Distension of the pulmonary vein – atrial junctions and plasma vasopressin in the chloralose-anaesthetized dog

1983 ◽  
Vol 61 (8) ◽  
pp. 905-910 ◽  
Author(s):  
N. Wilson ◽  
J. R. Ledsome
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Pulmonary Vein ◽  
Arginine Vasopressin ◽  
Left Atrial ◽  
Vagus Nerves ◽  
Plasma Vasopressin ◽  
Plasma Arginine ◽  
Atrial Receptors ◽  
Anaesthetized Dog

The effects of localized distension of the pulmonary vein–left atrial junctions on plasma arginine vasopressin (AVP) have been examined in chloralose anaesthetized dogs. Pulmonary vein distension caused an increase in heart rate and a decrease in plasma AVP concentration. Cooling the vagosympathetic nerves to 10 °C caused an increase in arterial pressure and plasma AVP concentration and prevented the changes in heart rate and plasma AVP concentration caused by pulmonary vein distension. Cooling the vagus nerves to 16 °C did not change heart rate, arterial pressure, or plasma AVP concentration but significantly reduced the changes in heart rate and plasma AVP concentration caused by pulmonary vein distension. Propranolol (0.5 mg/kg) decreased heart rate and prevented the increase in heart rate associated with pulmonary vein distension but did not abolish the decrease in plasma AVP concentration. It is concluded that distension of the pulmonary vein – left atrial junctions causes a decrease in plasma AVP concentration by stimulating atrial receptors with myelinated afferent fibres. The decrease in plasma AVP concentration is not secondary to the reflex changes in heart rate caused by pulmonary vein distension.

Release of atrial natriuretic peptide by atrial distension

1985 ◽  
Vol 63 (6) ◽  
pp. 739-742 ◽  
Author(s):  
J. R. Ledsome ◽  
N. Wilson ◽  
C. A. Courneya ◽  
A. J. Rankin
Keyword(s):  
Heart Rate ◽  
Atrial Natriuretic Peptide ◽  
Pulmonary Vein ◽  
Natriuretic Peptide ◽  
Coronary Sinus ◽  
Femoral Artery ◽  
Left Atrial ◽  
Cervical Vagotomy ◽  
Atrial Receptors ◽  
Atrial Natriuretic

A heterologous radioimmunoassay was used to measure the concentration of immunoreactive atrial natriuretic peptide (iANP) in plasma from the femoral artery of eight chloralose anaesthetized dogs. Mitral obstruction which increased left atrial pressure by 11 cmH2O increased plasma iANP from 97 ± 10.3 (mean ± SE) to 135 ± 14.3 pg/mL. Pulmonary vein distension increased heart rate but did not increase plasma iANP. Bilateral cervical vagotomy and administration of atenolol (2 mg/kg) did not prevent the increase in iANP with mitral obstruction. Samples of blood from the coronary sinus had plasma iANP significantly higher than simultaneous samples from the femoral artery confirming the cardiac origin of the iANP. Release of iANP depends on direct stretch of the atrium rather than on a reflex involving left atrial receptors.

Effects of bilateral vagal cold block on vasopressin in conscious dogs

1984 ◽  
Vol 246 (4) ◽  
pp. R566-R569
Author(s):  
V. S. Bishop ◽  
M. D. Thames ◽  
P. G. Schmid
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Afferent Nerve ◽  
Vagal Afferents ◽  
Inhibitory Influence ◽  
Conscious Dog ◽  
Afferent Nerves ◽  
Vagal Afferent ◽  
Plasma Arginine

Bilateral vagal cold block was used to interrupt afferent nerve traffic in the cervical vagi and thus to determine the tonic inhibitory influence of vagal afferents on plasma arginine vasopressin (AVP) concentrations in the conscious dog. Experiments were performed in conscious aortic baroreceptor-denervated dogs with carotid baroreflexes intact or with sinoaortic denervation. In the presence of intact carotid baroreflexes (n = 11) vagal cold block significantly increased arterial pressure (99 +/- 5 to 120 +/- 8 mmHg), heart rate (98 +/- 2 to 168 +/- 11 beats/min), and AVP (2.9 +/- 0.6 to 6.7 +/- 1.3 microU/ml). Chronic sinoaortic denervation did not significantly alter plasma AVP (4.4 +/- 1.0 microU/ml). However, vagal cold block in these totally denervated animals caused a significantly greater increase in arterial pressure (116 +/- 7 to 167 +/- 7 mmHg) and plasma AVP (4.4 +/- 1 to 33.4 +/- 4.8 microU/ml) compared with the responses observed in dogs with intact carotid baroreflexes. These results indicate that vagal afferent nerves exert a significant tonic inhibitory influence on the secretion of AVP in the conscious aortic baroreceptor-denervated dogs as well as in dogs with sinoaortic denervation.

