Systemic angiotensin II alters intrinsic heart rate through central mechanisms

2002 ◽  
Vol 58 (1) ◽  
pp. 61-65 ◽  
Author(s):  
Steven L Bealer
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Intrinsic Heart Rate

Chemoreflex and endocrine components of cardiovascular responses to acute hypoxemia in the llama fetus

1996 ◽  
Vol 271 (1) ◽  
pp. R73-R83 ◽  
Author(s):  
D. A. Giussani ◽  
R. A. Riquelme ◽  
F. A. Moraga ◽  
H. H. McGarrigle ◽  
C. R. Gaete ◽  
...  
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
High Altitude ◽  
Chronic Exposure ◽  
Perfusion Pressure ◽  
Carotid Sinus ◽  
Cardiovascular Responses ◽  
Pronounced Increase ◽  
Plasma Vasopressin ◽  
Plasma Angiotensin

We tested the hypothesis that the llama fetus has a blunted cardiovascular chemoreflex response to hypoxemia by investigating the effects of acute hypoxemia on perfusion pressure, heart rate, and the distribution of the combined ventricular output in 10 chronically instrumented fetal llamas at 0.6-0.7 gestation. Four llama fetuses had the carotid sinus nerves sectioned. In the intact fetuses, there was a marked bradycardia, an increase in perfusion pressure, and a pronounced peripheral vasoconstriction during hypoxemia. These cardiovascular responses during hypoxemia in intact fetuses were accompanied by a pronounced increase in plasma vasopressin, but not in plasma angiotensin II concentrations. Carotid denervation prevented the bradycardia at the onset of hypoxemia, but it did not affect the intense vasoconstriction during hypoxemia. Plasma vasopressin and angiotensin II levels were not measured in carotid-denervated fetuses. Our results do not support the hypothesis that the carotid chemoreflex during hypoxemia is blunted in the llama fetus. However, they emphasize that other mechanisms, such as increased vasopressin concentrations, operate to produce an intense vasoconstriction in hypoxemia. This intense vasoconstriction in the llama fetus during hypoxemia may reflect the influence of chronic exposure to the hypoxia of high altitude on the magnitude and gain of fetal cardiovascular responses to a superimposed acute episode of hypoxemia.

Angiotensin II induces insulin resistance independent of changes in interstitial insulin

1999 ◽  
Vol 277 (5) ◽  
pp. E920-E926 ◽  
Author(s):  
Joyce M. Richey ◽  
Marilyn Ader ◽  
Donna Moore ◽  
Richard N. Bergman
Keyword(s):  
Insulin Resistance ◽  
Heart Rate ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glucose Uptake ◽  
Peripheral Resistance ◽  
Glucose Turnover ◽  
Ang Ii

We set out to examine whether angiotensin-driven hypertension can alter insulin action and whether these changes are reflected as changes in interstitial insulin (the signal to which insulin-sensitive cells respond to increase glucose uptake). To this end, we measured hemodynamic parameters, glucose turnover, and insulin dynamics in both plasma and interstitial fluid (lymph) during hyperinsulinemic euglycemic clamps in anesthetized dogs, with or without simultaneous infusions of angiotensin II (ANG II). Hyperinsulinemia per se failed to alter mean arterial pressure, heart rate, or femoral blood flow. ANG II infusion resulted in increased mean arterial pressure (68 ± 16 to 94 ± 14 mmHg, P < 0.001) with a compensatory decrease in heart rate (110 ± 7 vs. 86 ± 4 mmHg, P < 0.05). Peripheral resistance was significantly increased by ANG II from 0.434 to 0.507 mmHg ⋅ ml−1⋅ min ( P < 0.05). ANG II infusion increased femoral artery blood flow (176 ± 4 to 187 ± 5 ml/min, P < 0.05) and resulted in additional increases in both plasma and lymph insulin (93 ± 20 to 122 ± 13 μU/ml and 30 ± 4 to 45 ± 8 μU/ml, P < 0.05). However, glucose uptake was not significantly altered and actually had a tendency to be lower (5.9 ± 1.2 vs. 5.4 ± 0.7 mg ⋅ kg−1⋅ min−1, P > 0.10). Mimicking of the ANG II-induced hyperinsulinemia resulted in an additional increase in glucose uptake. These data imply that ANG II induces insulin resistance by an effect independent of a reduction in interstitial insulin.

