Protein expression, vascular reactivity and soluble guanylate cyclase activity in mice lacking the endothelial cell nitric oxide synthase: contributions of NOS isoforms to blood pressure and heart rate control

Experiments were designed to examine the autonomic mechanisms underlying the decreases in blood pressure and heart rate elicited by electrical stimulation in the rat area postrema (AP). Vagotomy was found to significantly reduce the bradycardia observed in response to AP stimulation (control -123.5 +/- 23.5 beats/min; vagotomized -7 +/- 5.4 beats/min; P less than 0.001) but was without significant effect on blood pressure responses. Hexamethonium significantly reduced both heart rate (control -225.5 +/- 11.9 beats/min; hexamethonium -5.5 +/- 2.8 beats/min; P less than 0.001) and depressor (control -35.4 +/- 4.7 mmHg; hexamethonium -6.4 +/- 0.8 mmHg; P less than 0.001) responses to such stimulation, whereas combined alpha- and beta-adrenergic blockade was without effect. The muscarinic blocking agent atropine also abolished both blood pressure (control -22.0 +/- 4.3 mmHg; atropine 2.8 +/- 4.4 mmHg; P less than 0.01) and heart rate (control -187.0 +/- 41.9 beats/min; atropine 8.8 +/- 2.6 beats/min; P less than 0.01) responses to AP stimulation. These data suggest that AP stimulation influences two separate neural pathways eliciting distinct cardiovascular responses. It would appear that activation of one of these pathways results in activation of vagal efferents to the heart and thus bradycardia. A second parallel pathway influenced by AP stimulation apparently elicits depressor response through actions on cholinergic muscarinic receptors.

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Pharmacological Properties of Blood Pressure and Heart Rate Control in Suncus

The Japanese Journal of Pharmacology ◽

10.1254/jjp.62.315 ◽

1993 ◽

Vol 62 (3) ◽

pp. 315-324 ◽

Cited By ~ 14

Author(s):

Norio Matsuki ◽

Yuri Sakuma ◽

Hiroshi Saito

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Rate Control ◽

Pharmacological Properties ◽

Heart Rate Control

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NO production by cNOS and iNOS reflects blood pressure changes in LPS-challenged mice

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00004.2002 ◽

2003 ◽

Vol 285 (4) ◽

pp. E871-E875 ◽

Cited By ~ 51

Author(s):

Marcella M. Hallemeesch ◽

Ben J. A. Janssen ◽

Wouter J. de Jonge ◽

Peter B. Soeters ◽

Wouter H. Lamers ◽

...

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Blood Pressure Response ◽

No Production ◽

Baseline Conditions ◽

Pressure Changes ◽

Oxide Synthase ◽

Nos Isoforms ◽

Firm Evidence ◽

Lps Treatment

Increased nitric oxide (NO) production is the cause of hypotension and shock during sepsis. In the present experiments, we have measured the contribution of endothelial (e) and inducible (i) nitric oxide synthase (NOS) to systemic NO production in mice under baseline conditions and upon LPS treatment (100 μg/10 g ip LPS). NO synthesis was measured by the rate of conversion of l-[ guanidino-15N2]arginine to l-[ ureido-15N]citrulline, and the contribution of the specific NOS isoforms was evaluated by comparing NO production in eNOS-deficient [(–/–)] and iNOS(–/–) mice with that in wild-type (WT) mice. Under baseline conditions, NO production was similar in WT and iNOS(–/–) mice but lower in eNOS(–/–) mice [WT: 1.2 ± 0.2; iNOS(–/–): 1.2 ± 0.2; eNOS(–/–): 0.6 ± 0.3 nmol · 10 g body wt–1· min–1]. In response to the challenge with LPS (5 h), systemic NO production increased in WT and eNOS(–/–) mice but fell in iNOS(–/–) mice [WT: 2.7 ± 0.3; eNOS(–/–): 2.2 ± 0.6; iNOS(–/–): 0.7 ± 0.1 nmol · 10 g body wt–1· min–1]. After 5 h of LPS treatment, blood pressure had dropped 14 mmHg in WT but not in iNOS(–/–) mice. The present findings provide firm evidence that, upon treatment with bacterial LPS, the increase of NO production is solely dependent on iNOS, whereas that mediated by cNOS is reduced. Furthermore, the data show that the LPS-induced blood pressure response is dependent on iNOS.

