Sympathetic arterial baroreflex hysteresis in humans: different patterns during low- and high-pressure levels

2020 ◽  
Vol 319 (4) ◽  
pp. H787-H792
Author(s):  
Anthony V. Incognito ◽  
Milena Samora ◽  
Andrew D. Shepherd ◽  
Roberta A. Cartafina ◽  
Gabriel M. N. Guimarães ◽  
...  

The findings show that the arterial baroreflex processes diastolic pressure dependent on the direction of pressure change from the previous beat, yielding two distinct baroreflex response curves to falling and rising pressure. Overall, the falling pressure curve is rightward shifted and more sensitive. The rightward shift caused a hysteresis reversal at hypotensive pressures as the falling pressure saturation plateau of the sigmoid response curve occurred at higher pressures than the rising pressure curve.

2006 ◽  
Vol 290 (1) ◽  
pp. H200-H208 ◽  
Author(s):  
Kanji Matsukawa ◽  
Hidehiko Komine ◽  
Tomoko Nakamoto ◽  
Jun Murata

We have reported that baroreflex bradycardia by stimulation of the aortic depressor nerve is blunted at the onset of voluntary static exercise in conscious cats. Central command may contribute to the blunted bradycardia, because the most blunted bradycardia occurs immediately before exercise or when a forelimb is extended before force development. However, it remained unknown whether the blunted bradycardia is due to either reduced sensitivity of the baroreflex stimulus-response curve or resetting of the curve toward a higher blood pressure. To determine this, we examined the stimulus-response relationship between systolic (SAP) or mean arterial pressure (MAP) and heart rate (HR) at the onset of and during the later period of static exercise in seven cats ( n = 348 trials) by changing arterial pressure with infusion of nitroprusside and phenylephrine or norepinephrine. The slope of the MAP-HR curve decreased at the onset of exercise to 48% of the preexercise value (2.9 ± 0.4 beats·min−1·mmHg−1); the slope of the SAP-HR curve decreased to 59%. The threshold blood pressures of the stimulus-response curves, at which HR started to fall due to arterial baroreflex, were not affected. In contrast, the slopes of the stimulus-response curves during the later period of exercise returned near the preexercise levels, whereas the threshold blood pressures elevated 6–8 mmHg. The maximal plateau level of HR was not different before and during static exercise, denying an upward shift of the baroreflex stimulus-response curves. Thus central command is likely to attenuate sensitivity of the cardiac component of arterial baroreflex at the onset of voluntary static exercise without shifting the stimulus-response curve.


1983 ◽  
Vol 54 (1) ◽  
pp. 130-133 ◽  
Author(s):  
D. Sheppard ◽  
J. Epstein ◽  
M. J. Holtzman ◽  
J. A. Nadel ◽  
H. A. Boushey

We undertook a study to determine whether the apparent disparity between the dose of inhaled atropine required to inhibit the bronchoconstriction induced by inhaled methacholine and the dose required to inhibit the bronchoconstriction induced by eucapnic hyperpnea with cold air is a function of the route of administration of atropine. In six subjects with asthma, we constructed dose-response curves to inhaled methacholine and to eucapnic hyperpnea with cold air after treatment with inhaled atropine (0.5 mg delivered) and intravenous placebo, with inhaled placebo and intravenous atropine (0.5 mg injected), and with inhaled and intravenous placebos. Atropine by either route shifted the dose-response curves to both cold air and to methacholine to the right. In every subject, however, inhaled atropine caused a markedly greater rightward shift of the inhaled methacholine dose-response curve than did intravenous atropine, whereas inhaled and intravenous atropine had similar effects on the cold air dose-response curve. These findings suggest that the apparent disparity between the doses of atropine required to inhibit methacholine- and cold air-induced bronchoconstriction may be a function of the route of administration of atropine and thus does not imply a nonmuscarinic action of atropine. The findings support the view that cold air causes bronchoconstriction via muscarinic pathways.


1993 ◽  
Vol 74 (5) ◽  
pp. 2537-2542 ◽  
Author(s):  
W. M. Abraham ◽  
A. Ahmed ◽  
A. Cortes ◽  
M. J. Spinella ◽  
A. B. Malik ◽  
...  

