesthesia in isoflurane-anaesthetised pigs during surgical removal of the liver

2009 ◽  
Vol 80 (1) ◽  
Author(s):  
G.F. Stegmann
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Abdominal Surgery ◽  
Epidural Anaesthesia ◽  
Cardiovascular Effects ◽  
Surgical Removal ◽  
Arterial Blood ◽  
Combined Administration ◽  
Lumbar Epidural Anaesthesia ◽  
Surgical Preparation

In humans the combined administration of epidural anaesthesia and inhalation anaesthesia may result in cardiovascular instability associated with decreases in heart rate and blood pressure. Anaesthesia was induced with a combination of midazolam / ketamine in 18 female pigs with a mean body weight of 24.9±5.9 kg scheduled for surgical removal of the liver. After tracheal intubation, anaesthesia was maintained on a circle rebreathing circuit with isoflurane. Epidural anaesthesia was administered with ropivacaine (AL-group, n=8) at 0.2 mℓ / kg of a 7.5 mg / mℓ solution to the anaesthetised animals. The A-group (n = 10) received isoflurane anaesthesia only. The vaporiser was set at 2.5 % for the A-group and 1.5 % for the AL-group. Heart rate, invasive systolic, diastolic, and mean arterial blood pressure were monitored. Comparisons were made between treatments and within treatments comparing variables during surgical preparation and abdominal surgery. Differences between treatments were not statistically significant (P > 0.05) during surgical preparation or during abdominal surgery. For within treatment groups, the differences between surgical preparation and abdominal surgery were statistically significant (P < 0.05) for heart rate in the A-group, but not statistically significant (P > 0.05) for the other variables. It is concluded that abdominal surgery may be associated with statistically significant changes in heart rate in isoflurane-anaesthetised pigs and that the combined administration of epidural ropivacaine may prevent statistically significant changes in HR during abdominal surgery.

Regulation of arterial blood pressure in Australian tiger snakes

1978 ◽  
Vol 75 (1) ◽  
pp. 65-79 ◽  
Author(s):  
H. B. Lillywhite ◽  
R. S. Seymour
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Complete Recovery ◽  
Pressure Control ◽  
Pressure Regulation ◽  
Body Temperatures ◽  
Heating And Cooling ◽  
Arterial Blood ◽  
Preferred Temperatures ◽  
Head Up Tilt

1. Blood pressure was measured in the dorsal aorta of restrained, unanaesthetized tiger snakes (Notechis scutatus) at different body temperatures during graded, passive tilt. Aortic blood pressure in horizontal snakes showed no significant change over a range of body temperatures between 18 and 33 degrees C (mean of measurements on 16 snakes = 42.2 +/− I.98 mmHg), while heart rate increased logarithmically (Q10 approximately 2.5). Blood pressure was stable during heating and cooling between body temperatures of 15 and 30 degrees C, but the pressure was 10--50% higher during heating than during cooling. 2. Head-up tilt usually caused a brief fall in pressure at heart level followed by partial or complete recovery and tachycardia. At the cessation of tilt, there was a characteristic overshoot of the blood pressure followed by readjustment to control (pretilt) levels. Head-down tilt typically increased pressure which then either stabilized or returned toward pretilt levels. Heart rate changes during head-down tilt were not consistent in direction or magnitude. Stabilized pressures at mid-body usually increased following head-up tilt and decreased following head-down tilt, indicating physiological adjustment to posture change. Blood pressure control was evident at body temperatures ranging from 10 to 38 degrees C, but was most effective at the higher and behaviourally preferred temperatures. 3. Propranolol lowered heart rate but did not influence pressure in horizontal snakes. During head-up tilt propranolol eliminated or reduced tachycardia and sometimes reduced the efficacy of pressure compensation for tilt. Phentolamine increased heart rate, lowered blood pressure, and eliminated pressure regulation during tilt. The results suggest that sympathetically mediated reflexes assist central blood pressure regulation in the tiger snake, with vasomotor adjustments having greater importance than changes in heart rate.

