Effect of ingesting a meal and orthostasis on the regulation of splanchnic and systemic hemodynamics and the responsiveness of cardiovascular α1-adrenoceptors

2021 ◽  
Author(s):  
Farid Zreik ◽  
Reshef Meshulam ◽  
Ido Shichel ◽  
Muriel Webb ◽  
Oren Shibolet ◽  
...  
Keyword(s):  
Pressor Response ◽  
Plasma Renin ◽  
Systemic Circulation ◽  
Systemic Hemodynamics ◽  
Plasma Catecholamine ◽  
Neurohumoral Regulation ◽  
Before And After ◽  
Cardiovascular Homeostasis ◽  
Underlying Mechanisms ◽  
Meal Ingestion

Background: Postprandial orthostasis activates mechanisms of cardiovascular homeostasis in order to maintain normal blood pressure (BP) and adequate blood flow to vital organs. The underlying mechanisms of cardiovascular homeostasis in postprandial orthostasis still require elucidation. Methods: Fourteen healthy volunteers were recruited to investigate the effect of an orthostatic challenge (600-head-up-tilt for 20 minutes) on splanchnic and systemic hemodynamics before and after ingesting an 800-kilocalorie composite meal. The splanchnic circulation was assessed by ultrasonography of the superior mesenteric and hepatic arteries and portal vein. Systemic hemodynamics were assessed non-invasively by continuous monitoring of BP, heart rate (HR), cardiac output (CO), and the pressor response to an intravenous infusion on increasing doses of phenylephrine, an α1-adrenoceptor agonist. Neurohumoral regulation was assessed by spectral analysis of HR and BP, plasma catecholamine and aldosterone levels and plasma renin activity. Results: Postprandial mesenteric hyperemia was associated with an increase in CO, a decrease in SVR and cardiac vagal tone, and reduction in baroreflex sensitivity with no change in sympathetic tone. Arterial α1-adrenoceptor responsiveness was preserved and reduced in hepatic sinusoids. Postprandial orthostasis was associated with a shift of 500 ml of blood from mesenteric to systemic circulation with preserved sympathetic-mediated vasoconstriction Conclusions: Meal ingestion provokes cardiovascular hyperdynamism, cardiac vagolysis, and resetting of the baroreflex without activation of the sympathetic nervous system. Meal ingestion also alters α1-adrenoceptor responsiveness in the hepatic sinusoids and participates in the redistribution of blood volume from the mesenteric to the systemic circulation in order to maintain a normal BP during orthostasis.

α1-Adrenoceptor Blockade: Dissociation of Its Effects on Renin Release and Arterial Blood Pressure in Man

1981 ◽  
Vol 61 (s7) ◽  
pp. 307s-309s ◽  
Author(s):  
A. Morganti ◽  
Carla Sala ◽  
Anna Palermo ◽  
Lucia Turolo ◽  
A. Zanchetti
Keyword(s):  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Pressor Response ◽  
Plasma Renin ◽  
Test Dose ◽  
Blocking Agent ◽  
Renin Activity ◽  
Renin Release ◽  
Arterial Blood ◽  
Before And After

1. The possibility that the juxtaglomerular α1-adrenoceptors mediate an inhibitory action on renin release in man was examined in seven patients with essential hypertension, by measuring (i) the acute effects of prazosin (0.25 mg intravenously), a selective α1-adrenoceptor-blocking agent, on arterial pressure and plasma renin activity, the degree of α-blockade induced by the drug being assessed by comparing the pressor response with that to a test dose of phenylephrine before and after prazosin administration, and (ii) the increases in plasma renin activity in response to isoprenaline before and during the prazosin-induced α-blockade. 2. Twenty minutes after the infusion of prazosin, when the pressor response to phenylephrine was reduced by 80% with respect to control, (i) mean arterial pressure was practically unchanged, (ii) plasma renin activity was almost doubled and (iii) the increases in plasma renin activity in response to isoprenaline were significantly greater, both in absolute and percentage values, than those observed before prazosin. 3. The increments in baseline plasma renin activity induced by prazosin in the absence of decrease in arterial pressure and the enhancement in renin responsiveness to the β-adrenoceptor stimulus suggest that, in man, the juxtaglomerular α1-adrenoceptors exert a direct, suppressive action on renin release.

