scholarly journals Reflex cardiovascular responses originating in exercising muscles of mice

2001 ◽  
Vol 90 (2) ◽  
pp. 579-585 ◽  
Author(s):  
Jeffery M. Kramer ◽  
Arthur Aragones ◽  
Tony G. Waldrop
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Muscle Contraction ◽  
Cardiovascular Responses ◽  
Muscular Contraction ◽  
Dependent Manner ◽  
Direct Stimulation ◽  
Systemic Hypoxia ◽  
Dose Dependent ◽  
Stimulation Of

The cardiovascular responses induced by exercise are initiated by two primary mechanisms: central command and reflexes originating in exercising muscles. Although our understanding of cardiovascular responses to exercise in mice is progressing, a murine model of cardiovascular responses to muscle contraction has not been developed. Therefore, the purpose of this study was to characterize the cardiovascular responses to muscular contraction in anesthetized mice. The results of this study indicate that mice demonstrate significant increases in blood pressure (13.8 ± 1.9 mmHg) and heart rate (33.5 ± 11.9 beats/min) to muscle contraction in a contraction-intensity-dependent manner. Mice also demonstrate 23.1 ± 3.5, 20.9 ± 4.0, 21.7 ± 2.6, and 25.8 ± 3.0 mmHg increases in blood pressure to direct stimulation of tibial, peroneal, sural, and sciatic hindlimb somatic nerves, respectively. Systemic hypoxia (10% O2-90% N2) elicits increases in blood pressure (11.7 ± 2.6 mmHg) and heart rate (42.7 ± 13.9 beats/min), while increasing arterial pressure with phenylephrine decreases heart rate in a dose-dependent manner. The results from this study demonstrate the feasibility of using mice to study neural regulation of cardiovascular function during a variety of autonomic stimuli, including exercise-related drives such as muscle contraction.

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

Blocking properties of terguride at the 5-HT2 receptor subtypes mediating cardiovascular responses in the rat

2020 ◽  
Vol 98 (8) ◽  
pp. 511-521
Author(s):  
Oscar Alcántara-Vázquez ◽  
Ma. Trinidad Villamil-Hernández ◽  
Araceli Sánchez-López ◽  
Heinz H. Pertz ◽  
Carlos M. Villalón ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Diastolic Blood Pressure ◽  
Receptor Agonist ◽  
Cardiovascular Responses ◽  
Receptor Subtypes ◽  
Pithed Rats ◽  
Anaesthetized Rats ◽  
Dose Dependent

In vitro studies have suggested that terguride blocks the contractile and relaxant responses produced by 5-hydroxytryptamine (5-HT) via 5-HT2A/2B receptors. This study has now investigated terguride’s blocking properties on central/peripheral 5-HT2 receptors in anaesthetized or pithed rats. Male Wistar anaesthetized/pithed rats were cannulated for recording blood pressure and heart rate and for i.v. administration of several compounds. In both groups of rats, i.v. bolus injections of 5-HT or (±)-DOI (a 5-HT2 receptor agonist; 1–1000 μg/kg) produced dose-dependent increases in diastolic blood pressure and heart rate. These responses were dose-dependently antagonized by terguride (10–3000 μg/kg). In anaesthetized rats, i.v. bolus injections of BW723C86 (a 5-HT2B receptor agonist; 1–1000 μg/kg) produced dose-dependent increases in diastolic blood pressure and not dose-dependent increases in heart rate, while in pithed rats, these responses were attenuated. The vasopressor responses elicited by BW723C86 in anaesthetized rats were dose-dependently blocked by terguride (10–300 μg/kg), whereas its the tachycardic responses were dose-independently blocked. These results, taken together, suggest that terguride behaved as an antagonist at the 5-HT2 receptors located in the central nervous system and (or) the systemic vasculature. This is the first evidence demonstrating that terguride can block central/peripheral 5-HT2 receptors mediating cardiovascular responses in anaesthetized or pithed rats.