In this study we used conscious sheep to compare the relative potencies of inhaled endothelin- (ET) 1 and ET-3 and to determine whether a newly described selective ET-1 receptor antagonist, [diaminopropionic acid1-Asp15]ET-1 ([Dpr1-Asp15]ET-1), when given as an aerosol blocks ET-1-induced bronchoconstriction. Partial concentration-response curves to ET-1 and ET-3 were obtained by measuring the change in pulmonary airflow resistance (RL) after aerosol challenge. Both ET-1 (n = 6) and ET-3 (n = 4) caused concentration-dependent (10(-10)-10(-7) bronchoconstriction, but ET-3 was 400-fold less potent than ET-1. Pretreatment (30 min) with 25 breaths of 5 x 10(-8) M [Dpr1-Asp15]ET-1 caused a 100-fold rightward shift of the ET-1 concentration-response curve. The activity of the ET-1 antagonist (25 breaths of 5 x 10(-8) M) was compared with that of various control peptides (25 breaths of 10(-8) M). ET-1 (50 breaths of 10(-7) M) caused an increase in RL of 133 +/- 33% (SE) over baseline. [Dpr1-Asp15]ET-1 significantly inhibited this response by 54%. No protection was seen with a monocyclic control peptide or a thrombin receptor peptide. There was, however, a small protective effect (38%, P < 0.05) seen with [Dpr1-Asp15]ET-3, a structurally homologous ET-3 antagonist. [Dpr1-Asp15]ET-1 had no effect on carbachol (n = 3) or leukotriene D4-induced bronchoconstriction. Thus inhaled ET-1 and, to a lesser extent, ET-3 cause concentration-dependent bronchoconstriction in conscious sheep.


1991 ◽  
Vol 65 (02) ◽  
pp. 160-164 ◽  
Author(s):  
Marina Poggio ◽  
Armando Tripodi ◽  
Guglielmo Mariani ◽  
Pier Mannuccio Mannucci ◽  

SummaryBeing a putative predictor of ischemic heart disease, the measurement of factor VII (FVTI) coagulant activity will be presumably requested to clinical laboratories with increasing frequency. To assess the influence on FVII assays of different thromboplastins and FVII-deficient plasmas we compared performances of all possible combinations of 5 thromboplastins and 6 deficient plasmas. The reproducibility of the clotting times of the dose-response curves for human and rabbit thromboplastins were acceptable (CV lower than 7%), whereas bovine thromboplastin had a higher CV. Reproducibility was very similar for all deficient plasmas when they were used in combination with a given thromboplastin. Responsiveness of the dose-response curve did not depend on the deficient plasma but rather on the thromboplastin: one rabbit thromboplastin was the least responsive, the bovine thromboplastin the most responsive, the human and the remaining two rabbit thromboplastins had intermediate responsiveness. Assay sensitivity to cold-activated FVII varied according to the thromboplastin: the bovine thromboplastin was the most sensitive, the human thromboplastin the least sensitive, of the three rabbit thromboplastins two were relatively sensitive, one was almost insensitive. In conclusion, our results indicate that thromboplastin rather than deficient plasma is the crucial factor in the standardization of FVII assay.


1967 ◽  
Vol 56 (4) ◽  
pp. 619-625 ◽  
Author(s):  
Hans Jacob Koed ◽  
Christian Hamburger

ABSTRACT Comparison of the dose-response curves for LH of ovine origin (NIH-LH-S8) and of human origin (IRP-HMG-2) using the OAAD test showed a small, though statistically significant difference, the dose-response curve for LH of human origin being a little flatter. Two standard curves for ovine LH obtained with 14 months' interval, were parallel but at different levels of ovarian ascorbic acid. When the mean ascorbic acid depletions were calculated as percentages of the control levels, the two curves for NIH-LH-S8 were identical. The use of standards of human origin in the OAAD test for LH activity of human preparations is recommended.


1981 ◽  
Vol 27 (11) ◽  
pp. 1838-1844 ◽  
Author(s):  
G A Hudson ◽  
R F Ritchie ◽  
J E Haddow

Abstract Antiserum performance in a nephelometric system can be characterized by parameters derived from measuring reaction rates. The characterization process is derived from a series of dose-response curves (elicited nephelometric response vs antigen concentration) generated from various dilutions of the antiserum being tested. Antiserum titer can then be calculated by plotting the antigen concentration found at one-half the maximum nephelometric response (Hmax) of each dose-response curve (C50) vs the corresponding antiserum dilution. Antiserum avidity can be calculated by plotting Hmax against its corresponding antiserum concentration. After general expressions are determined for C50 and Hmax vs antiserum concentration, a single dose-response curve suffices for characterizing antisera with respect to titer and avidity. Direct evidence is provided for the validity of C50 and Hmax as measures of titer and avidity by correlating these parameters with antiserum binding strength and with the number of antibodies eluted from immobilized antigen. This method can be applied to evaluate and compare different antiserum lots having the same specificity, to identify reagent inadequacies by comparing antisera of different specificity, and to predict the optimal antiserum dilution to use in performing an assay.


