scholarly journals Role of endothelial nitric oxide in control of peripheral vascular conductance during muscle metaboreflex activation

2017 ◽  
Vol 313 (1) ◽  
pp. R29-R34
Author(s):  
Danielle Senador ◽  
Jasdeep Kaur ◽  
Alberto Alvarez ◽  
Hanna W. Hanna ◽  
Abhinav C. Krishnan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Peripheral Vasodilation ◽  
Dependent Flow ◽  
Flow Mediated Vasodilation ◽  
The Relationship

The muscle metaboreflex is a powerful pressor reflex induced by the activation of chemically sensitive muscle afferents as a result of metabolite accumulation. During submaximal dynamic exercise, the rise in arterial pressure is primarily due to increases in cardiac output, since there is little systemic vasoconstriction. Indeed, in normal animals, we have often shown a small, but significant, peripheral vasodilation during metaboreflex activation, which is mediated, at least in part, by release of epinephrine and activation of vascular β2-receptors. We tested whether this vasodilation is in part due to increased release of nitric oxide caused by the rise in cardiac output eliciting endothelium-dependent flow-mediated vasodilation. The muscle metaboreflex was activated via graded reductions in hindlimb blood flow during mild exercise with and without nitric oxide synthesis blockade [ NG-nitro-l-arginine methyl ester (l-NAME); 5 mg/kg]. We assessed the role of increased cardiac output in mediating peripheral vasodilation via the slope of the relationship between the rise in nonischemic vascular conductance (conductance of all vascular beds excluding hindlimbs) vs. the rise in cardiac output. l-NAME increased mean arterial pressure at rest and during exercise. The metaboreflex-induced increases in mean arterial pressure were unaltered by l-NAME, whereas the increases in cardiac output and nonischemic vascular conductance were attenuated. However, the slope of the relationship between nonischemic vascular conductance and cardiac output was not affected by l-NAME, indicating that the rise in cardiac output did not elicit vasodilation via increased release of nitric oxide. Thus, although nitric oxide is intrinsic to the vascular tonus, endothelial-dependent flow-mediated vasodilation plays little role in the small peripheral vasodilation observed during muscle metaboreflex activation.

Role of cardiac output in the pressor responses to graded muscle ischemia in man

1978 ◽  
Vol 45 (4) ◽  
pp. 574-580 ◽  
Author(s):  
F. Bonde-Petersen ◽  
L. B. Rowell ◽  
R. G. Murray ◽  
G. G. Blomqvist ◽  
R. White ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Conductance ◽  
Total Occlusion ◽  
Muscle Ischemia ◽  
Pressor Responses ◽  
Leg Exercise

Ten men repeatedly performed leg exercise (100–150 W) for 7 min with 30-min recovery periods interspersed. Both legs were made ischemic by total occlusion (OCCL), first for 3 min immediately after exercise and second for 30 s before exercise ended and 3 min into recovery. In addition legs were occluded for 3 min at rest (seated). OCCL at rest increased mean arterial pressure (MAP) by 9 Torr but did not affect cardiac output (CO) or heart rate (HR). OCCL at the end of exercise significantly raised MAP and HR above control values during 3-min recovery but CO was unaffected. OCCL 30 s before the end of exercise further increased MAP and HR significantly during recovery; MAP, CO, and HR were significantly increased above control values (CO by 2.1 1-min-1) during the 3rd min of recovery. We conclude that a strong reflex from ischemic legs maintains normal or elevated CO during leg OCCL. Thus CO was too high relative to total vascular conductance so that MAP was elevated.

Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism

1994 ◽  
Vol 267 (1) ◽  
pp. R84-R88 ◽  
Author(s):  
M. Huang ◽  
M. L. Leblanc ◽  
R. L. Hester
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Cardiac Output ◽  
No Synthase ◽  
Before And After ◽  
Regional Hemodynamics ◽  
Autonomic Blockade ◽  
Infusion Of Norepinephrine ◽  
Oxide Synthase

The study tested the hypothesis that the increase in blood pressure and decrease in cardiac output after nitric oxide (NO) synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) was partially mediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive microspheres. All measurements of pressure and flows were made before and after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervous system was blocked by 20 mg/kg hexamethonium. In this group of animals, an intravenous infusion of norepinephrine (20-140 ng/min) was used to maintain normal blood pressure. L-NAME treatment resulted in a significant increase in mean arterial pressure in both groups. L-NAME treatment decreased cardiac output approximately 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decrease in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in blood pressure and decreases in cardiac output and tissue flows after L-NAME treatment are not dependent on a neurogenic mechanism.

Regional vascular resistance vs. conductance: which index for baroreflex responses?

1991 ◽  
Vol 260 (2) ◽  
pp. H632-H637 ◽  
Author(s):  
D. S. O'Leary
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Pressure Regulation ◽  
Differential Analysis ◽  
Initial Value ◽  
Baseline Effect ◽  
Regional Vascular Resistance ◽  
Vascular Beds ◽  
The Relationship

When large changes in baseline blood flow occur in regional vascular beds (i.e., in skeletal muscle between rest and dynamic exercise or in skin between normothermia and hyperthermia) opposite conclusions are often drawn regarding the magnitude of a given vasomotor response (such as baroreflex vasoconstriction during hypotension) using regional resistance versus conductance. This report analyzes the relationship between changes in regional resistance or conductance and the contribution of the responses in the maintenance of blood pressure. The main supposition is that the appropriate index of baroreflex responses should reflect the importance of the response in the maintenance of blood pressure. Through differential analysis of the relationship between changes in resistance and conductance on arterial pressure, it can be seen that in terms of resistance, the effect of a given change in resistance on arterial pressure is greatly dependent on the baseline level of resistance. For conductance, while a modest baseline effect exists when cardiac output changes markedly, at a constant cardiac output, the same change in regional conductance always causes the same change in arterial pressure regardless of the initial value of conductance. Conclusions drawn are that while neither resistance nor conductance is a perfect index of vasomotor responses, changes in conductance far better reflect the importance of the response in pressure regulation than do changes in regional resistance.

Does nitric oxide contribute to the basal vasodilation of pregnancy in conscious rabbits?

2001 ◽  
Vol 281 (5) ◽  
pp. R1624-R1632 ◽  
Author(s):  
Virginia L. Brooks ◽  
Kathy A. Clow ◽  
Lisa S. Welch ◽  
George D. Giraud
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Cardiac Output ◽  
Mesenteric Artery ◽  
Vascular Tone ◽  
Ascending Aorta ◽  
No Production ◽  
Vascular Conductance ◽  
Vascular Beds ◽  
Conscious Rabbits

Pregnancy produces marked systemic vasodilation, but the mechanism is unknown. Experiments were performed in conscious rabbits to test the hypotheses that increased nitric oxide (NO) production contributes to the increased vascular conductance, but that the contribution varies among vascular beds. Rabbits were instrumented with aortic and vena caval catheters and ultrasonic flow probes implanted around the ascending aorta, superior mesenteric artery, terminal aorta, and/or a femoral artery. Hemodynamic responses to intravenous injection of N ω-nitro-l-arginine (l-NA; 20 mg/kg or increasing doses of 2, 5, 10, 15, and 20 mg/kg) were determined in rabbits first before pregnancy (NP) and then at the end of gestation (P). l-NA produced similar increases in arterial pressure between groups, but the following responses were larger ( P < 0.05) when the rabbits were pregnant: 1) decreases in total peripheral conductance [−3.7 ± 0.3 (NP), −5.0 ± 0.5 (P) ml · min−1 · mmHg−1], 2) decreases in mesenteric conductance [−0.47 ± 0.05 (NP), −0.63 ± 0.07 (P) ml · min−1 · mmHg−1], 3) decreases in terminal aortic conductance [−0.43 ± 0.05 (NP), −0.95 ± 0.19 ml · min−1 · mmHg−1 (P)], and 4) decreases in heart rate [−41 ± 4 (NP), −62 ± 5 beats/min (P)]. Nevertheless, total peripheral and terminal aortic conductances remained elevated in the pregnant rabbits ( P < 0.05) after l-NA. Furthermore, decreases in cardiac output and femoral conductance were not different between the reproductive states. We conclude that the contribution of NO to vascular tone increases during pregnancy, but only in some vascular beds. Moreover, the data support a role for NO in the pregnancy-induced increase in basal heart rate. Finally, unknown factors in addition to NO must also underlie the basal vasodilation observed during pregnancy.

