scholarly journals Hydrogen sulfide regulation of renal and mesenteric blood flow

2019 ◽  
Vol 317 (5) ◽  
pp. H1157-H1165 ◽  
Author(s):  
Humberto Morales-Loredo ◽  
Adelaeda Barrera ◽  
Joshua M. Garcia ◽  
Carolyn E. Pace ◽  
Jay S. Naik ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Hydrogen Sulfide ◽  
Vascular Resistance ◽  
Vascular Tone ◽  
Mesenteric Arteries ◽  
Renal Circulation ◽  
Inhalation Anesthesia ◽  
Regional Blood Flows ◽  
Isolated Arteries

Hydrogen sulfide (H2S) dilates isolated arteries, and knockout of the H2S-synthesizing enzyme cystathionine γ-lyase (CSE) increases blood pressure. However, the contributions of endogenously produced H2S to blood flow regulation in specific vascular beds are unknown. Published studies in isolated arteries show that CSE production of H2S influences vascular tone more in small mesenteric arteries than in renal arteries or the aorta. Therefore, the goal of this study was to evaluate H2S regulation of blood pressure, vascular resistance, and regional blood flows using chronically instrumented rats. We hypothesized that during whole animal CSE inhibition, vascular resistance would increase more in the mesenteric than the renal circulation. Under anesthesia, CSE inhibition [β-cyanoalanine (BCA), 30 mg/kg bolus + 5 mg·kg−1·min−1 for 20 min iv) rapidly increased mean arterial pressure (MAP) more than saline administration (%Δ: saline −1.4 ± 0.75 vs. BCA 7.1 ± 1.69, P < 0.05) but did not change resistance (MAP/flow) in either the mesenteric or renal circulation. In conscious rats, BCA infusion similarly increased MAP (%Δ: saline −0.8 ± 1.18 vs. BCA 8.2 ± 2.6, P < 0.05, n = 7) and significantly increased mesenteric resistance (saline 0.9 ± 3.1 vs. BCA 15.6 ± 6.5, P < 0.05, n = 12). The H2S donor Na2S (50 mg/kg) decreased blood pressure and mesenteric resistance ,but the fall in resistance was not significant. Inhibiting CSE for multiple days with dl-proparglycine (PAG, 50 mg·kg−1·min−1 iv bolus for 5 days) significantly increased vascular resistance in both mesenteric (ratio of day 1: saline 0.86 ± 0.033 vs. PAG 1.79 ± 0.38) and renal circulations (ratio of day 1: saline 1.26 ± 0.22 vs. 1.98 ± 0.14 PAG). These results support our hypothesis that CSE-derived H2S is an important regulator of blood pressure and vascular resistance in both mesenteric and renal circulations. Furthermore, inhalation anesthesia diminishes the effect of CSE inhibition on vascular tone. NEW & NOTEWORTHY These results suggest that CSE-derived H2S has a prominent role in regulating blood pressure and blood flow under physiological conditions, which may have been underestimated in prior studies in anesthetized subjects. Therefore, enhancing substrate availability or enzyme activity or dosing with H2S donors could be a novel therapeutic approach to treat cardiovascular diseases.

scholarly journals Simulated Sleep Apnea Alters Hydrogen Sulfide Regulation of Blood Flow and Pressure

2020 ◽  
Author(s):  
Adelaeda Barrera ◽  
Humberto Morales-Loredo ◽  
Joshua Garcia ◽  
Gisel Fregoso ◽  
Carolyn E. Pace ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Hydrogen Sulfide ◽  
Sleep Apnea ◽  
Vascular Resistance ◽  
Carotid Body ◽  
Animal Studies ◽  
Mesenteric Arteries ◽  
Carotid Bodies ◽  
Inner Diameter ◽  
Induced Changes

In sleep apnea, airway obstruction causes intermittent hypoxia (IH). In animal studies, IH-dependent hypertension is associated with loss of vasodilator hydrogen sulfide (H2S), and increased H2S activation of sympathetic nervous system (SNS) activity in the carotid body. We previously reported that inhibiting cystathionine γ-lyase (CSE) to prevent H2S synthesis augments vascular resistance in control rats. The goal of this study was to evaluate the contribution of IH-induced changes in CSE signaling to increased blood pressure and vascular resistance. We hypothesized that chronic IH exposure eliminates CSE regulation of blood pressure (BP) and vascular resistance. In rats instrumented with venous catheters, arterial telemeters, and flow probes on the main mesenteric artery, the CSE inhibitor DL-propargylglycine (PAG, 50 mg/kg/day i.v. for 5 days) increased BP in Sham rats but decreased BP in IH rats (in mmHg, Sham (n = 11): 114±4 to 131±6; IH (n = 8): 131±8 to 115±7 mmHg, p<0.05). PAG treatment increased mesenteric vascular resistance in Sham rats but decreased it in IH rats (Day 5/Day 1: Sham: 1.50 ± 0.07; IH: 0.85 ± 0.19, p<0.05). Administration of the ganglionic blocker hexamethonium (to evaluate SNS activity) decreased mesenteric resistance in PAG-treated Sham rats more than in saline-treated Sham rats or PAG-treated IH rats. CSE immunoreactivity in IH carotid bodies compared to those from Sham rats. However, CSE staining in small mesenteric arteries was less in arteries from IH compared to Sham rats but not different in larger arteries (inner diameter > 200 mm). These results suggest endogenous H2S regulates blood pressure and vascular resistance but this control is lost after IH exposure with decreased CSE expression in resistance size arteries. IH exposure concurrently increases carotid body CSE expression and relative SNS control of blood pressure suggesting both vascular and carotid body H2S generation contribute to blood pressure regulation.

