Vasopressin potentiates ventricular and arterial reflexes in the conscious nonhuman primate

1989 ◽  
Vol 256 (6) ◽  
pp. H1546-H1552 ◽  
Author(s):  
M. W. Barazanji ◽  
K. G. Cornish
Keyword(s):  
Blood Pressure ◽  
Nonhuman Primate ◽  
Nucleus Tractus Solitarius ◽  
Control Level ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Rule Out

The effect of arginine vasopressin (AVP) on the arterial baroreflex control of heart rate (HR) was studied in intact and sinoaortic-denervated (SAD) conscious, unrestrained monkeys. A baroreflex curve for mean arterial blood pressure (MABP) and HR was determined before and during intravenous infusion of AVP (2-4 mU.kg-1.min-1) and after the AVP vascular antagonist "Manning compound" [( d(CH2)5Tyr(Me)]AVP, 40 micrograms/kg), while AVP infusion was kept running. The sensitivity (slope) of the arterial baroreflex, as well as the reflex bradycardia induced by high blood pressure, increased significantly during AVP and returned to the control level after Manning compound. The effect of AVP on the Bezold-Jarisch reflex (induced by stimulating left ventricular receptors with 4 micrograms/kg veratridine injected in the left atrium) was also studied. The cardiovascular responses to veratridine were examined before and during AVP and after administration of Manning compound together with AVP infusion. AVP significantly potentiated the hypotension and the bradycardia produced by veratridine, whereas Manning compound blunted this potentiation. The ventricular reflex in SAD monkeys was significantly greater than in intact monkeys. We conclude that, in the conscious nonhuman primate, AVP potentiates the sensitivity of the baroreflex control of HR as well as the Bezold-Jarisch reflex. The potentiation of the Bezold-Jarisch reflex by AVP in the SAD animals is consistent with a central action, since the baroreceptors and ventricular receptors both have connections in the nucleus tractus solitarius. However, it does not rule out the possibility of peripheral actions on receptors or end organs.

Modulation of cardiovascular response to dynamic exercise by fastigial nucleus

1984 ◽  
Vol 56 (5) ◽  
pp. 1369-1377 ◽  
Author(s):  
K. J. Dormer
Keyword(s):  
Blood Pressure ◽  
Repeated Measures ◽  
Cardiovascular Response ◽  
Systolic Pressure ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Fastigial Nucleus ◽  
Ventricular Systolic Pressure ◽  
Arterial Blood

Mongrel dogs (n = 34) were used to record the cardiovascular responses during submaximal exercise-tolerance tests (ETT) before and after the placement of lesions in rostral portions of the cerebellar fastigial nucleus (FN). Sterile surgical procedures were used to implant solid-state pressure transducers into the left ventricle or descending aorta (anesthesia 1% halothane in O2) and multipolar stainless steel electrodes into FN (anesthesia alpha-chloralose 115 mg/kg iv). Heart rate (HR), maximal left ventricular systolic pressure ( LVPmax ) and its first derivative ( dLVP /dt), and mean arterial blood pressure (MAP) were recorded during a motorized treadmill ETT. Electrolytic direct-current or radio-frequency lesions were made through the indwelling FN electrodes, and the ETT was repeated following 10–14 days recovery. Two-way analysis of variance (ANOVA), with repeated measures on one, and one-way ANOVA for simple effects indicated a significant reduction in HR and MAP (P less than 0.01) but not LVPmax and dLVP /dt occurred during exercise as a result of rostral FN lesions. Although the trend for reduced LVPmax and dLVP /dt was also evident, a relatively greater decrease in blood pressure occurred in the peripheral vasculature during exercise. It was concluded that FN acts as a modulator of HR and MAP during dynamic exercise because of the observed deficits, and because FN is known to both send efferent projections to medullary vasomotor areas and receive projections from motor cortex and muscle and joint afferents.

Volume expansion attenuates baroreflex sensitivity in the conscious nonhuman primate

1989 ◽  
Vol 257 (3) ◽  
pp. R595-R598 ◽  
Author(s):  
K. G. Cornish ◽  
M. W. Barazanji ◽  
T. Yong ◽  
J. P. Gilmore
Keyword(s):  
Blood Pressure ◽  
Nonhuman Primate ◽  
Volume Expansion ◽  
Maximum Sensitivity ◽  
Response Curves ◽  
Baroreflex Control ◽  
Stimulus Response ◽  
Arterial Blood ◽  
Before And After ◽  
The Right