Influence of cardiac innervation on intrinsic heart rate in dogs

1990 ◽  
Vol 258 (4) ◽  
pp. H1132-H1137 ◽  
Author(s):  
J. M. Evans ◽  
D. C. Randall ◽  
J. N. Funk ◽  
C. F. Knapp
Keyword(s):  
Heart Rate ◽  
Intrinsic Rate ◽  
Conscious State ◽  
Autonomic Innervation ◽  
Autonomic Activity ◽  
Cardiac Innervation ◽  
Cardiac Denervation ◽  
Ganglionic Blockade ◽  
Intrinsic Heart Rate

Intrinsic heart rate is defined as the rate at which the heart beats when all cardiac neural and hormonal inputs are removed. We determined the effect of prevailing autonomic innervation of the heart on the intrinsic heart rate in chronically maintained, sedated, normally innervated dogs (n = 14), and in 14 other dogs that had previously (greater than 12 day) undergone complete surgical cardiac denervation. Intrinsic rate was determined in both groups using the following two procedures: 1) pharmacological effector blockade; and 2) pharmacological ganglionic blockade. The intrinsic rate determined by effector blockade was 142.9 +/- 7.2 (SE) beats/min in the dogs with intact cardiac innervation. When the same treatment was given after total surgical cardiac denervation, intrinsic rate was 97.9 +/- 4.8 beats/min. Intrinsic heart rate was significantly (P less than 0.05) lower in surgically denervated dogs. Ganglionic blockade in surgically denervated animals yielded an intrinsic rate of 90.0 +/- 8.5 beats/min, which was again significantly lower than the corresponding value of 128.4 +/- 5.5 beats/min in normal dogs. There was no difference in the intrinsic heart rate as determined by effector vs. ganglionic blockade in either group of dogs. An additional six dogs were subjected to selective surgical sinoatrial nodal parasympathectomy; their intrinsic rate (effector blockade) in the conscious state was 115.8 +/- 4.3 beats/min; this was significantly lower than the corresponding value for normal dogs and significantly greater than in dogs subject to total surgical cardiac denervation. The lower rate observed in the totally denervated and selectively denervated dogs after effector and/or ganglionic blockades implies that intrinsic heart rate depends on the level or nature of prevailing autonomic activity.

Dissociation of Direct and Indirect Effects of Angiotensin II on the Heart

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 683-684
Author(s):  
Jorge P van Kats ◽  
David W Silversides ◽  
Timothy L Reudelhuber
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Systolic Pressure ◽  
Weight Ratio ◽  
Renin Angiotensin System ◽  
Cardiac Cells ◽  
Heart Weight ◽  
Ang Ii ◽  
Direct Stimulation ◽  
Beneficial Effects

33 Cardiac angiotensin II (Ang II), either derived from the circulation or locally synthesized, is often suggested to be involved in the structural adaptations occurring in the heart in hypertension and following myocardial infarction. However, it is debated whether the proven beneficial effects of renin-angiotensin system blockade in these pathologies are related to an inhibition of the direct cardiac actions of the peptide. The objective of the present study was to investigate which of the effects of cardiac Ang II are due to direct stimulation of cardiac cells by Ang II. To test for cardiac specific functions of Ang II, transgenic mice were developed that express an Ang II-releasing fusion protein (J Biol Chem 1997;272:12994-99) exclusively in cardiomyocytes. Blood pressure, heart rate, cardiac and plasma Ang II content, Ang II receptor binding and organ morphology were monitored in transgenic (TG) and non-transgenic littermate mice (control). Cardiac Ang II levels in TG mice were 20-40 fold higher than in hearts of control mice (15±3 pg/100 mg ww). In 3 independent founder lines of TG mice, plasma Ang II concentration was not altered as compared to control (119±20 vs. 127±20 pg/mL). The heart weight to body weight ratio in TG mice (4.0±0.1 mg/g) was not different from controls (3.8±0.1 mg/g), neither was systolic pressure (137±4 and 138±7 mm Hg respectively) or heart rate (618±13 and 662±15 bpm respectively). Microscopic inspection of TG hearts did not reveal any differences with control regarding size and number of cardiomyocytes and organization of extracellular matrix proteins. TG mice had not become less sensitive for Ang II signaling since Ang II receptor number was not altered in TG mice (Bmax = 23±3 fmol/mg protein) as compared to control (22±2 fmol/mg protein). Our data show that very high Ang II levels in hearts of TG mice do not lead to myocardial enlargement or affect cardiovascular physiology. We conclude that elevated Ang II in the heart has no direct effects on cardiac cells and we hypothesize that effects of cardiac Ang II become apparent upon altered hemodynamic loading.

scholarly journals A randomized trial to evaluate a modified tracheal catheter with upper and lower balloons for anesthetic administration: effect on the cardiovascular, stress response, and comfort in patients undergoing laparoscopic cholecystectomy

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Yuenong Zhang ◽  
Zhiwen Zeng ◽  
Guangwen Xiao ◽  
Weiqiang Zhang ◽  
Weixiong Lin ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Clinical Trial ◽  
Heart Rate ◽  
Laparoscopic Cholecystectomy ◽  
Stress Response ◽  
Angiotensin Ii ◽  
Tracheal Intubation ◽  
Systolic Blood Pressure ◽  
Group A ◽  
Endotracheal Anesthesia