Angiotensin II-mediated catecholamine release during the pressor response in rats

1994 ◽  
Vol 142 (1) ◽  
pp. 19-28 ◽  
Author(s):  
D G Butler ◽  
D A Butt ◽  
D Puskas ◽  
G Y Oudit
Keyword(s):  
Angiotensin Ii ◽  
Pressor Response ◽  
Plasma Renin ◽  
Sympathetic Nerves ◽  
Catecholamine Release ◽  
Plasma Catecholamine ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Pressor Responses ◽  
Plasma Catecholamine Concentrations

Abstract Angiotensin II (ANG II)-mediated catecholamine release and its possible contribution to the pressor response was assessed in baroreceptor-denervated rats. Neonatal male Sprague-Dawley rats were injected with the sympatholytic drug, guanethidine monosulphate (50 mg/kg s.c., 6 days/week) for 40 days. Plasma catecholamine concentrations were measured using a 3H-radioenzymatic assay as follows: (a) before and 30 s after the injection of saline or ANG II (79·3 pmol/kg i.v.), at the peak of the pressor response, then 50 s and 80 s thereafter, in guanethidine-treated (GUAN) and saline-injected (SHAM) rats, and (b) before and after adrenalectomy (ADX), following the same time-sequence for ANG II as in (a). Peak pressor responses to graded doses of ANG II (6·6, 26·4, 53·0 and 79·3 pmol/kg i.v.) were measured in GUAN+ADX and ADX rats. Destruction of peripheral sympathetic nerves was confirmed by measurements of plasma noradrenaline (NA), adrenaline (AD) and dopamine (DA) concentrations and by changes in pressor responses and heart rates following i.v. doses of tyramine. ANG II induced significantly (P<0·05) greater pressor responses in GUAN+ADX rats than in ADX rats, especially after the 53·0 and 79·3 pmol/kg doses. Plasma AD concentrations increased within seconds after the pressor response to ANG II in both GUAN and SHAM rats but there was no change in plasma NA or DA concentrations (P<0·05). ANG-II-mediated AD release from the adrenal medulla may contribute to the overall pressor action of the peptide. The vasculature became more sensitive to ANG II at a time when NA and DA depletion occurred following sympathectomy and/or adrenalectomy. This heightened sensitivity to ANG II was not due to a decrease in circulating ANG II in sympathectomized rats because even though plasma renin activity fell from 6·54 ±0·52 to 3·77 ±0·26 ng ANG I/ml per h it remained within the normal range. Journal of Endocrinology (1994) 142, 19–28

Similar poststimulatory pressor responses with different mechanisms in response to excitation of the locus coeruleus before and after acute adrenalectomy

1987 ◽  
Vol 65 (6) ◽  
pp. 1136-1141 ◽  
Author(s):  
Guy Drolet ◽  
Pierre Gauthier
Keyword(s):  
Locus Coeruleus ◽  
Pressor Response ◽  
Primary Component ◽  
Adrenergic Blockade ◽  
Pressor Responses ◽  
Before And After ◽  
Underlying Mechanisms ◽  
Noradrenaline And Adrenaline ◽  
Stimulation Of ◽  
Intact Rats

Electrical stimulation of the locus coeruleus in anesthetized rats evoked a biphasic pressor response consisting of an initial sharp rise in blood pressure at the onset of stimulation, followed by a second elevation after cessation of the stimulus. This response, which was accompanied by an increase in plasma noradrenaline and adrenaline levels, was stable and could be easily reproduced over time. Sympathectomy by administration of guanethidine selectively abolished the primary pressor response. β-Adrenergic blockade by intravenous administration of sotalol enhanced the secondary pressor response without affecting the primary component. Adrenal demedullation performed 24–48 h before the experiments selectively prevented the secondary pressor component. In contrast, acute adrenalectomy carried out during the experiment to impair the adrenomedullary secretions eliminated the secondary pressor response to stimulation of the locus coeruleus only in sympathectomized or in sotalol-treated rats but not in intact rats in which the response persisted. The latter, however, could be abolished by the administration of either guanethidine or sotalol, and it disappeared following repeated stimulation of the locus coeruleus. The study demonstrates that similar poststimulatory pressor responses with different underlying mechanisms can be elicited on excitation of the locus coeruleus before and after acute adrenalectomy in the rat. The results also suggest that intraneuronal adrenaline may be involved in the response evoked in acutely adrenalectomized animals.

Effect of volume expansion on pressor response to angiotensin II in pregnant ewes

1981 ◽  
Vol 240 (6) ◽  
pp. H908-H913
Author(s):  
S. Matsuura ◽  
R. P. Naden ◽  
N. F. Gant ◽  
C. R. Parker ◽  
C. R. Rosenfeld
Keyword(s):  
Angiotensin Ii ◽  
Volume Expansion ◽  
Pressor Response ◽  
Plasma Concentrations ◽  
Isotonic Saline ◽  
Plasma Renin ◽  
Response Curves ◽  
Pregnant Sheep ◽  
Before And After ◽  
Near Term