Right atrial stretch decreases supraoptic neurosecretory activity and plasma vasopressin

1981 ◽  
Vol 241 (1) ◽  
pp. R44-R49
Author(s):  
R. P. Menninger
Keyword(s):  
Left Atrial ◽  
Supraoptic Nucleus ◽  
Right Atrial ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Neurosecretory Neurons ◽  
Plasma Arginine ◽  
Right Atrial Appendage ◽  
The Right ◽  
Atrial Receptors

It is generally held that left atrial stretch (LAS) but not right atrial stretch (RAS) reflexly inhibits vasopressin release and results in a diuresis. To reexamine the influence of RAS on the release of vasopressin and on the behavior of antidromically identified supraoptic neurosecretory neurons, RAS and LAS were applied in pentobarbital-anesthetized cats. Weighted 20 or 30 g sutures were placed in the left atrium pulmonary vein junction and at the base of the right atrial appendage. Antidromically identified supraoptic nucleus neurons were inhibited by both RAS and LAS applied independently and together, although fewer neurons were responsive to RAS alone. Simultaneous stretch of both atria resulted in greater inhibition of these neurons than did stretch of either atrium alone. Stretch of the right atrium alone also resulted in a significant decrease in plasma arginine vasopressin measured by radioimmunoassay. Differences between these results and other reports may stem from differences in the method of RAS or the specific right atrial receptors affected.

Plasma vasopressin during increases and decreases in blood volume in anaesthetized dogs

1985 ◽  
Vol 63 (3) ◽  
pp. 224-229 ◽  
Author(s):  
J. R. Ledsome ◽  
N. Wilson ◽  
C. A. Courneya
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Natural Logarithm ◽  
Plasma Vasopressin ◽  
Logarithmic Relationship ◽  
Atrial Receptors

In chloralose-anaesthetized dogs, plasma vasopressin concentration was measured by radioimmunoassay during step changes in blood volume of 4 mL/kg over a range of blood volume from +20 to −12 mL/kg. Blood volume was both increased and decreased over this range. There was a logarithmic relationship between blood volume and plasma vasopressin concentration over the range of blood volume examined. There was also a logarithmic relationship between blood volume and mean left atrial pressure. Linear regression between the natural logarithm of plasma vasopressin concentration and mean arterial pressure, heart rate, and mean left atrial pressure gave the highest correlation coefficient (r = 0.94) between vasopressin and mean arterial pressure. The results support the hypothesis that there are sensitive mechanisms controlling the release of vasopressin in response to changes in blood volume. Observations were also made of changes in atrial pressure and activity of left atrial receptors during changes in blood volume over the same range. The results suggest that changes in atrial receptor activity are unlikely to be the major cause of the large increases in plasma vasopressin concentration associated with hypovolemia.

Comparison of phenylephrine bolus and infusion methods in baroreflex measurements

1990 ◽  
Vol 69 (3) ◽  
pp. 962-967 ◽  
Author(s):  
J. T. Sullebarger ◽  
C. S. Liang ◽  
P. D. Woolf ◽  
A. E. Willick ◽  
J. F. Richeson
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Heart Rate Response ◽  
Pressor Response ◽  
Plasma Catecholamines ◽  
Systolic Arterial Pressure ◽  
Normal Subjects ◽  
Vagus Nerves ◽  
Baroreflex Control