Abstract Background We aimed to evaluate a modified endotracheal tube containing upper and lower balloons for anesthetic administration among patients undergoing laparoscopic cholecystectomy. Methods Ninety patients scheduled to undergo laparoscopic cholecystectomy were randomly allocated to 3 equal groups: group A (conventional tracheal intubation without endotracheal anesthesia); B (conventional tracheal intubation with endotracheal anesthesia); and C (tracheal intubation using a modified catheter under study). Blood pressure, heart rate, angiotensin II level, blood glucose level, airway pressure before anesthesia (T1) were measured immediately after intubation (T2), 5 min after intubation (T3), and immediately after extubation (T4). The post-extubation pain experienced was evaluated using the Wong-Baker Face Pain scale. Adverse reactions within 30 min after extubation were recorded. Results Systolic blood pressure, diastolic blood pressure, angiotensin II, and blood sugar level in group C at T2, T3 and T4, and heart rate at T2 and T4 were significantly lower than those in group A (P < 0.05); systolic blood pressure and blood sugar at T4, and angiotensin II levels at T2, T3, and T4 were significantly lower than those in group B (P < 0.05). Patients in group C reported the lowest post-extubation pain (P < 0.05 vs. Group A), and the lowest incidence of adverse events such as nausea, vomiting, and sore throat than that in groups A and B (P < 0.05). Conclusion The modified endotracheal anesthesia tube under study is effective in reducing cardiovascular and tracheal stress response, and increasing patient comfort, without inducing an increase in airway resistance. Trial registration The clinical trial was retrospectively registered at the Chinese Clinical Trial Registry with the Registration Number ChiCTR1900020832 at January 20th 2019.

Centrally induced cardiovascular and sympathetic responses to hydrocortisone in rats

1983 ◽  
Vol 245 (6) ◽  
pp. H1013-H1018 ◽  
Author(s):  
H. Takahashi ◽  
K. Takeda ◽  
H. Ashizawa ◽  
A. Inoue ◽  
S. Yoneda ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Sympathetic Nerve ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Angiotensin I Converting Enzyme ◽  
Angiotensin Ii Antagonist ◽  
Dose Dependent

Central effects of hydrocortisone were investigated by injecting it intracerebroventricularly (icv) while recording blood pressure and heart rate in awake rats. Dose-dependent increases in both blood pressure and heart rate occurred following injections of hydrocortisone. Pretreatment by icv injections of the angiotensin II antagonist, [Sar1-Ile8]angiotensin II, completely abolished vasopressor responses to subsequent injections of hydrocortisone. When rats were later anesthetized with urethan to allow recording of abdominal sympathetic nerve activity, hydrocortisone produced vasopressor responses accompanied by corresponding increases in sympathetic nerve firing, which were also abolished by central pretreatment with either [Sar1-Ile8]angiotensin II or angiotensin I converting-enzyme inhibitor, captopril. These results indicate that centrally administered hydrocortisone stimulates the brain renin-angiotensin system to produce vasopressor responses by increasing sympathetic nerve firing.

scholarly journals Acute sympathoexcitatory action of angiotensin II in conscious baroreceptor-denervated rats

2002 ◽  
Vol 283 (2) ◽  
pp. R451-R459 ◽  
Author(s):  
Ling Xu ◽  
Alan F. Sved
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Baroreceptor Reflex ◽  
Ang Ii ◽  
Nerve Activity ◽  
Induced Hypotension ◽  
Baroreceptor Reflexes

Angiotensin II (ANG II) has complex actions on the cardiovascular system. ANG II may act to increase sympathetic vasomotor outflow, but acutely the sympathoexcitatory actions of exogenous ANG II may be opposed by ANG II-induced increases in arterial pressure (AP), evoking baroreceptor-mediated decreases in sympathetic nerve activity (SNA). To examine this hypothesis, the effect of ANG II infusion on lumbar SNA was measured in unanesthetized chronic sinoaortic-denervated rats. Chronic sinoaortic-denervated rats had no reflex heart rate (HR) responses to pharmacologically evoked increases or decreases in AP. Similarly, in these denervated rats, nitroprusside-induced hypotension had no effect on lumbar SNA; however, phenylephrine-induced increases in AP were still associated with transient decreases in SNA. In control rats, infusion of ANG II (100 ng · kg−1 · min−1 iv) increased AP and decreased HR and SNA. In contrast, ANG II infusion increased lumbar SNA and HR in sinoaortic-denervated rats. In rats that underwent sinoaortic denervation surgery but still had residual baroreceptor reflex-evoked changes in HR, the effect of ANG II on HR and SNA was variable and correlated to the extent of baroreceptor reflex impairment. The present data suggest that pressor concentrations of ANG II in rats act rapidly to increase lumbar SNA and HR, although baroreceptor reflexes normally mask these effects of ANG II. Furthermore, these studies highlight the importance of fully characterizing sinoaortic-denervated rats used in experiments examining the role of baroreceptor reflexes.

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