Vascular refractoriness to infused angiotensin II (AII) characterizes normal human and ovine pregnancy. To ascertain whether the refractoriness in the gravid ewe is mediated by either endogenous plasma concentrations of renin and AII or vasomotor reflexes, effects of acute volume expansion (VE) on the pressor response to AII were studied in chronically instrumented nonpregnant and near-term pregnant sheep. Dose-response curves describing the pressor response (delta BP) were determined before and after infusions of 1.0 1 of isotonic saline (NS) or 0.5 1 of 10% dextran (D). In nonpregnant sheep, hematocrit (Hct) and plasma renin activity (PRA) fell in all animals after NS (n = 7) and D (n = 6) (P less than 0.005). After VE with NS and D, delta BP increased at each dose of AII (P less than 0.05). The pressor response to AII in pregnant sheep was not altered by NS although decreases in Hct and PRA were comparable to those in nonpregnant sheep. Baroreceptor responses were not altered. Vascular refractoriness to infused AII in pregnant sheep is not due primarily to changes in plasma concentrations of renin-AII but more likely to another factor, vessel wall refractoriness. In this respect, the ewe is similar to the human.

SERIAL ESTIMATION OF PLASMA RENIN CONCENTRATION DURING PREGNANCY AND AFTER PARTURITION

1966 ◽  
Vol 35 (4) ◽  
pp. 373-378 ◽  
Author(s):  
J. J. BROWN ◽  
D. L. DAVIES ◽  
P. B. DOAK ◽  
A. F. LEVER ◽  
J. I. S. ROBERTSON
Keyword(s):  
Pregnant Women ◽  
Plasma Renin ◽  
Plasma Renin Concentration ◽  
Before And After ◽  
Normal Women ◽  
Made In

SUMMARY Plasma renin concentration has been measured in normal women at intervals throughout pregnancy. Further measurements have been made in the days and hours before and after delivery of the foetus and placenta. Plasma renin was consistently raised in the majority of pregnant women and did not change markedly until 24 hr. or more after delivery. The significance of these findings is discussed.

scholarly journals Detection of Anthrax Toxin in the Serum of Animals Infected with Bacillus anthracis by Using Engineered Immunoassays

2006 ◽  
Vol 13 (6) ◽  
pp. 671-677 ◽  
Author(s):  
Robert Mabry ◽  
Kathleen Brasky ◽  
Robert Geiger ◽  
Ricardo Carrion ◽  
Gene B. Hubbard ◽  
...  
Keyword(s):  
Bacillus Anthracis ◽  
Protective Antigen ◽  
Lethal Factor ◽  
Systemic Circulation ◽  
Rapid Identification ◽  
Anthrax Toxin ◽  
Soluble Form ◽  
Before And After

ABSTRACT Several strategies that target anthrax toxin are being developed as therapies for infection by Bacillus anthracis. Although the action of the tripartite anthrax toxin has been extensively studied in vitro, relatively little is known about the presence of toxins during an infection in vivo. We developed a series of sensitive sandwich enzyme-linked immunosorbent assays (ELISAs) for detection of both the protective antigen (PA) and lethal factor (LF) components of the anthrax exotoxin in serum. The assays utilize as capture agents an engineered high-affinity antibody to PA, a soluble form of the extracellular domain of the anthrax toxin receptor (ANTXR2/CMG2), or PA itself. Sandwich immunoassays were used to detect and quantify PA and LF in animals infected with the Ames or Vollum strains of anthrax spores. PA and LF were detected before and after signs of toxemia were observed, with increasing levels reported in the late stages of the infection. These results represent the detection of free PA and LF by ELISA in the systemic circulation of two animal models exposed to either of the two fully virulent strains of anthrax. Simple anthrax toxin detection ELISAs could prove useful in the evaluation of potential therapies and possibly as a clinical diagnostic to complement other strategies for the rapid identification of B. anthracis infection.

scholarly journals Does Social Exclusion Alter Sensory and Pain Thresholds in Children and Adolescents with Functional Abdominal Pain? – Results from a Preliminary Study

Pain Medicine ◽  
2018 ◽  
Vol 20 (8) ◽  
pp. 1472-1478
Author(s):  
Marco Daniel Gulewitsch ◽  
Aiste Jusyte ◽  
Katja Weimer ◽  
Michael Schönenberg
Keyword(s):  
Abdominal Pain ◽  
Social Exclusion ◽  
Experimental Studies ◽  
Control Group ◽  
Childhood And Adolescence ◽  
Sensory Threshold ◽  
Functional Abdominal Pain ◽  
Pain Thresholds ◽  
Before And After ◽  
Underlying Mechanisms