Role of Bradycardia and Cold per se in Increasing Mechanical Efficiency of Hypothermic Heart

1958 ◽  
Vol 192 (2) ◽  
pp. 331-334 ◽  
Author(s):  
Henry Badeer ◽  
Avedis Khachadurian
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Oxygen Uptake ◽  
Arterial Pressure ◽  
Mechanical Efficiency ◽  
Metabolic Effect ◽  
Stroke Work ◽  
Per Se ◽  
Lung Preparation

The relative influence of bradycardia and of cold per se on the oxygen consumption and mechanical efficiency of the dog heart was investigated in the modified heart-lung preparation (11 experiments). Myocardial oxygen uptake was determined under constant arterial pressure and cardiac output in a) normothermia, b) normothermia with bradycardia induced by a cold thermode on the pacemaker, and c) hypothermia producing the same bradycardia as in ( b). At 36.8°C with a rate of 153 beats/min. the efficiency was 8.5% ± 0.3(S.E.), whereas with a rate of 110/min. efficiency was 9.1% ± 0.4(S.E.), a change that is statistically not significant. In hypothermia of 31.5°C with a rate of 110/min. the efficiency was 10.8% ± 0.3(S.E.), an increase that is statistically significant. Performing the same stroke work the hypothermic myocardium consumed less oxygen than the normothermic. It is concluded that the metabolic effect of cold per se is the chief factor responsible for increasing the mechanical efficiency of the hypothermic heart when pressure-volume work is kept constant.

Does autonomic blockade reveal a potent contribution of nitric oxide to locomotion-induced vasodilation?

2000 ◽  
Vol 279 (2) ◽  
pp. H726-H732 ◽  
Author(s):  
Don D. Sheriff ◽  
Christopher D. Nelson ◽  
Ryan K. Sundermann
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
No Production ◽  
Vascular Conductance ◽  
Absolute Level ◽  
Autonomic Blockade ◽  
The Absolute ◽  
Ganglionic Transmission ◽  
Treadmill Locomotion

We sought to test the role of nitric oxide (NO) in governing skeletal muscle (iliac) vascular conductance during treadmill locomotion in dogs ( n = 6; 3.2 and 6.4 km/h at 0% grade, and 6.4 km/h at 10% grade). As seen previously, the increase in muscle vascular conductance accompanying treadmill locomotion was little influenced by NO synthase inhibition alone with N ω-nitro-l-arginine methyl ester (l-NAME, 10 mg/kg iv), but the absolute value of conductance achieved during locomotion was reduced. Such ambiguous results provide an unclear picture regarding the importance of NO during locomotion. However, muscle vasodilation is normally restrained by the sympathetic system during locomotion. Thus a significant contribution by NO to the increase in vascular conductance that accompanies locomotion could be masked by partial withdrawal of the competing influence of sympathetic vasoconstrictor nerve activity secondary to the rise in arterial pressure following systemicl-NAME administration. To test this possibility, we compared the rise in muscle vascular conductance before and afterl-NAME treatment while ganglionic transmission was blocked by hexamethonium. Under these conditions, l-NAME significantly reduced both the rise in vascular conductance (by 32%, P < 0.001) and the absolute level of vascular conductance (by 30%, P < 0.001) achieved during locomotion with no effect on blood flow. Thus augmented NO production normally provides a significant drive to relax vascular smooth muscle in active skeletal muscle during locomotion. Potential deficits stemming from the absence of NO following l-NAME treatment are masked by less intense sympathetic restraint when autonomic function is intact.

