scholarly journals Role of central AT1 and V1 receptors in cardiovascular adaptation to hemorrhage in SD and renin TGR rats

1999 ◽  
Vol 276 (6) ◽  
pp. H1918-H1926 ◽  
Author(s):  
Piotr Paczwa ◽  
Ewa Szczepańska-Sadowska ◽  
Slawomir Łoń, Ursula Ganten ◽  
Detlev Ganten
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Effects ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Sd Rats ◽  
Vasopressin Receptors ◽  
In Series ◽  
Regulation Of Blood Pressure

In acute experiments, intracranially applied angiotensin II and vasopressin elicit significant cardiovascular effects. The purpose of the present study was to find out whether chronic intrabrain elevation of these peptides, occurring in the renin transgenic TGR(mRen2)27 (TGR) rats, results in an alteration of the cardiovascular control. Mean arterial blood pressure (MAP) and heart rate responses to hypovolemia were examined in hypertensive TGR and normotensive Sprague-Dawley (SD) rats under control conditions and during blockade of central AT1 or V1 receptors. Both groups received cerebroventricular infusions of either 1) cerebrospinal fluid ( series 1), 2) AT1 receptors antagonist (AT1ANT, series 2), or 3) V1 receptors antagonist (V1ANT, series 3). Blockade of AT1 and V1 receptors decreased MAP in TGR but not in SD rats. In SD rats, bleeding elicited a similar decrease of MAP in each series and a transient increase of heart rate in series 3. In TGR, hemorrhage caused bradycardia and decrease of MAP, which was greater than in SD rats. Hemorrhagic hypotension in TGR was abolished by V1ANT and bradycardia by V1ANT or AT1ANT. The results demonstrate remarkable differences in cardiovascular adjustment to hemorrhage in SD and TGR rats and provide evidence for enhanced involvement of central V1 and AT1 receptors in the regulation of blood pressure during hypovolemia in TGR. Central V1 vasopressin receptors play a crucial role in eliciting posthemorrhagic hypotension and bradycardia in this strain.

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.

Abstract 15839: Effect of Serotonin Neuron Depletion on Arterial Blood Pressure Regulation in Young Rats

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Jennifer Magnusson ◽  
Kevin Cummings
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Recovery Period ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Sprague Dawley ◽  
Baroreflex Control ◽  
Hypoxic Conditions ◽  
Arterial Blood

Infants dying of Sudden Infant Death Syndrome (SIDS) have reduced brainstem serotonin (5-hydroxytryptamine, 5-HT) where some cases die following episodes of severe bradycardia and hypoxemia. The specific role of central 5-HT in resting arterial blood pressure (BP) and on baroreflex sensitivity during neonatal life has not been studied. In adult animals, systemic depletion of 5-HT increases BP with no effect on heart rate (HR) and reduces the sensitivity of the baroreflex. Other studies have also shown that a loss of central 5-HT beginning in embryogenesis reduces resting BP and HR in adulthood. Based on these reports, we hypothesized that loss of brainstem 5-HT neurons in the neonatal period would reduce baseline BP and HR as well as reduce baroreflex gain. To test this, we utilized 3-week old Sprague Dawley rats treated centrally with 5,7-dihydroxytryptamine (5,7-DHT, n=4; ~120 ug in saline, i.c.v.), a chemical that is toxic to serotonergic neurons. Littermate controls were injected with saline (CTRL, n=5, ~3ul, i.c.v.). We measured BP with a femoral artery catheter. HR was derived from BP. Following a recovery period, we measured resting variables for 15 minutes and then injected phenylephrine (PE; 3mg/kg s.c.) followed by sodium nitroprusside (SNP; 2.5mg/kg s.c.), separated by 15 minutes, to induce pressor or depressor responses, respectively. For both responses, baroreflex gain was calculated as the [[Unable to Display Character: &#8710;]]HR at the maximum [[Unable to Display Character: &#8710;]]BP following drug injection. We found that a loss of 5-HT neurons did not alter baseline BP (p>0.05) but did reduce baseline HR when compared to control littermates (p<0.02). 5-HT neuron deficiency tended to reduce baroreflex gain in response to PE (CTRL: -2.756 ± 0.483 beats/mmHg; 5,7-DHT: -1.499 ± 0.348 beats/mmHg; p=0.058), but not SNP (CTRL: -2.408 ± 0.351 beats/mmHg; 5,7-DHT: -3.316 ± 1.214 beats/mmHg; p>0.05). Our data indicate that brainstem 5-HT maintains resting HR, and is involved in baroreflex control of HR in response to hypertensive stimuli. Reduced brainstem 5-HT may predispose an infant to SIDS via altered autonomic control of BP and HR. The role of 5-HT in BP regulation during hypoxic conditions remains to be elucidated.