Abstract Objective Functional abdominal pain (AP) is a prevalent issue in childhood and adolescence. The contribution of psychosocial factors in the development and maintenance of this health problem is rather unclear, and experimental studies about underlying mechanisms are lacking. This study investigates whether experimentally induced social exclusion decreases sensory and pain thresholds in children suffering from AP. Subjects Twenty children/adolescents with AP and 22 healthy controls. Methods Children/adolescents participated in the Cyberball paradigm, which affects an experience of social exclusion. Thermal sensory and pain thresholds were measured before and after Cyberball. Results Children/adolescents with AP showed a divergent reaction regarding their sensory threshold after social exclusion: The control group exhibited a tendency toward a decreased sensory threshold whereas the AP group remained stable. Concerning the pain threshold, no effect of social exclusion could be identified. The increase of both thresholds (“numbing”) after Cyberball was positively correlated with symptoms of mental health issues. Conclusions This is the first study to investigate changes in sensory and pain thresholds following painful social interactions in a sample of children/adolescents with a chronic pain condition. Results suggest that AP and control children differ in their reaction of sensory thresholds, which might indicate an altered processing of social exclusion. Replication and further methodological improvements are needed.

Salt-sensitive hypertension in ANP knockout mice is prevented by AT1 receptor antagonist losartan

1999 ◽  
Vol 277 (3) ◽  
pp. R624-R630 ◽  
Author(s):  
Luis G. Melo ◽  
Anthony T. Veress ◽  
Chee K. Chong ◽  
Uwe Ackermann ◽  
Harald Sonnenberg
Keyword(s):  
Receptor Antagonist ◽  
Knockout Mice ◽  
Plasma Renin ◽  
Plasma Catecholamine ◽  
Ang Ii ◽  
Dietary Salt ◽  
Water Control ◽  
Dietary Regimen ◽  
Arterial Blood ◽  
Salt Sensitive Hypertension

Mice harboring a functional deletion of the pro-atrial natriuretic peptide (ANP) gene (−/−) develop salt-sensitive hypertension relative to their wild-type (+/+) counterparts after prolonged (>1 wk) maintenance on high-salt (HS, 8% NaCl) diet. We reported recently that the sensitization of arterial blood pressure (ABP) to dietary salt in the −/− mice is associated with failure to downregulate plasma renin activity. To further characterize the role and mechanism of ANG II in the sensitization of ABP to salt in the ANP “knockout” mice, we measured ABP, heart rate (HR), and plasma catecholamine and aldosterone concentrations in −/− and +/+ mice maintained on HS for 4 wk and treated with daily injections of AT1 receptor antagonist DuP-753 (losartan) or distilled water (control). Daily food and water intake and fluid and electrolyte excretion were also measured during the first and last weeks of the dietary regimen. Cumulative urinary excretion of fluid and electrolytes did not differ significantly between genotypes and was not altered by chronic treatment with losartan. Basal ABP and HR were significantly elevated in control −/− mice compared with control +/+ mice. Losartan did not affect ABP or HR in +/+ mice, but reduced ABP and HR in the −/− mice to the levels in the +/+ mice. Total plasma catecholamine was elevated by approximately ten-fold in control −/− mice compared with control +/+ mice. Losartan reduced plasma catecholamine concentration significantly in −/− mice and abrogated the difference in plasma catecholamine between −/− and +/+ mice on HS diet. Plasma aldosterone did not differ significantly between genotypes and was not altered by losartan. We conclude that salt sensitivity of ABP in ANP knockout mice is mediated, at least in part, by a synergistic interaction between ANG II and sympathetic nerve activity.

scholarly journals Chronic pain relief after the exposure of nitrous oxide during dental treatment: longitudinal retrospective study

2015 ◽  
Vol 73 (7) ◽  
pp. 578-581 ◽  
Author(s):  
Francisco Moreira Mattos Júnior ◽  
Rafael Villanova Mattos ◽  
Manoel Jacobsen Teixeira ◽  
Silvia Regina Dowgan Tesseroli de Siqueira ◽  
Jose Tadeu Tesseroli de Siqueira
Keyword(s):  
Chronic Pain ◽  
Nitrous Oxide ◽  
Dental Treatment ◽  
Chronic Pain Patients ◽  
Before And After ◽  
Nitrous Oxide Oxygen ◽  
Oxygen Nitrous Oxide ◽  
Prevalence Of Pain ◽  
Underlying Mechanisms ◽  
Pain Patients

The objective was to investigate the effect of nitrous/oxygen in chronic pain. Seventy-seven chronic pain patients referred to dental treatment with conscious sedation with nitrous oxide/oxygen had their records included in this research. Data were collected regarding the location and intensity of pain by the visual analogue scale before and after the treatment. Statistical analysis was performed comparing pre- and post-treatment findings. It was observed a remarkable decrease in the prevalence of pain in this sample (only 18 patients still had chronic pain, p < 0.001) and in its intensity (p < 0.001). Patients that needed fewer sessions received higher proportions of nitrous oxide/oxygen. Nitrous oxide may be a tool to be used in the treatment of chronic pain, and future prospective studies are necessary to understand the underlying mechanisms and the effect of nitrous oxide/oxygen in patients according to the pain diagnosis and other characteristics.

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