Central cholinergic control of vasopressin release in conscious rats

1986 ◽  
Vol 251 (2) ◽  
pp. E146-E150 ◽  
Author(s):  
K. Iitake ◽  
L. Share ◽  
Y. Ouchi ◽  
J. T. Crofton ◽  
D. P. Brooks
Keyword(s):  
Blood Pressure ◽  
Muscarinic Receptors ◽  
Dependent Manner ◽  
Conscious Rat ◽  
Vasopressin Release ◽  
Conscious Rats ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Dose Dependent ◽  
Stimulation Of

Intracerebroventricular (icv) administration of carbachol into conscious rats evoked a substantial increase in vasopressin secretion and blood pressure in a dose-dependent manner. These effects were blocked by pretreatment with the muscarinic blocker, atropine (10 micrograms icv), but not by the nicotinic blocker, hexamethonium (10 micrograms icv). Hexamethonium did, however, block the increase in blood pressure, the decrease in heart rate, and the very small elevation in the plasma vasopressin concentration induced by nicotine (10 micrograms icv). These results indicate that stimulation of either central nicotinic or muscarinic receptors can affect the cardiovascular system and suggest that the cholinergic stimulation of vasopressin secretion may involve primarily muscarinic receptors in the conscious rat.

scholarly journals Dosing study of esmolol for reducing hemodynamic changes during lightwand intubation

2020 ◽  
Vol 15 (4) ◽  
pp. 417-423
Author(s):  
Jin Ku Kang ◽  
Sie Hyeon Yoo ◽  
Jin Hun Chung ◽  
Nan Seol Kim ◽  
Ho Soon Jung ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Normal Saline ◽  
Elective Surgery ◽  
Rate Pressure Product ◽  
Hemodynamic Changes ◽  
Direct Stimulation ◽  
Before And After ◽  
Different Doses ◽  
Stimulation Of

Background: Lightwand is a convenient tool that can be used instead of a laryngoscope for intubation. Tracheal intubation causes direct stimulation of the larynx, drastically increasing hemodynamic values including blood pressure and heart rate. This study aims to identify the effect of different doses of esmolol on hemodynamic changes during lightwand intubation.Methods: The study subjects included 140 patients who underwent general anesthesia for elective surgery. The patients were randomly divided into four groups (35 patients in each group). The ‘C’ group only received 20 ml of normal saline, while the ‘E0.5’, ‘E1’, and ‘E2’ groups received 20 ml of normal saline containing esmolol—0.5 mg/kg, 1 mg/kg, and 2 mg/kg, respectively, injected 2 min prior to intubation. The patients’ blood pressure, heart rate, and rate-pressure product were measured six times, before and after the intubation.Results: The degree of heart rate elevation was suppressed in the E1 and E2 groups compared to the C group, and RPP after intubation significantly decreased in the E2 group compared to the C group.Conclusions: 1–2 mg/kg of a single esmolol injection prior to lightwand intubation effectively blunts heart rate elevation, and 2 mg/kg of esmolol injection blunts rate-pressure product elevation.

scholarly journals Effects of oily fish intake on cardiometabolic markers in healthy 8- to 9-y-old children: the FiSK Junior randomized trial

2019 ◽  
Vol 110 (6) ◽  
pp. 1296-1305 ◽  
Author(s):  
Stine Vuholm ◽  
Jesper M Rantanen ◽  
Marie N Teisen ◽  
Ken D Stark ◽  
Christian Mølgaard ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Glucose Homeostasis ◽  
Hdl Cholesterol ◽  
Fish Intake ◽  
Dependent Manner ◽  
Oily Fish ◽  
Fish Group ◽  
Cardiometabolic Markers ◽  
Dose Dependent