Phenylephrine (PE) bolus and infusion methods have both been used to measure baroreflex sensitivity in humans. To determine whether the two methods produce the same values of baroreceptor sensitivity, we administered intravenous PE by both bolus injection and graded infusion methods to 17 normal subjects. Baroreflex sensitivity was determined from the slope of the linear relationship between the cardiac cycle length (R-R interval) and systolic arterial pressure. Both methods produced similar peak increases in arterial pressure and reproducible results of baroreflex sensitivity in the same subjects, but baroreflex slopes measured by the infusion method (9.9 +/- 0.7 ms/mmHg) were significantly lower than those measured by the bolus method (22.5 +/- 1.8 ms/mmHg, P less than 0.0001). Pretreatment with atropine abolished the heart rate response to PE given by both methods, whereas plasma catecholamines were affected by neither method of PE administration. Naloxone pretreatment exaggerated the pressor response to PE and increased plasma beta-endorphin response to PE infusion but had no effect on baroreflex sensitivity. Thus our results indicate that 1) activation of the baroreflex by the PE bolus and infusion methods, although reproducible, is not equivalent, 2) baroreflex-induced heart rate response to a gradual increase in pressure is less than that seen with a rapid rise, 3) in both methods, heart rate response is mediated by the vagus nerves, and 4) neither the sympathetic nervous system nor the endogenous opiate system has a significant role in mediating the baroreflex control of heart rate to a hypertensive stimulus in normal subjects.

Dependent effect of drinking volume on vasopressin but not atrial peptide in humans

1989 ◽  
Vol 257 (4) ◽  
pp. R762-R764 ◽  
Author(s):  
T. D. Williams ◽  
J. R. Seckl ◽  
S. L. Lightman
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Hormone Secretion ◽  
Plasma Osmolality ◽  
Reflex Inhibition ◽  
Analog Scale ◽  
Dependent Effect ◽  
Plasma Arginine

The act of drinking causes a fall in plasma arginine vasopressin (AVP) concentration that precedes changes in plasma osmolality. To investigate the specificity of this drinking stimulus on hormone secretion, six volunteers (5 male, 1 female, aged 22-39 yr) were water deprived for 36 h and then drank 15 ml/kg water at 10-12 degrees C using 15-20 swallowing actions/min over 3.5 +/- 0.5 min (mean +/- SE). This caused a fall in plasma AVP from 4.5 +/- 0.7 to 3.2 +/- 0.5 pmol/l (P less than 0.05) and in thirst (by 5.7 +/- 0.6 on a 10-cm linear analog scale) (P less than 0.05) 5 min after drinking. No significant changes occurred in mean arterial pressure, heart rate, or plasma atrial natriuretic peptide (ANP) concentration. A second study was undertaken to determine whether the reflex inhibition of AVP secretion is activated simply by the act of swallowing regardless of the volume of liquid consumed. The six volunteers were water deprived for 36 h and then sipped and swallowed 1 ml/kg water at 10-12 degrees C using 15-20 swallowing actions/min over 3.0 +/- 0.1 min. There was no change in plasma AVP concentration, although thirst was reduced by 2.3 +/- 0.6 (P less than 0.05) at 5 min. Plasma AVP 10 min after sipping and swallowing (4.2 +/- 0.8 pmol/l) was significantly greater than at 10 min after drinking 15 ml/kg (2.8 +/- 0.5 pmol/l) (P less than 0.05) despite the fact that plasma osmolality at this stage was similar in both studies. We conclude that the drinking-mediated reflex inhibition of AVP secretion in humans is dependent on swallowing an adequate volume and is not accompanied by changes in hemodynamics or in plasma ANP concentration.

"Summation" of the increase in heart rate from stimulation of atrial receptors

1980 ◽  
Vol 58 (6) ◽  
pp. 666-672
Author(s):  
P. V. Greenwood ◽  
C. T. Kappagoda
Keyword(s):  
Heart Rate ◽  
Left Atrial ◽  
Superior Vena ◽  
Right Atrial ◽  
Propranolol Hydrochloride ◽  
Superior Vena Caval ◽  
The Right ◽  
Atrial Receptors ◽  
Stimulation Of ◽  
Wire Cage