We examined the effect of intravascular volume expansion (VE) on the arterial baroreflex control of pulse rate (PR) in conscious, chronically instrumented monkeys tethered in their cages. A total of five monkeys was studied after surgical implantation of catheters in the descending aorta, the left atrium, and the internal jugular vein. Mean arterial blood pressure (MABP)-PR stimulus response curves were constructed by decreasing and increasing blood pressure with nitroprusside and phenylephrine, respectively. The data were analyzed with a regression analysis that generated a sigmoid curve and the maximum sensitivity (slope) of the curve. The data were obtained before and after VE with an isotonic isoncotic dextran solution equal to 20% of the estimated blood volume. After VE, the MABP-PR curve shifted to the right at the high blood pressures, and there was a significant decrease in the maximum sensitivity from 5.65 +/- 1.44 for control to 2.14 +/- 0.63 after VE (P less than 0.05). We concluded that VE attenuates the baroreflex control of heart rate in the conscious nonhuman primate.

Muscle metaboreflex activation speeds the recovery of arterial blood pressure following acute hypotension in humans

2013 ◽  
Vol 304 (11) ◽  
pp. H1568-H1575 ◽  
Author(s):  
Masashi Ichinose ◽  
Kazuhito Watanabe ◽  
Naoto Fujii ◽  
Narihiko Kondo ◽  
Takeshi Nishiyasu
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Maximum Voluntary Contraction ◽  
Cardiovascular Responses ◽  
Arterial Baroreflex ◽  
Isometric Handgrip ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Arterial Blood ◽  
Acute Hypotension

It has been suggested that the arterial baroreflex and muscle metaboreflex are both activated during heavy exercise and that they interact to modulate primary cardiovascular reflex responses. This proposed interaction and its consequences are not fully understood, however. The purpose of present study was to test our hypothesis that dynamic arterial baroreflex-mediated cardiovascular responses to acute systemic hypotension in humans are augmented when the muscle metaboreflex is active and that this results in a faster recovery of arterial blood pressure. Acute hypotension was induced nonpharmacologically in 12 healthy subjects by releasing bilateral thigh cuffs after 9 min of suprasystolic resting ischemia, with and without muscle metaboreflex activation via postexercise muscle ischemia (PEMI) after 1 min of isometric handgrip exercise at 50% maximum voluntary contraction. The thigh-cuff release evoked rapid reductions in mean arterial pressure (MAP) and increases in heart rate, cardiac output (Doppler), and total vascular conductance (TVC) under control conditions and during PEMI. The reductions in MAP from baseline were greater and the increases in TVC were smaller during PEMI than control. In addition, arterial baroreflex-mediated peripheral vasoconstriction was augmented during PEMI, as evidenced by a near doubling of the rate of recovery of MAP and TVC. These results show that when the muscle metaboreflex is activated in humans, arterial baroreflex-mediated peripheral vasoconstriction elicited in response to acute hypotension is augmented, which halves the time needed for MAP recovery. Such modulation of baroreflex function would be advantageous for maintaining an elevated arterial blood pressure during activation of the muscle metaboreflex.

scholarly journals Impaired carotid baroreflex control of arterial blood pressure in multiple sclerosis

2016 ◽  
Vol 116 (1) ◽  
pp. 81-87 ◽  
Author(s):  
Mu Huang ◽  
Dustin R. Allen ◽  
David M. Keller ◽  
Paul J. Fadel ◽  
Elliot M. Frohman ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Vascular Conductance ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Carotid Baroreflex ◽  
Relapsing Remitting ◽  
Neck Pressure

Multiple sclerosis (MS), a progressive neurological disease, can lead to impairments in the autonomic control of cardiovascular function. We tested the hypothesis that individuals with relapsing-remitting MS ( n = 10; 7 females, 3 males; 13 ± 4 yr from diagnosis) exhibit impaired carotid baroreflex control of blood pressure and heart rate compared with sex, age, and body weight-matched healthy individuals (CON: n = 10; 7 females, 3 males). At rest, 5-s trials of neck pressure (NP; +40 Torr) and neck suction (NS; −60 Torr) were applied to simulate carotid hypotension and hypertension, respectively, while mean arterial pressure (MAP; finger photoplethysmography), heart rate (HR), cardiac output (CO; Modelflow), and total vascular conductance (TVC) were continuously measured. In response to NP, there was a blunted increase in peak MAP responses (MS: 5 ± 2 mmHg) in individuals with MS compared with healthy controls (CON: 9 ± 3 mmHg; P = 0.005), whereas peak HR responses were not different between groups. At the peak MAP response to NP, individuals with MS demonstrated an attenuated decrease in TVC (MS, −10 ± 4% baseline vs. CON, −15 ± 4% baseline, P = 0.012), whereas changes in CO were similar between groups. Following NS, all cardiovascular responses (i.e., nadir MAP and HR and percent changes in CO and TVC) were not different between MS and CON groups. These data suggest that individuals with MS have impaired carotid baroreflex control of blood pressure via a blunted vascular conductance response resulting in a diminished ability to increase MAP in response to a hypotensive challenge.