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.

scholarly journals Missing pieces of the Piezo1/Piezo2 baroreceptor hypothesis: an autonomic perspective

2019 ◽  
Vol 122 (3) ◽  
pp. 1207-1212 ◽  
Author(s):  
Sean D. Stocker ◽  
Alan F. Sved ◽  
Michael C. Andresen
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Arterial Blood Pressure ◽  
Tissue Perfusion ◽  
Cellular Mechanism ◽  
Baroreceptor Function ◽  
Arterial Blood ◽  
The Central Nervous System ◽  
Regulation Of Blood Pressure

Baroreceptors play a pivotal role in the regulation of blood pressure through moment to moment sensing of arterial blood pressure and providing information to the central nervous system to make autonomic adjustments to maintain appropriate tissue perfusion. A recent publication by Zeng and colleagues (Zeng WZ, Marshall KL, Min S, Daou I, Chapleau MW, Abboud FM, Liberles SD, Science 362: 464–467, 2018) suggests the mechanosensitive ion channels Piezo1 and Piezo2 represent the cellular mechanism by which baroreceptor nerve endings sense changes in arterial blood pressure. However, before Piezo1 and Piezo2 are accepted as the sensor of baroreceptors, the question must be asked of what criteria are necessary to establish this and how well the report of Zeng and colleagues (Zeng WZ, Marshall KL, Min S, Daou I, Chapleau MW, Abboud FM, Liberles SD, Science 362: 464–467, 2018) satisfies these criteria. We briefly review baroreceptor function, outline criteria that a putative neuronal sensor of blood pressure must satisfy, and discuss whether the recent findings of Zeng and colleagues suitably meet these criteria. Despite the provocative hypothesis, there are significant concerns regarding the evidence supporting a role of Piezo1/Piezo2 in arterial baroreceptor function.

Role of sinoaortic reflexes in hemodynamic patterns of natural defense behaviors in the cat

1981 ◽  
Vol 240 (3) ◽  
pp. H421-H429 ◽  
Author(s):  
G. Baccelli ◽  
R. Albertini ◽  
A. Del Bo ◽  
G. Mancia ◽  
A. Zanchetti
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Carotid Sinus ◽  
Emotional Behavior ◽  
Natural Defense ◽  
Arterial Blood ◽  
Hemodynamic Pattern ◽  
Before And After

To evaluate whether sinoaortic afferents contribute to the hemodynamic pattern of fighting, cardiovascular changes associated with fighting were studied in cats before and after sinoaortic denervation. Sinoaortic denervation exaggerates the decrease in heart rate, cardiac output, and arterial pressure during immobile confrontation (hissing, staring but no movement). During nonsupportive fighting (fighting with forelimbs while lying on one side) and supportive fighting ( fighting while standing on four feet) sinoaortic denervation reduces the increase in heart rate and cardiac output, minimizes the mesenteric vasoconstriction, induces a fall in arterial blood pressure, but does not affect iliac vasoconstriction or vasodilatation. The hemodynamic pattern of fighting is similarly changed by temporary inactivation of carotid sinus baroreflexes by common carotid occlusion as by chronic section of sinoaortic nerves. It is concluded that sinoaortic reflexes play an important role in the cardiovascular patterns accompanying natural fighting. They favor cardiac action and allow a marked visceral vasoconstriction to occur, thus minimizing or preventing a fall in blood pressure during emotional behavior.

scholarly journals Improved cardiovascular autonomic modulation in transgenic rats expressing an Ang-(1-7)-producing fusion protein

2017 ◽  
Vol 95 (9) ◽  
pp. 993-998 ◽  
Author(s):  
Daniela Ravizzoni Dartora ◽  
Maria-Claudia Irigoyen ◽  
Karina Rabello Casali ◽  
Ivana C. Moraes-Silva ◽  
Mariane Bertagnolli ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiovascular Effects ◽  
Chronic Administration ◽  
Acute Administration ◽  
Autonomic Modulation ◽  
Sprague Dawley ◽  
Transgenic Rats ◽  
Sd Rats ◽  
Sympathetic Modulation ◽  
Acute Elevation

Angiotensin-(1-7) counterbalances angiotensin II cardiovascular effects. However, it has yet to be determined how cardiovascular autonomic modulation may be affected by chronic and acute elevation of Ang-(1-7). Hemodynamics and cardiovascular autonomic profile were evaluated in male Sprague-Dawley (SD) rats and transgenic rats (TGR) overexpressing Ang-(1-7) [TGR(A1-7)3292]. Blood pressure (BP) was directly measured while cardiovascular autonomic modulation was evaluated by spectral analysis. TGR received A-779 or vehicle and SD rats received Ang-(1-7) or vehicle and were monitored for 5 h after i.v. administration. In another set of experiments with TGR, A-779 was infused for 7 days using osmotic mini pumps. Although at baseline no differences were observed, acute administration of A-779 in TGR produced a marked long-lasting increase in BP accompanied by increased BP variability (BPV) and sympathetic modulation to the vessels. Likewise, chronic administration of A-779 with osmotic mini pumps in TGR increased heart rate, sympathovagal balance, BPV, and sympathetic modulation to the vessels. Administration of Ang-(1-7) to SD rats increased heart rate variability values in 88% accompanied by 8% of vagal modulation increase and 18% of mean BP reduction. These results show that both acute and chronic alteration in the Ang-(1-7)-Mas receptor axis may lead to important changes in the autonomic control of circulation, impacting either sympathetic and (or) parasympathetic systems.