Cardiovascular and neuroendocrine responses to baroreceptor denervation in baboons

1990 ◽  
Vol 258 (4) ◽  
pp. R930-R938 ◽  
Author(s):  
R. E. Shade ◽  
V. S. Bishop ◽  
J. R. Haywood ◽  
C. K. Hamm
Keyword(s):  
Blood Pressure ◽  
Aortic Arch ◽  
Carotid Sinus ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Plasma Norepinephrine ◽  
Arterial Blood ◽  
Bilateral Carotid ◽  
Vasopressin Secretion ◽  
Blood Pressure Responses

The purpose of this study was to describe the hormonal and blood pressure responses to partial (carotid sinus) and complete (carotid sinus + aortic arch) baroreceptor denervation in baboons. Experiments were performed in eight adult male baboons maintained on a tether system for the continuous measurement of mean arterial blood pressure (MAP) and heart rate (HR). Bilateral carotid sinus denervation (CSD) immediately increased MAP from 83 +/- 2.2 to 124 +/- 7.3 mmHg. MAP gradually decreased over the next 14 days to intact levels. There were also transient decreases in HR variability and increases in blood pressure variability after CSD. Subsequent denervation of the aortic arch to produce sinoaortic denervation (SAD) resulted in another abrupt large increase in MAP followed by a small but significant increase in MAP of 11 mmHg that was maintained for up to 4 wk after SAD. The short-term variability of HR and blood pressure was chronically decreased and increased, respectively, after SAD. Plasma renin activity, vasopressin, and epinephrine were not changed from intact levels either after CSD or SAD. Plasma norepinephrine was only transiently increased by CSD and chronically elevated by 72% over intact levels after SAD. Thus CSD in the baboon does not produce a sustained increase in MAP. SAD chronically increases MAP and is associated with evidence for an increased sympathetic tone. There is no indication that either increased renin secretion or vasopressin secretion contributes to the chronic cardiovascular effects of SAD in baboons.

scholarly journals Cardiovascular effects of epidural morphine or ropivacaine in isoflurane-anaesthetised pigs during surgical devascularisation of the liver

2010 ◽  
Vol 81 (3) ◽  
Author(s):  
G.F. Stegmann
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Abdominal Surgery ◽  
Arterial Blood Pressure ◽  
Cardiovascular Effects ◽  
Group Differences ◽  
Epidural Administration ◽  
Isoflurane Anaesthesia ◽  
Treatment Groups ◽  
Arterial Blood

The cardiovascular effects of non-abdominal and abdominal surgery during isoflurane anaesthesia (A-group) or isoflurane anaesthesia supplemented with either epidural ropivacaine (AR-group; 0.75 % solution, 0.2 mℓ/kg) or morphine (AM-group; 0.1 mg/kg diluted in saline to 0.2mℓ/kg) were evaluated in 28 healthy pigs with a mean body weight of 30.3 kg SD ± 4.1 during surgical devascularisation of the liver. Anaesthesia was induced with the intramuscular injection of midazolam (0.3 mg/kg) and ketamine (10 mg/kg). Anaesthesia was deepened with intravenous propofol to enable tracheal intubation and maintained with isoflurane on a circle rebreathing circuit. The vaporiser was set at 2.5% for the A-group and 1.5% for the AR- and AM-groups. Differences between treatment groups were not statistically significant (P>0.05) for any of the variables. Differences between AM- and AR-groups were marginally significant heart rate (HR) (P = 0.06) and mean arterial blood pressure (MAP) (P = 0.08). Within treatment groups, differences for the A-group were statistically significant (P<0.05) between non-abdominal and abdominal surgery for HR, systolic blood pressure, diastolic blood pressure (DIA) and MAP. Within the AM-group differences were statistically significant (P < 0.05) for DIA and MAP, and within the AR group differences for all variables were not statistically significant (P > 0.05). It was concluded that in isoflurane-anaesthetised pigs, the epidural administration of ropivacaine decreased heart rate and improved arterial blood pressure during surgery.