Intracoronary epinephrine attenuates baroreflex control of heart rate in the conscious dog

1984 ◽  
Vol 247 (2) ◽  
pp. R237-R245
Author(s):  
M. J. Holmberg ◽  
A. J. Gorman ◽  
K. G. Cornish ◽  
I. H. Zucker
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Rate Curve ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Conscious Dog ◽  
Arterial Blood ◽  
The Mean

In the present study, the reflex effects of low-dose (12.5-50 ng X kg-1 X min-1) intracoronary epinephrine infusion on the arterial baroreflex control of heart rate were studied. Mean arterial blood pressure-heart rate curves were constructed by changing mean arterial blood pressure with graded occlusions of the descending aorta and inferior vena cava. Intracoronary epinephrine increased left ventricular dP/dtmax by an average of 309 +/- 67.0 mmHg/s but did not alter resting mean arterial blood pressure or heart rate. Peak sensitivity, the maximum absolute slope along the mean arterial blood pressure-heart rate curve, and heart rate range were 32.7 +/- 3.2 and 26.7 +/- 2.5% less during intracoronary epinephrine compared with control, respectively. Intracoronary epinephrine did not alter the median, threshold, or saturation pressure of the mean arterial blood pressure-heart rate curve. Lidocaine block of the pericoronary nerves, which blocked the ventricular afferent pathway, eliminated the effects of intracoronary epinephrine on the arterial baroreflex. Atropine abolished the effects of intracoronary epinephrine on arterial baroreflex control of heart rate. We conclude that intracoronary epinephrine reflexly attenuates the arterial baroreflex control of heart rate in the conscious dog through activation of ventricular receptors. This response is mediated by cardiac parasympathetic efferents common to both reflex arcs.

Cardiovascular regulation and expressions of NO synthase-tyrosine hydroxylase in nucleus tractus solitarius of ovine fetus

2003 ◽  
Vol 284 (4) ◽  
pp. H1057-H1063 ◽  
Author(s):  
Sheng-Xing Ma ◽  
Qun Fang ◽  
Brian Morgan ◽  
Michael G. Ross ◽  
Conrad R. Chao
Keyword(s):  
Blood Pressure ◽  
Tyrosine Hydroxylase ◽  
Arterial Blood Pressure ◽  
Nucleus Tractus Solitarius ◽  
Cardiovascular Responses ◽  
No Synthase ◽  
No Donor ◽  
Fetal Sheep ◽  
Medial Nucleus ◽  
Arterial Blood

The purpose of this study was to examine cardiovascular responses to fourth cerebral ventricle (4V) administration of nitroglycerin (NTG) or an inhibitor of nitric oxide (NO) synthase (NOS) in the near-term ovine and to determine whether, during birth, neuronal NOS (nNOS) is induced in noradrenergic A1 neurons in the medial nucleus tractus solitarius (mNTS). In chronically instrumented fetal sheep, 4V injection of NTG (1.2 nmol), an NO donor, produced an arterial blood depressor and a moderate decrease in heart rate. Arterial blood pressure is increased by 4V administration of N G-nitro-l-arginine methyl ester (10 nmnol), an inhibitor of NOS, in fetuses. Sections of the medulla from fetuses and newborn lambs were examined by using immunolabeling with tyrosine hydroxylase (TH) antibody combined with NADPH diaphorase (NADPHd) histochemistry, a marker of nNOS activity. The NADPHd-positive cells and TH-positive cells containing NADPHd reactivity were significantly increased in the mNTS of newborns compared with the fetuses. The results suggest that during birth, there is upregulation of NADPHd/nNOS in the noradrenergic neurons of mNTS resulting in a centrally mediated reduction of fetal arterial blood pressure.