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.

scholarly journals Glucocorticoids act in the dorsal hindbrain to increase arterial pressure

2004 ◽  
Vol 286 (1) ◽  
pp. H458-H467 ◽  
Author(s):  
Deborah A. Scheuer ◽  
Andrea G. Bechtold ◽  
Sylvan S. Shank ◽  
Susan F. Akana
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glucocorticoid Receptors ◽  
Cardiovascular Effects ◽  
Systemic Circulation ◽  
Dorsal Hindbrain ◽  
Regulation Of Blood Pressure ◽  
Experimental Strategies

Glucocorticoid receptors (GRs) are present at a high density in the nucleus of the solitary tract (NTS), an area of the dorsal hindbrain (DHB) that is critical for blood pressure regulation. However, whether these receptors play any role in the regulation of blood pressure is unknown. We tested the hypothesis that glucocorticoids act in the DHB to increase arterial pressure using two experimental strategies. In one approach, we implanted pellets of corticosterone (Cort) or sham pellets onto the DHB over the NTS. Compared with rats with sham pellets, rats with DHB Cort pellets had an increased ( P < 0.05) mean arterial pressure (111 ± 2 vs. 104 ± 1 mmHg) and heart rate (355 ± 9 vs. 326 ± 5 beats/min) after 4 days. In the second approach, we implanted subcutaneous Cort pellets to increase the systemic Cort concentration and then subsequently implanted pellets of the GR antagonist mifepristone (Mif; previously RU-38486) or sham pellets onto the DHB. Two days of DHB Mif treatment reduced ( P < 0.05) mean arterial pressure in those rats with elevated plasma Cort levels (118 ± 2 vs. 108 ± 1 mmHg for sham vs. Mif DHB pellets). Cort and Mif pellets placed on the dura had no effects on arterial pressure or heart rate, ruling out systemic cardiovascular effects of the steroids. DHB Cort treatment had no effects on plasma Cort concentration or adrenal weight, indicating that the contents of the DHB Cort pellet did not diffuse into the systemic circulation or into the forebrain areas that regulate plasma Cort concentration in concentrations sufficient to produce physiological effects. Immunohistochemistry for the occupied GRs demonstrated that the Cort and Mif from the DHB pellets were delivered to the DHB with minimal diffusion to the ventral hindbrain or forebrain. We conclude that glucocorticoids act in the DHB to increase arterial pressure.

Cardiovascular actions of trout urotensin II in the conscious trout, Oncorhynchus mykiss

1996 ◽  
Vol 271 (5) ◽  
pp. R1335-R1343 ◽  
Author(s):  
J. C. Le Mevel ◽  
K. R. Olson ◽  
D. Conklin ◽  
D. Waugh ◽  
D. D. Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Cardiovascular Effects ◽  
Pressor Effect ◽  
Urotensin Ii ◽  
Cardinal Vein ◽  
Vascular Rings ◽  
Arterial Blood ◽  
Dose Dependent

The central and peripheral cardiovascular effects of synthetic trout urotensin II (UII) were investigated in the conscious rainbow trout. Intracerebroventricular injection of 50 pmol UII produced a slight (3%) but significant (P < 0.05) increase in heart rate but had no effect on mean arterial blood pressure. Injection of 500 pmol UII icv produced a significant (P < 0.05) rise (8%) in blood pressure with no change in heart rate. In contrast to the weak pressor effect of centrally administered UII, intra-arterial injection of UII produced a dose-dependent increase in arterial blood pressure and decrease in heart rate with significant (P < 0.05) effects on both parameters observed at a dose of 25 pmol. Higher doses of the peptide produced a sustained decrease in cardiac output that accompanied the bradycardia and rise in arterial blood pressure. The UII-induced bradycardia, but not the increase in pressure, was abolished by pretreatment with phentolamine. Trout UII produced a sustained and dose-dependent contraction of isolated vascular rings prepared from trout efferent branchial [-log 50% of the concentration producing maximal contraction (pD2) = 8.30] and celiacomesenteric (pD2 = 8.22) arteries but was without effects on vascular rings from the anterior cardinal vein. The data indicate that the pressor effect of UII in trout is mediated predominantly, if not exclusively, by an increase in systemic vascular resistance. The UII-induced hypertensive response does not seem to involve release of catecholamines, but the bradycardia may arise from adrenergic-mediated activation of cardioinhibitory baroreflexes.

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