Forearm and finger blood flow responses to passive body tilts

1979 ◽  
Vol 46 (2) ◽  
pp. 288-292 ◽  
Author(s):  
Y. A. Mengesha ◽  
G. H. Bell
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Pulse Rate ◽  
Forearm Blood Flow ◽  
Body Tilt ◽  
Finger Blood Flow ◽  
Arterial Blood ◽  
Forearm Vascular Resistance

Ten to fifteen healthy subjects, ages 18--30 yr, were used to assess the correlation of forearm blood flow with graded passive body tilts and vascular resistance and also to discern the relative effects of body tilts on finger blood flow. In the head-up tilts forearm blood flow and arterial blood pressure fell progressively, whereas forearm vascular resistance and pulse rate increased. In the head-down tilts the forearm blood flow and the arterial blood pressure increased, whereas the forearm vascular resistance and pulse rate decreased. These changes were found to be significantly correlated with the different tilt angles and with one another. In a preliminary study it was found that infrared heating of the carpometacarpal region produced finger vasodilatation similar to the forearm vasodilatation observed by Crockford and Hellon (6). However, unlike forearm blood flow, finger blood flow showed no appreciable response to either the head-up or head-down tilts. This indicates that the sympathetic tone and the volume of blood in the finger are not appreciably altered by this test procedure at least 1 min after the body tilt is assumed.

Increased vascular resistance in paralyzed legs after spinal cord injury is reversible by training

2002 ◽  
Vol 93 (6) ◽  
pp. 1966-1972 ◽  
Author(s):  
Maria T. E. Hopman ◽  
Jan T. Groothuis ◽  
Marcel Flendrie ◽  
Karin H. L. Gerrits ◽  
Sibrand Houtman
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Cord Injury

The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.

Changes in Blood Pressure in the Rainbow Trout During Hypoxia

1967 ◽  
Vol 46 (2) ◽  
pp. 297-305 ◽  
Author(s):  
G. F. HOLETON ◽  
D. J. RANDALL
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Rainbow Trout ◽  
Vascular Resistance ◽  
Ventral Aorta

1. Methods for cannulating the ventral aorta of the trout, which permit the measurement of blood pressure in the unanaesthetized, unrestrained, intact fish are described. 2. Rate and amplitude of breathing and blood pressure in the dorsal and ventral aortae increase during hypoxia. These changes are associated with a marked bradycardia. 3. There are increases in vascular resistance to blood flow in both respiratory and systemic circulations during hypoxia. 4. Post hypoxia is associated with large increases in ventral aortic and dorsal aortic pressures.

L-propionylcarnitine increases postischemic blood flow but does not affect recovery of energy charge

1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Contractile Function ◽  
Energy Charge ◽  
Left Ventricular ◽  
Arterial Blood

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.

Effect of K ATP + channel inhibition on total and regional vascular resistance in guinea pig pregnancy

1998 ◽  
Vol 275 (2) ◽  
pp. H680-H688 ◽  
Author(s):  
Linda Keyes ◽  
David M. Rodman ◽  
Douglas Curran-Everett ◽  
Kenneth Morris ◽  
Lorna G. Moore
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Guinea Pig ◽  
Vascular Resistance ◽  
Coronary Vascular Resistance ◽  
Ang Ii ◽  
Channel Activity ◽  
Vasoconstrictor Response ◽  
Regional Vascular Resistance