Role of endogenous ANG II and AT1 receptors in regulating arterial baroreflex responses in newborn lambs

1997 ◽  
Vol 272 (6) ◽  
pp. R1862-R1873 ◽  
Author(s):  
J. L. Segar ◽  
A. Minnick ◽  
A. M. Nuyt ◽  
J. E. Robillard
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Ang Ii ◽  
Central Administration ◽  
Arterial Baroreflex ◽  
Response Curves ◽  
Baroreflex Control ◽  
At1 Receptors ◽  
Arterial Blood ◽  
Baroreflex Function

The present study was designed to test the hypothesis that endogenous angiotensin II (ANG II) influences baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) early in life and to determine whether these actions are mediated by angiotensin AT1 or AT2 receptors. To test this hypothesis, we studied the effects of systemic and central administration of losartan, a selective AT1 receptor antagonist, and PD-123319, a selective AT2 antagonist, on baroreflex-mediated control of HR and RSNA in conscious newborn lambs. Systemic administration of losartan decreased resting mean arterial blood pressure (MABP) from 70 +/- 3 to 58 +/- 4 mmHg (P < 0.05) without producing reflex increases in HR or RSNA. The baroreflex response curves were shifted to the left as indicated by a decrease in the arterial pressure at the midpoint of the curve for HR (83 +/- 3 to 75 +/- 4 mmHg) and RSNA (74 +/- 2 to 69 +/- 3 mmHg; P < 0.05 for both). Losartan also reset HR and RSNA baroreflex curves when changes in baseline blood pressure were prevented by simultaneous infusion of phenylephrine. In contrast, a sustained decrease in arterial pressure of 10-12 mmHg with nitroprusside failed to shift the baroreflex function curves. PD-123319 had no effect on baseline HR, MABP, RSNA, or baroreflex responses. Lateral ventricle administration of losartan but not PD-123319 also produced a decrease in arterial pressure (81 +/- 4 to 73 +/- 3 mmHg, P < 0.05) and reset the baroreflex for HR and RSNA toward lower pressure. These results demonstrate that, early in life, endogenous ANG II exerts a tonic effect on baroreflex control of HR and RSNA to shift the curves toward higher pressure levels. The alterations in arterial baroreflex function appear independent of direct ANG II effects on arterial pressure and are mediated by AT1 receptors.

Comparison of cardiovascular response to passive tilt in young and elderly men

1988 ◽  
Vol 66 (11) ◽  
pp. 1425-1432 ◽  
Author(s):  
D. A. Cunningham ◽  
R. J. Petrella ◽  
D. H. Paterson ◽  
P. M. Nichol
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Age Effects ◽  
Hemodynamic Responses ◽  
Arterial Blood ◽  
Postural Changes

To test the hypothesis that altered hemodynamic responses to postural changes are associated with aging, cardiovascular responses to head-up tilt (HUT) and head-down tilt (HDT) were examined in 12 healthy young (average age, 24.6 ± 1.7 years) and 12 healthy elderly (average age, 68.6 ± 2.2 years) men. Subjects were passively tilted from supine to 30°, 60°, and 90° HUT and HDT. Responses to these perturbations were determined 5 min after tilting with measures of heart rate (HR), blood pressure (SBP, DBP), and echocardiographically determined left ventricular diameter in systole and diastole (LVIDs, LVIDd). In HUT there were no significant age effects. In both young and elderly, SBP decreased significantly (p < 0.05), and DBP and HR increased significantly. Ejection fraction (EF), mean arterial blood pressure (MABP), and rate-pressure product (RPP) were unchanged in both groups. In HDT, the hemodynamic responses of the young and elderly were in opposite directions and significant age effects were found for SBP, DBP, HR, LVIDs, EF, MABP, and RPP. In HDT, the young appear to increase cardiac output primarily due to an increase in EF and end-diastolic volume (LVIDd), while HR is unchanged and SBP is decreased. MABP is unchanged, suggesting a small decrease in total peripheral resistance. The elderly may increase cardiac output slightly, owing to an increase in LVIDd with no change in EF, and a large increase in HR. Afterload increased markedly, therefore attenuating any increase in cardiac output. These results suggest that in healthy men, the cardiovascular response to HUT is not age related, while conversely there appear to be significant differences between young and elderly in response to HDT.

scholarly journals Association arterial stiffness reduction with improved left ventricular longitudinal and torsional deformation after 3 years of antihypertensive treatment

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Tzortzis ◽  
I Ikonomidis ◽  
H Triantafyllidi ◽  
J Thymis ◽  
A Frogoudaki ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Ace Inhibitors ◽  
Antihypertensive Treatment ◽  
Left Ventricular ◽  
Torsional Deformation ◽  
Flow Reserve ◽  
Stiffness Reduction ◽  
Arterial Blood ◽  
Lv Mass

