Mechanisms of action of sodium cromoglycate

1985 ◽  
Vol 63 (6) ◽  
pp. 760-765 ◽  
Author(s):  
D. F. Biggs ◽  
V. Goel
Keyword(s):  
Blood Pressure ◽  
Sodium Cromoglycate ◽  
Arterial Blood Pressure ◽  
Vagal Stimulation ◽  
Cardiovascular Responses ◽  
Bilateral Stimulation ◽  
Vagus Nerves ◽  
Arterial Blood ◽  
Efferent Pathways ◽  
Stimulation Of

The effects of sodium cromoglycate (SCG) on cardiovascular and pulmonary responses to phenylbiguanide, capsaicin, and vagal stimulation were studied in anesthetized guinea pigs. Phenylbiguanide had no bronchospastic activity but induced reflex changes in arterial blood pressure which were reduced or abolished by SCG. Capsaicin induced nonreflex bronchospasm, and decreases in arterial blood pressure that were unaffected by SCG. Sodium cromoglycate, given before or after atropine, had no effect on the bronchospasm and cardiovascular responses to unilateral or bilateral stimulation of the vagus nerves. We conclude that SCG may influence both the afferent and efferent pathways of responses to drugs.

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.

Bradykinin in reflex cardiovascular responses to static muscular contraction

1986 ◽  
Vol 61 (1) ◽  
pp. 271-279 ◽  
Author(s):  
C. L. Stebbins ◽  
J. C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Response ◽  
Time Derivative ◽  
Cardiovascular Responses ◽  
Carboxypeptidase B ◽  
Arterial Blood ◽  
Static Contraction ◽  
Stimulation Of

We examined the contribution of bradykinin to the reflex hemodynamic response evoked by static contraction of the hindlimb of anesthetized cats. During electrical stimulation of ventral roots L7 and S1, we compared the cardiovascular responses to hindlimb contraction before and after the following interventions: inhibition of converting enzyme (kininase II) with captopril (3–4 mg/kg, n = 6); inhibition of kallikrein activity with aprotinin (Trasylol, 20,000–30,000 KIU/kg, n = 8); and injection of carboxypeptidase B (500–750 U/kg, n = 7). Treatment with captopril augmented the rise in mean arterial blood pressure and maximal time derivative of pressure (dP/dt) caused by static contraction from 21 +/- 3 to 39 +/- 7 mmHg and 1,405 +/- 362 to 2,285 +/- 564 mmHg/s, respectively. Aprotinin attenuated the contraction-induced rise in mean arterial blood pressure (28 +/- 4 to 9 +/- 2 mmHg) and maximal dP/dt (1,284 +/- 261 to 469 +/- 158 mmHg/s). Carboxypeptidase B reduced the cardiovascular response to static contraction. Thus the mean arterial blood pressure response was decreased from 36 +/- 12 to 24 +/- 11 mmHg, maximal dP/dt from 1,618 +/- 652 to 957 +/- 392 mmHg/s, and heart rate from 12 +/- 2 to 7 +/- 1 beats/min. These data suggest that stimulation of muscle afferents by bradykinin contributes to a portion of the reflex cardiovascular response to static contraction.

The release of vasopressin without oxytocin in response to haemorrhage

1967 ◽  
Vol 166 (1005) ◽  
pp. 443-458 ◽  
Keyword(s):  
Blood Pressure ◽  
Mammary Gland ◽  
Guinea Pig ◽  
Arterial Blood Pressure ◽  
Vagal Stimulation ◽  
Critical Value ◽  
Inhibitory Substance ◽  
Blood Samples ◽  
Arterial Blood ◽  
Stimulation Of

Blood samples were collected from anaesthetized cats during haemorrhage or stimulation of the peripheral end of the vagus. Vasopressin and oxytocin were estimated in the samples by assaying alcohol extracts for antidiuretic activity in the water loaded rat and for milk-ejecting activity in the lactating guinea-pig. Haemorrhage caused vasopressin to be released into the blood with out detectable amounts of oxytocin. A similar result was obtained with vagal stimulation provided that the fall of blood pressure which it produced exceeded a critical value of about 80 mmHg. Failure to detect oxytocin in blood samples containing vasopressin was not due to the presence of adrenaline or any other inhibitory substance in the extracts blocking the response of the mammary gland to oxytocin. The stimulus for the independent release of vasopressin by haemorrhage appears to be the associated fall in arterial blood pressure.