ABSTRACT Background Fish oil improves cardiometabolic markers in adults, but results in children are inconsistent. Few children meet the recommended fish intake and no randomized trials have investigated how fish intake per se affects children's cardiometabolic profile. Objective We investigated whether oily fish consumption modulated serum triacylglycerol and diastolic blood pressure (coprimary outcomes) and other cardiometabolic markers in healthy Danish children and whether effects were sex-specific. Methods In a randomized controlled 12-wk trial, 199 children (aged 8–9 y) received ∼300 g/wk of oily fish or poultry (control). We measured blood pressure, heart rate, and heart rate variability (HRV) via 3-h continuous electrocardiograms and collected fasting blood samples for analysis of erythrocyte EPA [20:5n–3 (ω-3)] + DHA (22:6n–3) and serum triacylglycerol, LDL and HDL cholesterol, glucose, and insulin. Results One hundred and ninety-seven children (99%) completed the trial. The fish group consumed a median (IQR) of 375 (325–426) g oily fish/wk and the poultry group consumed 400 (359–452) g poultry/wk, which resulted in 2.25 (95% CI: 1.88, 2.62) fatty acid percentage-point higher erythrocyte EPA + DHA in the fish group (P < 0.001). In the fish group, serum triacylglycerol decreased by 0.05 mmol/L (95% CI: 0.00, 0.11 mmol/L) (P = 0.04) and HDL cholesterol increased by 0.07 mmol/L (95% CI: 0.01, 0.13 mmol/L) (P = 0.02); the triacylglycerol effect showed dose-dependency with erythrocyte EPA + DHA (r = −0.15, P = 0.04), whereas HDL showed a tendency for such an association(r = 0.13, P = 0.08). Additional analyses indicated sex-specificity (Pdiet*sex < 0.10), because triacylglycerol was reduced by 0.09 mmol/L (95% CI: 0.02, 0.16 mmol/L) in boys only (girls: −0.00; 95% CI: −0.07, 0.07 mmol/L) and heart rate was reduced by 3.4 bpm (95% CI: 0.2, 6.6 bpm) in girls only (boys: 0.6; 95% CI: −2.6, 3.8 bpm). Blood pressure, HRV, and glucose homeostasis were unaffected. Conclusions Oily fish intake improved serum triacylglycerol and HDL cholesterol in a dose-dependent manner in 8- to 9-y-old children, but had no effect on blood pressure, HRV, or glucose homeostasis. This supports recommendations for fish intake in children and underlines the importance of initiatives to increase children's intake of oily fish. This trial was registered at clinicaltrials.gov as NCT02809508.

Temporal relationships of barosensory attenuation in conscious rabbits

1976 ◽  
Vol 230 (6) ◽  
pp. 1480-1486 ◽  
Author(s):  
MP Gimpl ◽  
AL Brickman ◽  
MP Kaufman ◽  
N Schneiderman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Hypothalamic Stimulation ◽  
Aortic Nerve ◽  
Temporal Relationships ◽  
Train Stimulation ◽  
Posterior Hypothalamic Stimulation ◽  
Simple Summation ◽  
Stimulation Of

Electrical stimulation of anterior or posterior hypothalamus with 10-s trains elicited heart rate and blood pressure decreases. Presentation of anterior hypothalamic stimulation coincident with or 5, 10, or 15 s prior to 5-s train stimulation of aortic nerve (AN) summated with depressor-decelerator responses to AN stimulation. The summating effect was more pronounced for heart rate than for blood pressure. Simultaneous onset of AN and posterior hypothalamic stimulation did not influence AN responses. In contrast, when AN stimulation was delayed until 5, 10, or 15 s after onset of posterior hypothalamic stimulation, small, moderate, and full attenuation of AN responses occurred, respectively. Since AN and posterior hypothalamic stimulation each led to depressor-decelerator responses, attenuation of AN responses cannot be attributed to simple summation of cardiovascular responses elicited by intracranial and aortic nerve stimulation.