Abstract Background We investigated the effects of antihypertensive treatment on vascular function, longitudinal and torsional deformation in hypertensives. Methods In 200 untreated patients with arterial hypertension (age 52.5±11.6 years, 56% females), we measured at baseline and after a 3-year of antihypertensive treatment (160 received ACEi± diuretics and 40 CCBs± diuretics): a) 24h ambulatory blood pressure b) Carotid-femoral pulse wave velocity (PWV) b) Coronary flow reserve (CFR), LV mass index (LVMI), the global longitudinal strain (GLS) and diastolic (LongSRSE) strain rate, peak twisting (Tw-deg) and untwisting at mitral valve opening (UtwMVO), at peak E (UtwE) and at the end of the E wave (UtwendE) of the mitral inflow as well as twisting (TwVel-deg/sec) velocity using speckle tracking imaging. We calculated the % change of LV untwisting as difference between peakTw and UtwMVO, UtwpeakE and UtwendE. Results Compared to baseline, there was an improvement of GLS (−19.9±3.4 vs. −18.7±3.1%), LongSRS (−1.08±0.22 vs. −0.98±0.26 1/s), LongSRE (1.09±0.36 vs. 0.99±0.31 1/s), peak Tw (16.2±5.1 vs. 18.7±5.9 deg), Tw velocity, and the %LV untwisting (31.04±19.28 vs 26.02±15.69% at MVO, 60.04±19.78 vs 53.96±19.76% at peakE and 79.98±14.24 vs 75.90±17.01% at endE) post-treatment. In parallel, CFR (2.72±0.61 vs. 2.55±0.64), PWV (10.34±1.93 vs. 11.2±2.08 m/s) and LVMI were improved (p&lt;0.01 for all comparisons). By ANOVA, the interaction term between changes of all the above parameters and antihypertensive treatment (ACE inhibitors vs calcium channel blockers) was not significant (p&gt;0.05). By multivariate analysis, the reduction of 24h meanBP and PWV independently determined the respective improvement of GLS (b=0.478 and b=0.248 respectively), LongS (b=0.428 and b=0.201 respectively) as well as Twisting (b=0.449 and b=0.294 respectively) after adjusting for changes in LV mass, CFR and atherosclerotic risk factors (p&lt;0.05). Conclusions Long-term optimal blood pressure control with ACE inhibitors and CCBs improves LV longitudinal and torsional mechanics in hypertensives in parallel with arterial stiffness and blood pressure. This improvement in LV deformation and twisting was independently related to changes in arterial blood pressure and arterial stiffness. Funding Acknowledgement Type of funding source: None

Effect of chronic left ventricular failure on beta-endorphin

1992 ◽  
Vol 73 (6) ◽  
pp. 2675-2680 ◽  
Author(s):  
E. Mellow ◽  
E. Redei ◽  
K. Marzo ◽  
J. R. Wilson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Chronic Heart Failure ◽  
Left Ventricular ◽  
Plasma Norepinephrine ◽  
Endogenous Opiates ◽  
Beta Endorphin ◽  
Arterial Blood ◽  
Norepinephrine Concentration ◽  
C 30

Stimulation of endogenous opiate secretion worsens circulatory dysfunction in several forms of shock, in part by inhibiting sympathetic activity. To investigate whether endogenous opiates have a similar effect in chronic heart failure (HF), we measured beta-endorphin concentrations and hemodynamic responses to naloxone infusion (2 mg/kg bolus + 2 mg.kg-1 x h-1) in six control (C) dogs and eight dogs with low-output HF produced by 3 wk of rapid ventricular pacing. The dogs with HF exhibited reduced arterial blood pressure (C, 123 +/- 4 vs. HF, 85 +/- 7 mmHg; P < 0.01) and cardiac outputs (C, 179 +/- 14 vs. HF, 76 +/- 2 ml.min-1 x kg-1; P < 0.01) and elevated plasma norepinephrine concentrations (C, 99 +/- 12 vs. HF, 996 +/- 178 pg/ml; P < 0.01) but normal beta-endorphin concentrations (C, 30 +/- 11 vs. HF, 34 +/- 12 pg/ml; P = NS). Naloxone produced similar transitory increases in blood pressure (C, 14 +/- 5 vs. HF, 26 +/- 25%) and cardiac output (C, 37 +/- 13 vs. HF, 22 +/- 15%) in both groups (both P = NS). No significant changes in norepinephrine concentration or systemic vascular resistance were observed in either group. These findings suggest that beta-endorphin secretion does not exacerbate circulatory dysfunction in chronic heart failure.

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