Reduced parasympathetic control of heart rate in obese dogs

1995 ◽  
Vol 269 (2) ◽  
pp. H629-H637 ◽  
Author(s):  
B. N. Van Vliet ◽  
J. E. Hall ◽  
H. L. Mizelle ◽  
J. P. Montani ◽  
M. J. Smith
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Rate Control ◽  
Saturated Fat ◽  
Pressure Control ◽  
Resting Heart Rate ◽  
Arterial Blood ◽  
Parasympathetic Control ◽  
The Mean ◽  
Affect Heart Rate

We investigated why resting heart rate is elevated in dogs fed a high saturated fat diet for 12.7 +/- 1.8 wk. Obese dogs exhibited elevated body weight (59%), blood pressure (14%), and heart rate (25%). Differences in resting heart rate (control, 58 +/- 5 beats/min; obese, 83 +/- 7 beats/min) were abolished after hexamethonium, indicating an autonomic mechanism. Hexamethonium also reduced blood pressure in obese (20 +/- 4 mmHg) but not control (9 +/- 6 mmHg) animals. Propranolol did not affect heart rate in either group, excluding a beta-adrenergic mechanism. Subsequent administration of atropine increased heart rate more in control than in obese dogs (110 +/- 9 vs. 57 +/- 11 beats/min). The sensitivity of the cardiac limb of the baroreflex (Oxford method) was reduced by 46% in the obese group, confirming impairment of the parasympathetic control of heart rate. The standard deviation of blood pressure measurements was normal when expressed as a percentage of the mean arterial blood pressure (control, 11.2 +/- 0.4%; obese, 11.2 +/- 0.5%). Our results indicate that the development of obesity in dogs fed a high saturated fat diet is accompanied by an attenuated resting and reflex parasympathetic control of heart rate.

scholarly journals Cardiovascular assessment in horses sedated with xylazine or amitraz

2008 ◽  
Vol 60 (2) ◽  
pp. 329-334 ◽  
Author(s):  
R.L. Linardi ◽  
J.C. Canola ◽  
C.A.A. Valadão
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Effects ◽  
Left Ventricular ◽  
Av Block ◽  
Drug Injection ◽  
Arterial Blood ◽  
Cardiovascular Side Effects ◽  
Cardiovascular Assessment ◽  
Second Degree

Cardiovascular effects due to intravenous (IV) xylazine (1.0mg/kg) or amitraz (0.1 or 0.4mg/kg) were evaluated in horses. Left ventricular function indexes, heart rate (HR), and cardiac output (CO) were measured by echocardiography. Second degree atrioventricular (AV) block was detected by electrocardiography. Invasive arterial blood pressure (AP) was also evaluated. All parameters were measured immediately before and during 60 minutes after drug injection. HR, CO, and second degree AV block were different between xylazine and amitraz-0.4mg/kg groups. Xylazine induced initial hypertension 10 minutes after injection, and hypotension was observed 30 minutes after amitraz-0.4mg/kg administration. Except for the second degree AV block which occurred only at five minutes, there was no change in the echocardiographic measurements after administration of amitraz-0.1mg/kg. Thus, amitraz-0.4mg/kg and xylazine (1.0mg/kg) induced similar cardiovascular side effects, but long-lasting action of amitraz-0.4mg/kg in the cardiovascular system was observed.