In dogs anaesthetized with chloralose, application of stimuli which are likely to activate left atrial (L.A.) and right atrial (R.A.) receptors (complex unencapsulated endings) has been shown to result in an increase in heart rate. The present investigation was undertaken to determine whether the response elicited by the application of one stimulus (i.e., to the left atrium) could be enhanced by the application of a second stimulus (i.e., to the right atrium) in the same animal.The L.A. receptors were stimulated by distending a small balloon at the right upper pulmonary vein-L.A. junction and the R.A. receptors by "expanding" a spherical wire cage positioned at the superior vena caval (S.V.C.)-R.A. junction. Pressures in the S.V.C., R.A., L.A., and femoral artery were measured and the electrocardiogram monitored.In eight dogs stimulation of L.A. receptors resulted in an increase in heart rate (H.R.) of 18.5 beats/min (SEM 6.0; N = 23). In the same animals stimulation of R.A. receptors resulted in an increase in H.R. of 14.6 beats/min (SEM 2.0; N = 25). Application of both stimuli simultaneously resulted in an increase of 32.2 beats/min (SEM 8.0; N = 13). In four dogs propranolol hydrochloride (0.5 mg/kg) markedly diminished the response. In three dogs the response was abolished by bretylium tosylate (10 mg/kg).It is concluded that the increase in H.R. resulting from the application of these two stimuli could be "summated" and these findings support the proposition that the receptors in the two atria act as a functional entity.

Plasma arginine vasopressin during neck suction in upright sitting man

1987 ◽  
Vol 114 (2) ◽  
pp. 243-248 ◽  
Author(s):  
P. Norsk ◽  
F. Bonde-Petersen ◽  
J. Warberg
Keyword(s):  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Venous Pressure ◽  
Haemoglobin Concentration ◽  
Plasma Osmolality ◽  
Systolic Arterial Pressure ◽  
Plasma Sodium ◽  
Fluid Restriction ◽  
Vasopressin Secretion ◽  
Plasma Arginine

Abstract. In order to examine the influence of carotid baroreceptor stimulation on arginine vasopressin secretion, 8 normal healthy males were subjected to static neck suction of −3.3 kPa for 20 min in the upright sitting position after overnight food and fluid restriction. The plasma concentration of arginine vasopressin did not change significantly during neck suction. However, in 3 subjects the termination of neck suction induced large increases in plasma arginine vasopressin from 1.8 to 63.7 ng/l, from 0.7 to 34.3 ng/l and from 2.1 to 19.0 ng/l, respectively. Two subjects experienced symptoms such as nausea and paleness during neck suction. Systolic arterial pressure increased slightly but significantly during neck suction from 15.3 ± 0.3 to 15.7 ± 0.4 kPa (N = 7, P < 0.05), whereas mean arterial pressure, diastolic arterial pressure, central venous pressure, heart rate, plasma osmolality, plasma sodium and potassium were unchanged. Haemoglobin concentration in blood and haematocrit increased significantly during and after neck suction, whereas plasma volume decreased. We conclude that neck suction with a negative pressure of 3.3 kPa in upright sitting man does not significantly affect plasma arginine vasopressin. However, termination of the stimulation induces large increases in some subjects. This may be explained by a direct effect on the vagus nerve or by a selective deloading of carotid baroreceptors.

Distension of pulmonary vein-left atrial junction: Heart rate responses in conscious and anesthetized dogs

1980 ◽  
Vol 110 (1) ◽  
pp. 47-52 ◽  
Author(s):  
T. O. NEVALAINEN ◽  
M. O. K. HAKUMÄKI ◽  
S. J. HYÖDYNMAA ◽  
M. V. O. NÄRHI ◽  
H. S. S. SARAJAS
Keyword(s):  
Heart Rate ◽  
Pulmonary Vein ◽  
Left Atrial ◽  
Anesthetized Dogs

Cardiovascular Effects of Vasopressin Infused into the Vertebral Circulation of Conscious Dogs

1981 ◽  
Vol 61 (3) ◽  
pp. 345-347 ◽  
Author(s):  
J. F. Liard ◽  
O. Dériaz ◽  
M. Tschopp ◽  
J. Schoun
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Inferior Vena ◽  
Vena Cava ◽  
Electromagnetic Flowmeter ◽  
Cardiovascular Effects ◽  
Conscious Dogs ◽  
Left Vertebral Artery ◽  
Plasma Vasopressin ◽  
The Central Nervous System

1. Seven conscious dogs received arginine-vasopressin infusions (100 and 1000 fmol min−1 kg−1) through catheters implanted in the left vertebral artery or the inferior vena cava while arterial pressure, cardiac output (electromagnetic flowmeter) and heart rate were measured. 2. Despite similar increases in plasma vasopressin concentrations, intravertebral administration induced a lesser increase in mean arterial pressure and a greater decrease in heart rate than the same infusion given intravenously. 3. These results suggest that vasopressin has an effect on structures of the central nervous system involved in cardiovascular control, possibly by affecting the baroreceptor reflex.

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