scholarly journals Muscle metaboreflex-induced coronary vasoconstriction functionally limits increases in ventricular contractility

2010 ◽  
Vol 109 (2) ◽  
pp. 271-278 ◽  
Author(s):  
Matthew Coutsos ◽  
Javier A. Sala-Mercado ◽  
Masashi Ichinose ◽  
ZhenHua Li ◽  
Elizabeth J. Dawe ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Left Ventricular Contractility ◽  
Coronary Vasodilation ◽  
Cardiac Work ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Coronary Vasoconstriction

Muscle metaboreflex activation during dynamic exercise induces a substantial increase in cardiac work and oxygen demand via a significant increase in heart rate, ventricular contractility, and afterload. This increase in cardiac work should cause coronary metabolic vasodilation. However, little if any coronary vasodilation is observed due to concomitant sympathetically induced coronary vasoconstriction. The purpose of the present study is to determine whether the restraint of coronary vasodilation functionally limits increases in left ventricular contractility. Using chronically instrumented, conscious dogs ( n = 9), we measured mean arterial pressure, cardiac output, and circumflex blood flow and calculated coronary vascular conductance, maximal derivative of ventricular pressure (dp/d tmax), and preload recruitable stroke work (PRSW) at rest and during mild exercise (2 mph) before and during activation of the muscle metaboreflex. Experiments were repeated after systemic α1-adrenergic blockade (∼50 μg/kg prazosin). During prazosin administration, we observed significantly greater increases in coronary vascular conductance (0.64 ± 0.06 vs. 0.46 ± 0.03 ml·min−1·mmHg−1; P < 0.05), circumflex blood flow (77.9 ± 6.6 vs. 63.0 ± 4.5 ml/min; P < 0.05), cardiac output (7.38 ± 0.52 vs. 6.02 ± 0.42 l/min; P < 0.05), dP/d tmax (5,449 ± 339 vs. 3,888 ± 243 mmHg/s; P < 0.05), and PRSW (160.1 ± 10.3 vs. 183.8 ± 9.2 erg·103/ml; P < 0.05) with metaboreflex activation vs. those seen in control experiments. We conclude that the sympathetic restraint of coronary vasodilation functionally limits further reflex increases in left ventricular contractility.

Hyperosmotic NaCl and severe hemorrhagic shock: role of the innervated lung

1981 ◽  
Vol 241 (6) ◽  
pp. H883-H890 ◽  
Author(s):  
O. U. Lopes ◽  
V. Pontieri ◽  
M. Rocha e Silva ◽  
I. T. Velasco
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Metabolic Response ◽  
Term Survival ◽  
Long Term Survival ◽  
Vagal Blockade ◽  
Intravenous Infusions ◽  
Acid Base Equilibrium

Infusions of hyperosmotic NaCl (2,400 mosmol/l; 4 ml/kg) were given to dogs in severe hemorrhagic hypotension by intravenous injection (72 expts) or intra-aortic injection (25 expts). In 46 experiments intravenous infusions were given during bilateral blockage of the cervical vagal trunks (local anesthesia or cooling). Intravenous infusions (without vagal blockade) restore arterial pressure, cardiac output, and acid-base equilibrium to normal and cause mesenteric flow to overshoot prehemorrhage levels by 50%. These effects are stable, and indefinite survival was observed in every case. Intra-aortic infusions of hyperosmotic NaCl produce only a transient recovery of arterial pressure and cardiac output but no long-term survival. Intravenous infusions with vagal blockage produce only a transient recovery of cardiac output, with non long-term survival. Measurement of pulmonary artery blood osmolarity during and after the infusions shows that a different pattern is observed in each of these three groups and strongly indicates that the first passage of hyperosmotic blood through the pulmonary circulation at a time when vagal conduction is unimpaired is essential for the production of the full hemodynamic-metabolic response, which is needed for indefinite survival.