Thromboxane A2 acts on the brain to mediate hemodynamic, adrenocorticotropin, and cortisol responses

1998 ◽  
Vol 274 (5) ◽  
pp. R1353-R1360 ◽  
Author(s):  
Timothy A. Cudd
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
De Novo ◽  
Blood Pressure Response ◽  
Protective Function ◽  
Prostaglandin Synthase ◽  
Artificial Cerebrospinal Fluid ◽  
Cortisol Responses ◽  
Blood Pressure Responses ◽  
The Brain

Conditions that increase the formation of thromboxane A2(TxA2) also result in activation of hemodynamic and adrenocortical responses. The purpose of this study was to test the hypothesis that TxA2 acts directly on the brain to mediate these responses. Adult sheep were chronically instrumented with vascular and intracerebroventricular catheters. The TxA2 analog U-46619 (0, 100, or 1,000 ng ⋅ kg−1 ⋅ min−1) and artificial cerebrospinal fluid (CSF) were infused intracerebroventricularly for 30 min. Heart rate increased in response to 100 ng ⋅ kg−1 ⋅ min−1U-46619 infusions. Heart rate did not change over preinfusion values in response to the highest infusion rate, but values were elevated compared with the postinfusion period. Mean arterial pressure, ACTH, cortisol, hematocrit, and arterial pH (pHa) increased, and arterial partial CO2 pressure ([Formula: see text]) fell in response to 1,000 ng ⋅ kg−1 ⋅ min−1infusions of U-46619. Plasma vasopressin concentrations and arterial partial O2 pressure did not change. In a second study, U-46619 or artificial CSF was infused intracerebroventricularly during prostaglandin synthase blockade. Blockade reduced but did not prevent blood pressure responses to U-46619 infusion, suggesting that the U-46619 infusions increased prostaglandin synthase metabolism to contribute de novo TxA2 or a second metabolite to augment the blood pressure response. Heart rate, pHa,[Formula: see text], ACTH, and cortisol responses to U-46619 were not different with blockade. We conclude that TxA2 acts on the brain to mediate blood pressure, heart rate, pHa,[Formula: see text], hematocrit, ACTH, and cortisol responses. These findings support the hypothesis that TxA2 acts directly on the brain to promote cardiovascular and hormonal responses that may serve a protective function during conditions when TxA2 formation is increased.

Atrial natriuretic factor-induced vasodepression occurs through central nervous system

1988 ◽  
Vol 255 (3) ◽  
pp. H616-H622 ◽  
Author(s):  
E. R. Levin ◽  
M. A. Weber ◽  
S. Mills
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Fourth Ventricle ◽  
Saline Control ◽  
Arterial Blood ◽  
Adrenergic Antagonist ◽  
Adrenergic Nervous System ◽  
The Brain ◽  
Atrial Natriuretic

To characterize the blood pressure and heart rate effects of atrial natriuretic peptide (ANP) in the brain, we administered 20 micrograms/kg of atriopeptin III in 5 microliters of 0.9 normal saline into the fourth ventricle of awake, freely moving, spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. ANP produced a 13 +/- 1 mmHg decrease in mean arterial blood pressure (MAP) in the SHR (P less than 0.001 vs. base line or saline control, n = 10) and a 9 +/- 2 mmHg decrease in the WKY (P less than 0.02). Heart rate did not change significantly in response to ANP. To determine whether an interaction with the adrenergic nervous system played a role in the effects of ANP, we administered 100 ng yohimbine HCL, an alpha 2-antagonist, by intracerebroventricular injection, 45 min before ANP and completely prevented the ANP-induced decrease in MAP. In contrast, 100 ng intracerebroventricular prazosin, an alpha 1-adrenergic antagonist, had no significant influence on the MAP effect induced by ANP. A third group of SHR was pretreated with intracerebroventricular 6-OH dopamine to deplete central catecholamines or with saline. The rats pretreated with 6-OH dopamine (n = 6) had no significant response to ANP, which was administered 9 days later. This was significantly different from the saline-pretreated control group (n = 6), which responded with a 19 +/- 3 mmHg decrease in MAP (P less than 0.025). These studies indicate that the administration of ANP into the fourth ventricle of the brain decreases the MAP of rats through an interaction with the central alpha 2-adrenergic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

Sign in / Sign up

Export Citation Format

Share Document