scholarly journals Plasticity in breathing and arterial blood pressure following acute intermittent hypercapnic hypoxia in infant rat pups with a partial loss of 5-HT neurons

2015 ◽  
Vol 309 (10) ◽  
pp. R1273-R1284 ◽  
Author(s):  
Jennifer Magnusson ◽  
Kevin J. Cummings
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Partial Loss ◽  
Rat Pups ◽  
Arterial Blood ◽  
Hypercapnic Hypoxia ◽  
Long Term Facilitation

The role of serotonin (5-HT) neurons in cardiovascular responses to acute intermittent hypoxia (AIH) has not been studied in the neonatal period. We hypothesized that a partial loss of 5-HT neurons would reduce arterial blood pressure (BP) at rest, increase the fall in BP during hypoxia, and reduce the long-term facilitation of breathing (vLTF) and BP following AIH. We exposed 2-wk-old, 5,7-dihydroxytryptamine-treated and controls to AIH (10% O2; n = 13 control, 14 treated), acute intermittent hypercapnia (5% CO2; n = 12 and 11), or acute intermittent hypercapnic hypoxia (AIHH; 10% O2, 5% CO2; n = 15 and 17). We gave five 5-min challenges of AIH and acute intermittent hypercapnia, and twenty ∼20-s challenges of AIHH to mimic sleep apnea. Systolic BP (sBP), diastolic BP, mean arterial pressure, heart rate (HR), ventilation (V̇e), and metabolic rate (V̇o2) were continuously monitored. 5,7-Dihydroxytryptamine induced an ∼35% loss of 5-HT neurons from the medullary raphe. Compared with controls, pups deficient in 5-HT neurons had reduced resting sBP (∼6 mmHg), mean arterial pressure (∼5 mmHg), and HR (56 beats/min), and experienced a reduced drop in BP during hypoxia. AIHH induced vLTF in both groups, reflected in increased V̇e and V̇e/V̇o2, and decreased arterial Pco2. The sBP of pups deficient in 5-HT neurons, but not controls, was increased 1 h following AIHH. Our data suggest that a relatively small loss of 5-HT neurons compromises resting BP and HR, but has no influence on ventilatory plasticity induced by AIHH. AIHH may be useful for reversing cardiorespiratory defects related to partial 5-HT system dysfunction.

Life Events, Cardiovascular Reactivity, and Risk Behavior in Adolescent Boys

PEDIATRICS ◽  
1995 ◽  
Vol 96 (6) ◽  
pp. 1101-1105
Author(s):  
Sai-Woon Liang ◽  
John M. Jemerin ◽  
Jeanne M. Tschann ◽  
Charles E. Irwin ◽  
Diane W. Wara ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Risk Behavior ◽  
Arterial Blood Pressure ◽  
Life Events ◽  
Cardiovascular Reactivity ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Adolescent Boys ◽  
Positive Life Events ◽  
Arterial Blood

Background. Risk behavior contributes to injuries, one of the most important sources of morbidity and mortality in adolescents. Although research has shown that environmental stress makes adolescents more likely to engage in risk behavior and to sustain injuries, the magnitude of these associations has been small. Little is known about the role of individual differences in psychobiologic reactivity to stress in moderating the impact of stressful events. In this study, we examined associations among environmental stressors, cardiovascular reactivity to stress, and the level of risk behavior in adolescent boys. Methods. Twenty-four 14- to 16-year-old boys underwent a laboratory protocol designed to measure responses to psychologically and physically stressful tasks. Changes in heart rate and mean arterial blood pressure were measured serially at standard points in the protocol, and levels of positive and negative life events and recent risk behavior were measured using self-report questionnaires. Results. Neither life events nor cardiovascular reactivity were independently associated with risk behavior. Positive life events and mean arterial blood pressure reactivity significantly interacted, however, in predicting risk behavior (R2 increment = .25). Boys with high reactivity who reported numerous positive life events engaged in markedly less risk behavior than their peers. Conclusion. We conclude that adolescents with exaggerated cardiovascular responses to laboratory stressors are associated with less risk behavior in a setting of positive life circumstances. This result suggests that reactivity may exert protective, rather than harmful, influences in some environments.