scholarly journals Role of pH in a nitric oxide-dependent increase in cytosolic Cl− in retinal amacrine cells

2011 ◽  
Vol 106 (2) ◽  
pp. 641-651 ◽  
Author(s):  
Emily McMains ◽  
Evanna Gleason
Keyword(s):  
Nitric Oxide ◽  
Cell Voltage ◽  
Amacrine Cells ◽  
Excitatory Synapses ◽  
Cytosolic Ph ◽  
Ph Imaging ◽  
Gabaergic Synapses ◽  
The Relationship ◽  
Cytosolic Acidification

Nitric oxide (NO) synthase-expressing neurons are found throughout the vertebrate retina. Previous work by our laboratory has shown that NO can transiently convert inhibitory GABAergic synapses onto cultured retinal amacrine cells into excitatory synapses by releasing Cl− from an internal store in the postsynaptic cell. The mechanism underlying this Cl− release is currently unknown. Because transport of Cl− across internal membranes can be coupled to proton flux, we asked whether protons could be involved in the NO-dependent release of internal Cl−. Using pH imaging and whole cell voltage-clamp recording, we addressed the relationship between cytosolic pH and cytosolic Cl− in cultured retinal amacrine cells. We found that NO reliably produces a transient decrease in cytosolic pH. A physiological link between cytosolic pH and cytosolic Cl− was established by demonstrating that shifting cytosolic pH in the absence of NO altered cytosolic Cl− concentrations. Strong buffering of cytosolic pH limited the ability of NO to increase cytosolic Cl−, suggesting that cytosolic acidification is involved in generating the NO-dependent elevation in cytosolic Cl−. Furthermore, disruption of internal proton gradients also reduced the effects of NO on cytosolic Cl−. Taken together, these results suggest a cytosolic environment where proton and Cl− fluxes are coupled in a dynamic and physiologically meaningful way.

Mechanism of decreased cardiac output during ANP infusion in conscious anephric dogs

1992 ◽  
Vol 262 (1) ◽  
pp. R120-R125
Author(s):  
H. L. Mizelle ◽  
C. A. Gaillard ◽  
R. D. Manning ◽  
J. E. Hall
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Blood Cells ◽  
Venous Return ◽  
Control Period ◽  
Peripheral Resistance ◽  
Circulating Blood Volume

Atrial natriuretic peptide (ANP) may decrease cardiac output (CO) by lowering circulating blood volume (BV) or by altering the vasculature in a manner that would decrease venous return. The purpose of this study was to determine the role of decreased BV in mediating the decrease in CO during acute infusion of ANP. BV was measured by dilution of 51Cr-labeled red blood cells in seven trained conscious splenectomized dogs studied after unilateral (UNX) and total (TNX) nephrectomy. BV, hematocrit (Hct), CO, mean arterial pressure (MAP), and total peripheral resistance (TPR) were determined during a 90-min control period and 270 min of infusion of ANP (20 ng.kg-1.min-1 iv). In UNX dogs, ANP decreased BV from 60.9 +/- 1.4 to 58.6 +/- 1.4 ml/kg and increased Hct from 39.3 +/- 1.8% to 41.1 +/- 1.8% (P less than 0.05). MAP was not changed and CO fell to a low that was 86 +/- 2% of control (P less than 0.05) 240 min after starting ANP. TPR increased significantly during ANP infusion. All variables returned to control after ANP was stopped. In the same dogs studied 24 h after TNX, MAP averaged 111 +/- 5 mmHg during control and did not change during ANP infusion. CO fell to a low of 82 +/- 3% of control (P less than 0.05) after 120 min of infusion and remained reduced until after the ANP was stopped.(ABSTRACT TRUNCATED AT 250 WORDS)

Sign in / Sign up

Export Citation Format

Share Document