Decreased vascular resistance and vasoconstrictor response during pregnancy enables an increase in cardiac output and regional blood flow to the uterine circulation. We sought to determine whether inhibition of vascular smooth muscle ATP-sensitive potassium ([Formula: see text]) channel activity during pregnancy increased systemic and/or regional vascular resistance and resistance response to ANG II. A total of 32 catheterized, awake, pregnant or nonpregnant guinea pigs were treated with either the [Formula: see text]channel inhibitor glibenclamide (3.5 mg/kg) or vehicle (DMSO) ( n = 8/group). In nonpregnant and pregnant animals, glibenclamide raised blood pressure and systemic, uterine, and coronary vascular resistance, diminishing cardiac output and organ blood flow. Glibenclamide produced a greater rise in coronary vascular resistance in the pregnant than nonpregnant groups and increased renal and cerebral vascular resistance in the pregnant animals only. ANG II infusion raised blood pressure and systemic and renal vascular resistance and lowered cardiac output and renal blood flow in vehicle-treated animals. Glibenclamide augmented ANG II-induced systemic vasoconstriction in the nonpregnant and pregnant groups and the rise in uteroplacental vascular resistance in the pregnant animals. We concluded that [Formula: see text] channel activity likely modulates systemic, uterine, and coronary vascular resistance and opposes ANG II-induced systemic vasoconstriction in nonpregnant and pregnant guinea pigs. Pregnancy augments[Formula: see text] channel activity in the uterine, coronary, renal, and cerebral vascular beds and the uteroplacental circulation during ANG II infusion. Thus increased[Formula: see text] channel activity appears to influence regional control of vascular resistance during guinea pig pregnancy but cannot account for the characteristic decrease in systemic vascular resistance and ANG II-induced systemic vasoconstrictor response.

EFFECTS OF PROSTAGLANDIN F2α ON OVARIAN BLOOD FLOW AND VASCULAR RESISTANCE IN THE PSEUDOPREGNANT RABBIT

1975 ◽  
Vol 79 (2) ◽  
pp. 337-350 ◽  
Author(s):  
Per Olof Janson ◽  
Ivan Albrecht ◽  
Kurt Ahrén
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Prostaglandin F2α ◽  
Interstitial Tissue ◽  
Corpora Lutea ◽  
Luteal Function ◽  
Direct Measurements ◽  
Before And After

ABSTRACT In the search for data supporting the hypothesis that the luteolytic effect of prostaglandins (PG) is initiated by a vascular mechanism, some haemodynamic parameters including ovarian blood flow and vascular resistance were measured in pseudopregnant anaesthetized rabbits before and after exogenous administration of PGF2α. The measurements were performed on days 5–10 of pseudopregnancy induced by 500 IU HCG iv. Infusion of 50 μg/kg PGF2α iv over a one-minute period caused significant falls in cardiac output, heart rate and blood pressure after 1–3 min. Blood pressure and cardiac output were normalized after 16–49 min. Blood flow in the ovarian vein (direct measurements) decreased and returned to initial values parallel to the blood pressure and no change in resistance in the vascular bed drained by the vein was noted. Total ovarian blood flow and resistance, as measured in surgically intact ovaries before and after PG infusion, using 35 or 15 μm 169Yb and 46Sc-labelled microspheres, changed and remained constant respectively, according to the same pattern as in the direct measurements. The distribution of blood flow between the corpora lutea and the interstitial tissue of the ovary measured by 15 μm radioactive microspheres. PGF2α caused an interstitial vasodilation whereas no significant change in luteal vascular resistance was noted. Since luteal blood flow represented a predominant part of total ovarian flow in the type of ovary studied, the interstitial vasodilatation caused only negligible changes in blood flow to the whole ovary. The present study does not support the hypothesis of a PG-induced luteal blood flow reduction preceding luteolysis. The possible significance of the interstitial vasodilatation for luteal function remains to be elucidated.

Patterned cardiovascular responses to sleep and nonrespiratory arousals in a porcine model

1998 ◽  
Vol 85 (4) ◽  
pp. 1285-1291 ◽  
Author(s):  
Sandrine H. Launois ◽  
Joseph H. Abraham ◽  
J. Woodrow Weiss ◽  
Debra A. Kirby
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Eye Movement ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Arterial Blood

Patients with obstructive sleep apnea experience marked cardiovascular changes with apnea termination. Based on this observation, we hypothesized that sudden sleep disruption is accompanied by a specific, patterned hemodynamic response, similar to the cardiovascular defense reaction. To test this hypothesis, we recorded mean arterial blood pressure, heart rate, iliac blood flow and vascular resistance, and renal blood flow and vascular resistance in five pigs instrumented with chronic sleep electrodes. Cardiovascular parameters were recorded during quiet wakefulness, during non-rapid-eye-movement and rapid-eye-movement sleep, and during spontaneous and induced arousals. Iliac vasodilation (iliac vascular resistance decreased by −29.6 ± 4.1% of baseline) associated with renal vasoconstriction (renal vascular resistance increased by 10.3 ± 4.0%), tachycardia (heart rate increase: +23.8 ± 3.1%), and minimal changes in mean arterial blood pressure were the most common pattern of arousal response, but other hemodynamic patterns were observed. Similar findings were obtained in rapid-eye-movement sleep and for acoustic and tactile arousals. In conclusion, spontaneous and induced arousals from sleep may be associated with simultaneous visceral vasoconstriction and hindlimb vasodilation, but the response is variable.