Static muscular contraction elicits a pressor reflex in the chicken

1997 ◽  
Vol 272 (3) ◽  
pp. R759-R765 ◽  
Author(s):  
I. C. Solomon ◽  
T. P. Adamson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Sciatic Nerve ◽  
Arterial Pressure ◽  
Gastrocnemius Muscle ◽  
Muscular Contraction ◽  
Arterial Blood ◽  
Static Contraction ◽  
Stimulation Of

Static muscular contraction has been shown to increase arterial blood pressure and heart rate in humans and other mammals. It is not clear, however, whether birds exhibit a similar response to this maneuver. Therefore, we designed these experiments to determine if the chicken exhibits a cardiovascular response to static muscular contraction and if the observed responses are evoked through a reflex involving muscle afferents. Static contraction of the gastrocnemius muscle was evoked by electrically stimulating the sciatic nerve at 1.5-3.0 times motor threshold (30-40 Hz; 0.025 ms) in 13 chloralose-anesthetized cockerels. We measured arterial blood pressure and muscle tension before and during static contraction and calculated mean arterial pressure and heart rate from the arterial pressure trace. We found that static contraction of the gastrocnemius muscle increased mean arterial pressure from 71 +/- 4 to 95 +/- 4 mmHg (P < 0.05) and increased heart rate from 304 +/- 8 to 345 +/- 10 beats/min (P < 0.05). Furthermore, we found that stimulation of the sciatic nerve after paralysis of the birds with vecuronium bromide or stimulation of the cut peripheral end of the sciatic nerve (using the same stimulation parameters described above) evoked no change in mean arterial pressure or heart rate. We conclude that static muscular contraction of the gastrocnemius muscle in the chicken elicits a pressor response and that this response is due to a reflex arising from the contracting muscles.

scholarly journals Corticotropin-releasing hormone projections from the paraventricular nucleus of the hypothalamus to the nucleus of the solitary tract increase blood pressure

2019 ◽  
Vol 121 (2) ◽  
pp. 602-608 ◽  
Author(s):  
Lei A. Wang ◽  
Dianna H. Nguyen ◽  
Steve W. Mifflin
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Paraventricular Nucleus ◽  
Cardiovascular Responses ◽  
Solitary Tract ◽  
Increase Blood Pressure ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Optogenetic Stimulation ◽  
Stimulation Of

Activation of corticotropin-releasing hormone (CRH) type 2 receptors (CRHR2) in the nucleus of the solitary tract (NTS) contributes to the development of hypertension, but the source of CRH inputs to the NTS that increases blood pressure remains unknown. This study tested the hypothesis that activation of CRH-containing projections from the paraventricular nucleus of the hypothalamus (PVN) to the NTS increase blood pressure. We expressed channelrhodopsin 2 (ChR2), a light-sensitive ion channel, into CRH-containing neurons in the PVN. This was achieved by injecting Cre-inducible virus expressing ChR2 into the PVN of CRH-Cre mice. CRH-Cre mice are genetically modified mice expressing Cre recombinase only in neurons producing CRH. We found that optogenetic stimulation of CRH-containing somas in the PVN or CRH-containing fibers in the NTS originating from the PVN significantly increased blood pressure and heart rate. Microinjection of K-41498 (CRHR2 antagonist) into the NTS attenuated the pressor and tachycardiac responses induced by optogenetic stimulation of CRH-containing somas in the PVN. In vitro loose-patch recordings revealed that optogenetic stimulation of CRH-containing fibers in the NTS originating from the PVN significantly increased the discharge frequency of NTS neurons. This effect was attenuated by pretreatment of K-41498 and was abolished by pretreatment of kynurenic acid (nonselective glutamate receptor antagonist). These results suggest that activation of PVN-NTS CRH-containing projections increases blood pressure and heart rate. The cardiovascular responses may be mediated at least in part by the corelease of CRH and glutamate from NTS CRH-containing axons originating from the PVN. NEW & NOTEWORTHY Optogenetic stimulation of paraventricular nucleus of the hypothalamus (PVN) corticotropin-releasing hormone (CRH)-containing somas or nucleus of the solitary tract (NTS) CRH-containing fibers originating from the PVN increased blood pressure and heart rate. Corelease of CRH and glutamate from NTS CRH-containing axons originating from the PVN may contribute to the pressor and tachycardiac responses elicited by optogenetic stimulation of PVN CRH-containing somas.