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Respiratory sinus arrhythmia: time domain characterization using autoregressive moving average analysis

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1995.268.6.h2232 ◽

1995 ◽

Vol 268 (6) ◽

pp. H2232-H2238 ◽

Cited By ~ 10

Author(s):

J. K. Triedman ◽

M. H. Perrott ◽

R. J. Cohen ◽

J. P. Saul

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Time Domain ◽

Rate Control ◽

Moving Average ◽

Autoregressive Moving Average ◽

Heart Rate Control ◽

Sinus Arrhythmia ◽

Arterial Blood ◽

Autonomic Blockade

Fourier-based techniques are mathematically noncausal and are therefore limited in their application to feedback-containing systems, such as the cardiovascular system. In this study, a mathematically causal time domain technique, autoregressive moving average (ARMA) analysis, was used to parameterize the relations of respiration and arterial blood pressure to heart rate in eight humans before and during total cardiac autonomic blockade. Impulse-response curves thus generated showed the relation of respiration to heart rate to be characterized by an immediate increase in heart rate of 9.1 +/- 1.8 beats.min-1.l-1, followed by a transient mild decrease in heart rate to -1.2 +/- 0.5 beats.min-1.l-1 below baseline. The relation of blood pressure to heart rate was characterized by a slower decrease in heart rate of -0.5 +/- 0.1 beats.min-1.mmHg-1, followed by a gradual return to baseline. Both of these relations nearly disappeared after autonomic blockade, indicating autonomic mediation. Maximum values obtained from the respiration to heart rate impulse responses were also well correlated with frequency domain measures of high-frequency "vagal" heart rate control (r = 0.88). ARMA analysis may be useful as a time domain representation of autonomic heart rate control for cardiovascular modeling.

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Effects of antihypertensive drugs on blood pressure and vascular reactivity in the hypertension induced by chronic nitric oxide synthase inhibition.

American Journal of Hypertension ◽

10.1016/0895-7061(95)97773-k ◽

1995 ◽

Vol 8 (4) ◽

pp. 110A

Author(s):

J NAVARRO

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Nitric Oxide Synthase ◽

Vascular Reactivity ◽

Antihypertensive Drugs ◽

Oxide Synthase

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CYCLOOXYGENASE INHIBITION REDUCES BLOOD PRESSURE ELEVATION AND VASCULAR REACTIVITY DYSFUNCTION CAUSED BY INHIBITION OF NITRIC OXIDE SYNTHASE IN RATS

Clinical and Experimental Hypertension ◽

10.1081/ceh-100100073 ◽

2000 ◽

Vol 22 (2) ◽

pp. 203-215 ◽

Cited By ~ 18

Author(s):

Valdeci da Cunha ◽

Luciana V. Rossoni ◽

Patricia A. Oliveira ◽

Silmara Poton ◽

Silvio Cesar Pretti ◽

...

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Nitric Oxide Synthase ◽

Vascular Reactivity ◽

Blood Pressure Elevation ◽

Cyclooxygenase Inhibition ◽

Pressure Elevation ◽

Oxide Synthase

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Comparative Study between Ivabradine Versus Bisoprolol Effects for Heart Rate Control on Hemodynamics and Clinical Outcomes in Patients with Septic Shock

Journal of Advances in Medicine and Medical Research ◽

10.9734/jammr/2021/v33i1330955 ◽

2021 ◽

pp. 58-68

Author(s):

Omnia Ali El-Miseery ◽

Hesham Elsaid Elashry ◽

Magdy Elsaid Elbably ◽

Ahmed Mohammed Hamed

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Septic Shock ◽

Cardiac Output ◽

Clinical Outcomes ◽

Nasogastric Tube ◽

Rate Control ◽

Conventional Therapy ◽

The Other ◽

Heart Rate Control

Background: Septic shock is associated with excessive sympathetic outflow, high plasma catecholamine levels, myocardial depression, vascular hypo-reactivity, and autonomic dysfunction. Typically, patients have a low resistance, high cardiac output circulation with tachycardia and arterial hypotension that may be poorly or even nonresponsive to exogenous catecholamine vasopressors. The aim of the present study was to compare the effect of ivabradine vs bisoprolol for heart rate control on the hemodynamics and clinical outcomes in patients with septic shock. Methods: The study was carried out on 90 patients, aging from 18 to 60 years of both sex presented with septic shock in ICU. Patients were randomly classified into 3 equal groups each of 30 patients. Group I (Control group) received conventional therapy. Group II (Bisoprolol group) received conventional therapy plus bisoprolol 5 mg once daily & one placebo pill on 12 hrs interval via nasogastric tube for 7 days. Group III (Ivabradine group) received conventional therapy plus ivabradine 5 mg twice daily on 12 hrs interval via nasogastric tube for 7 days. Results: Both bisoprolol and ivabradine effectively lowered heart rate in septic shock patients but ivabradine was more effective than bisoprolol. Both bisoprolol and ivabradine did not affect mean blood pressure, with ivabradine being more effective in maintaining blood pressure than bisoprolol. Noradrenaline dose was lower in ivabradine group in comparison with the other two groups. As regard to stroke volume & cardiac output, there was improvement in ivabradine group in comparison with bisoprolol and control groups. As regard to serum lactate level, there was improvement in ivabradine group in comparison with the other two groups. Both bisoprolol & ivabradine resulted in reduction in LOS & 28-day mortality with no significant difference between both groups. Conclusions: Controlling heart rate in septic shock patients with either bisoprolol or ivabradine improves outcomes. Ivabradine is better than bisoprolol in maintaining hemodynamics and improving tissue perfusion parameters.

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