Effects of oxygen on regional hemodynamics in hemorrhagic shock

1996 ◽  
Vol 271 (1) ◽  
pp. H203-H211 ◽  
Author(s):  
H. Bitterman ◽  
V. Brod ◽  
G. Weisz ◽  
D. Kushnir ◽  
N. Bitterman
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Biceps Femoris ◽  
Total Blood ◽  
Biceps Femoris Muscle ◽  
Arterial Blood ◽  
Femoris Muscle

This study investigated mechanisms of the hemodynamic effects of oxygen in hemorrhagic shock induced by bleeding 30% of the total blood volume in anesthetized rats. An ultrasonic flowmeter was used to monitor regional blood flow. Changes in tissue perfusion were assessed by the laser-Doppler technique. The inhalation of 100% oxygen induced a significant increase in mean arterial blood pressure (MABP) and vascular resistance in the hindquarters, with a concomitant decrease in blood flow in the distal aorta and biceps femoris muscle. In contrast, oxygen did not change vascular resistance in the superior mesenteric artery (SMA) and renal beds and induced a significant increase in blood flow to the renal artery, SMA, and small bowel in hemorrhaged rats. L-Arginine (100 mg/kg iv) but not D-arginine or the vehicle (0.9% NaCl) completely abolished the effects of oxygen on blood pressure and reversed its effects on blood flow and resistance in the hindquarters and biceps femoris muscle. Administration of the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (50 mg/kg iv) significantly increased MABP and the resistance in the three vascular beds. Pretreatment of hemorrhaged rats with a superoxide dismutase mimic, the NO-stable radical 2,2,6,6-tetramethylpiperidine-N-oxyl (5 mg/kg iv), resulted in significantly diminished effects of oxygen on hindquarter hemodynamics. These results demonstrate a differential effect of oxygen, which increases vascular resistance in the hindquarters without a significant effect in the splanchnic and renal beds, thus favoring an increase in splanchnic and renal perfusion. It is suggested that inactivation of NO by reactive oxygen species may underlie the effects of oxygen on hindquarter vascular tone during shock.

P735Interleukin-33 induced eosinophilia restores perivascular adipose tissue function in obesity

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Saxton ◽  
R J Potter ◽  
S B Withers ◽  
R Grencis ◽  
A M Heagerty
Keyword(s):  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Plasma Insulin ◽  
Vascular Tone ◽  
Mesenteric Arteries ◽  
Obese Mice ◽  
High Fat ◽  
Perivascular Adipose Tissue

Abstract Background/Purpose Perivascular adipose tissue (PVAT) is essential in the modulation of vascular tone. Recently we have shown that resident eosinophils play a vital role in regulating PVAT function. In obesity, eosinophil numbers are reduced and PVAT anticontractile function is lost, resulting in increased vascular tone, which will contribute to development of hypertension and type-2 diabetes. Evidence suggests that eosinophilia resulting from parasitic infection may be useful in improving glucose tolerance; therefore, we investigated the effects of eosinophilia on PVAT function in health and obesity. Methods Control mice and a high fat fed mouse model of obesity were administered intraperitoneal injections of interleukin-33 (IL-33, 0.1μg) over a five day period. Blood pressure, blood glucose and plasma insulin were measured and compared with un-injected control and obese mice. Wire myography was used to assess the vascular contractility of mesenteric arteries (<250μm, +/− PVAT) from both injected and un-injected control and obese mice in response to noradrenaline. ELISAs and immunohistochemistry were used to examine eosinophil numbers. Results High fat feeding induced significant elevations in blood pressure, blood glucose and plasma insulin, which were reduced using IL-33 injections. Eosinophilia was confirmed in blood plasma using an eosinophil cationic protein ELISA. Using wire myography, mesenteric arteries from control mice PVAT exerted an anticontractile effect on the vessels, which was enhanced in control mice injected with IL-33. In obese mice, the PVAT anticontractile effect was lost, but was restored in IL-33 injected obese mice. Using immunohistochemistry, we confirm that eosinophils numbers in PVAT were reduced in obesity and increased in IL-33 treated PVAT. Conclusions IL-33 injections induced eosinophilia in both control and obese mice. IL-33 treatment restored PVAT function in obesity, and enhanced the anticontractile function of PVAT in healthy animals. In addition, only five consecutive injections of IL-33 reversed development of hypertension and type-2 diabetes in obese mice. These data suggest that IL-33 induced eosinophilia presents a novel approach to treatment of hypertension and type-2 diabetes in obesity. Acknowledgement/Funding British Heart Foundation

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