Arterial blood pressure control during hindlimb and forelimb contraction in the dog

1985 ◽  
Vol 248 (5) ◽  
pp. H678-H687
Author(s):  
O. Beaty
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Heart Rate ◽  
Muscle Contraction ◽  
Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Pressure Control ◽  
Arterial Blood ◽  
Vascular Bed ◽  
Skeletal Muscle Contraction

This study examined the differential reflex cardiovascular responses evoked by separate contractions of the right hindlimb and forelimb and established the mechanism of a regional reflex vasodilation associated with hindlimb skeletal muscle contraction. The two groups of skeletal muscle were contracted separately by electrical stimulation (2-48 Hz) of the peripheral motor nerves. The left nonexercising hindlimb was perfused at constant flow. All blood pressure-regulating mechanisms were intact. Arterial blood pressure (ABP), left nonexercising hindlimb perfusion pressure (HLPP), and heart rate (HR) were recorded. HR was increased by skeletal muscle contraction. This response was independent of muscle group and contraction frequency. Increases in both ABP and HLPP were produced by high-frequency contractions (greater than 16 Hz) of either the hindlimb or forelimb. Decreases were evoked only by hindlimb contractions (greater than 8 Hz). The nonexercising skeletal muscle vascular bed contributed to this systemic depressor response by vasodilating. The mechanism involved a contraction-induced withdrawal of sympathetic nerve activity to that vascular bed. Concomitant with this response was an increase in heart rate that was blocked with propranolol. Similar heart rate changes evoked by forelimb contractions also were blocked with propranolol. These data indicate that sympathetic outflow to resting skeletal muscle depends on the origin and magnitude of the afferent signal from the contracting skeletal muscle.

Somatostatin inhibition of secretagogue and forskolin-stimulated gastric acid secretion

1988 ◽  
Vol 254 (4) ◽  
pp. G531-G537
Author(s):  
F. Michelangeli ◽  
M. C. Ruiz ◽  
C. L. Rodriguez ◽  
A. Pelacca
Keyword(s):  
Acid Secretion ◽  
Histamine Release ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Direct Stimulation ◽  
Histamine Stimulation ◽  
Ussing Chambers ◽  
Cyclic Monophosphate ◽  
Dose Dependent ◽  
Stimulation Of

The action of somatostatin (SS) on acid secretion and histamine release was studied in isolated gastric mucosa of toads mounted in Ussing chambers. SS inhibited H+ secretion and histamine release stimulated by cholinergic and gastrinergic secretagogues. Exogenous histamine stimulation of H+ secretion was blocked noncompetitively by SS in a dose-dependent manner. In mucosae maximally stimulated by histamine or forskolin and cimetidine, acetylcholine (ACh) and tetragastrin (TG) induced a direct stimulation of the oxyntopeptic cell not inhibited by SS. Indomethacin, an inhibitor of prostaglandin synthesis, did not prevent SS inhibition of histamine stimulation. Pretreatment with SS abolished forskolin stimulation of H+ secretion. SS induced a small inhibition of the stimulatory effect of N6, 2'-O-dibutyryladenosine 3',5'-cyclic monophosphate. These results suggest that SS inhibits acid secretion stimulated by secretagogues through different mechanisms: 1) inhibition of histamine release by ACh and TG, 2) inhibition of endogenous and exogenous histamine stimulation through a blockade of adenylate cyclase, and 3) an inhibitory effect subsequent to the synthesis of adenosine 3',5'-cyclic monophosphate. The direct activation of the oxyntopeptic cell by ACh and TG does not seem to be affected by somatostatin.

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