Vagal neuroeffector mechanisms affecting transpulmonary pressure in the intact rat

1995 ◽  
Vol 79 (4) ◽  
pp. 1233-1241 ◽  
Author(s):  
J. R. Haselton ◽  
A. Y. Reynolds ◽  
H. D. Schultz
Keyword(s):  
Smooth Muscle ◽  
Untreated Control ◽  
Vagal Stimulation ◽  
Muscle Tone ◽  
Transpulmonary Pressure ◽  
Bilateral Stimulation ◽  
Vagus Nerves ◽  
Prostaglandin F2 Alpha ◽  
Combined Administration ◽  
Stimulation Of

Experiments were conducted with chloralose-urethan anesthetized rats to assess the effects of 1) bilateral stimulation of the cervical vagus nerves and 2) parasympathomimetic and sympathomimetic agents. Transpulmonary pressure (Ptp) was used as an index of airway smooth muscle tone, and peak inspiratory Ptp (Ptppeak) values were used for a comparison of responses. In untreated animals, vagal stimulation elicited an increase in Ptppeak of 155%. Cooling of the vagus nerves to 15 degrees C abolished the response of Ptppeak to vagal stimulation. Although isoproterenol (1–10 micrograms/kg i.v.) did not alter resting Ptppeak, it did prevent vagal stimulation from evoking an increase in Ptppeak. Nadolol (1.5 mg/kg i.v.) augmented the increase in Ptppeak elicited by vagal stimulation. Vagal stimulation did not evoke any change in Ptppeak after the administration of both nadolol and atropine or after combined administration of nadolol, atropine, and either serotonin aerosol or prostaglandin F2 alpha. In rats pretreated with capsaicin 1 wk before the experiment, vagal stimulation evoked an increase in Ptppeak that was not statistically different from that of untreated control animals. Therefore, nonadrenergic noncholinergic systems did not appear to play an independent role in the response of the airways to the activation of the vagus nerves.

Measurement Of Bradykinin-Induced Venous Dilation By Ultrasound And Correlation With Heart Rate, Arterial And Venous Pressure And Endothelial Damage

1981 ◽  
Author(s):  
G J Stewart ◽  
R G Schaub ◽  
R E Cartee
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Carotid Arteries ◽  
Jugular Vein ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Endothelial Damage ◽  
Whole Body ◽  
Arterial Blood

This study was done to correlate known cardiovascular responses to bradykinin (increased heart rate, lowered arterial blood pressure) with recently demonstrated endothelial damage and proposed venous dilation. Healthy dogs of mixed breed were used. Blood pressures and heart rate were monitored and recorded on a Narco physiograph. The diameter of a jugular vein was monitored with an ADR ultrasound machine using a 10 MHz probe with linear array of crystals and recorded on polaroid prints. Jugular veins and carotid arteries were removed and prepared for scanning electron microscopy after removal of blood and partial in situ fixation by whole body perfusion. The response of arterial pressure was dose dependent with no change at 6 ug/min, variable drop at 12 ug/min and 22-40% drop at 60 ug/min and above. Venous pressure increased in 1 dog but was unchanged in 4 others. The increase of heart rate paralled the drop in arterial blood pressure. The diameter of a jugular vein increased in 3 of 3 monitored dogs by 25, 33, 50% of baseline diameter (average increase 36%) with high (300 ug/min) bradykinin. Endothelial damage (microtears) occurred around 70-80% of branches, at some valves and on the main vessel occassionally. The tears were infiltrated with leukocytes and some red cells and platelets indicating that tearing occurred while blood was still circulating, i.e. before dissection for removal of vessels. Carotid arteries showed no tears. Dilation of arteries would be limited by their elastic layers (missing in veins). These observations show that venous dilation and endothelial tearing around side branches are part of the cardiovascular response to blood born bradykinin. They also show that venous dilation can be measured by ultrasound.

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