1995 ◽  
Vol 269 (1) ◽  
pp. F78-F85 ◽  
Author(s):  
C. L. Chou ◽  
S. R. DiGiovanni ◽  
A. Luther ◽  
S. J. Lolait ◽  
M. A. Knepper

We conducted this study to determine what receptor mediates the effect of oxytocin to increase osmotic water permeability (Pf) in the rat inner medullary collecting duct (IMCD). Reverse transcription-polymerase chain reaction (RT-PCR) experiments demonstrated that mRNA for both the oxytocin receptor and the V2 receptor is present in the rat terminal IMCD. In isolated perfused IMCD segments, we found that the V2 vasopressin receptor antagonist [d(CH2)5(1),D-Ile2,Ile4,Arg8]vasopressin, but not oxytocin receptor antagonists, blocked the hydrosmotic response to 200 pM oxytocin. The selective oxytocin receptor agonist [Thr4,Gly7]oxytocin did not increase water permeability. Oxytocin also increased urea permeability in IMCD segments. Studies in IMCD suspensions showed that oxytocin increases adenosine 3',5'-cyclic monophosphate production in a dose-dependent fashion with a half-maximal (EC50) response at 5.2 nM. The dose-response curves were virtually identical for IMCD suspensions from Sprague-Dawley rats and Brattleboro rats. The oxytocin dose-response curve was displaced to the right of the vasopressin dose-response curve (EC50, 0.44 nM). From these results, we conclude that the V2 receptor mediates the hydrosmotic action of oxytocin in rat IMCD.


1972 ◽  
Vol 43 (2) ◽  
pp. 181-191
Author(s):  
J. B. Elder ◽  
G. Gillespie ◽  
E. H. G. Campbell ◽  
I. E. Gillespie ◽  
G. P. Crean ◽  
...  

1. The acid secretory responses to a range of small doses of pentagastrin in 0·15 m-NaCl have been studied in thirty-one preoperative duodenal ulcer subjects. Acid output increased significantly above basal values when a dose of 0·064 μg h−1 kg−1 was given. 2. Control observations in sixteen duodenal ulcer patients using the saline solvent alone at identical rates of infusion showed no significant increase in acid output. 3. From the dose-response curves sub-threshold and threshold doses of pentapeptide are suggested for duodenal ulcer patients before truncal vagotomy. 4. Considerable variation in acid response was noted between patients given the same body-weight dose of pentapeptide. The results suggest that a ‘twilight zone’ of stimulation exists between the dose of pentagastrin by which few patients are stimulated and the dose by which the majority are stimulated. This may reflect some variation in the sensitivity to stimulation by pentagastrin from one patient to another.


2013 ◽  
Vol 712-715 ◽  
pp. 1201-1204
Author(s):  
Hai Feng Zhao ◽  
Yan Xu

The numerical simulation method is adopted to calculate the flow field of the secondary throttle choke used in the oil field. The relationships among the flow of the secondary throttle choke, differential pressure and diameters are studied. The results of numerical simulation coincide with the experiment values, which verify that the method is correct. The results show that the flow increases with the increasing of differential pressure of the throttle choke at both ends, but the increment of the flow gradually decreases. The structure could maintain the flow not to change basically when differential pressure change in a certain scope. When the throttle diameter turns out to be small, the flow decreases, and flow-pressure curve gradually becomes aclinic. Compared with the first-class throttle diameter, the second-class throttle diameter is the main factor which effects flow changes.


2002 ◽  
Vol 103 (s2002) ◽  
pp. 353S-356S ◽  
Author(s):  
Benjamin A. DE CAMPO ◽  
Roy G. GOLDIE ◽  
Arco Y. JENG ◽  
Peter J. HENRY

The present study examined the roles of endothelin-converting enzyme (ECE), neutral endopeptidase (NEP) and mast cell chymase as processors of the endothelin (ET) analogues ET-1(1–21), ET-1(1–31) and big ET-1 in the trachea of allergic mice. Male CBA/CaH mice were sensitized with ovalbumin (10µg) delivered intraperitoneal on days 1 and 14, and exposed to aerosolized ovalbumin on days 14, 25, 26 and 27 (OVA mice). Mice were killed and the trachea excised for histological analysis and contraction studies on day 28. Tracheae from OVA mice had 40% more mast cells than vehicle-sensitized mice (sham mice). Ovalbumin (10µg/ml) induced transient contractions (15±3% of the Cmax) in tracheae from OVA mice. The ECE inhibitor CGS35066 (10µM) inhibited contractions induced by big ET-1 (4.8-fold rightward shift of dose-response curve; P<0.05), but not those induced by either ET-1(1–21) or ET-1(1–31). The chymase inhibitors chymostatin (10µM) and Bowman-Birk inhibitor (10µM) had no effect on contractions induced by any of the ET analogues used. The NEP inhibitor CGS24592 (10µM) inhibited contractions induced by ET-1(1–31) (6.2-fold rightward shift; P<0.05) but not ET-1(1–21) or big ET-1. These data suggest that big ET-1 is processed predominantly by a CGS35066-sensitive ECE within allergic airways rather than by mast cell-derived proteases such as chymase. If endogenous ET-1(1–31) is formed within allergic airways, it is likely to undergo further conversion by NEP to more active products.


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