Intrahepatic adenosine-mediated activation of hepatorenal reflex is via A1 receptors in rats

2006 ◽  
Vol 84 (11) ◽  
pp. 1177-1184 ◽  
Author(s):  
Zhi Ming ◽  
W. Wayne Lautt
Keyword(s):  
Arterial Pressure ◽  
Receptor Antagonist ◽  
Adenosine Receptors ◽  
Venous Pressure ◽  
Systemic Arterial Pressure ◽  
Urine Flow ◽  
Process Mean ◽  
Water Excretion ◽  
Hepatorenal Reflex ◽  
Water And Sodium Excretion

Previous studies have shown that intrahepatic adenosine is involved in activation of the hepatorenal reflex that regulates renal sodium and water excretion. The present study aims to determine which subtype of adenosine receptors is implicated in the process. Mean arterial pressure, portal venous pressure and flow, and renal arterial flow were monitored in pentobarbital anesthetized rats. Urine was collected from the bladder. Intraportal administration of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), a selective adenosine A1 receptor antagonist, increased urine flow by 24%, 89%, and 143% at the dose of 0.01, 0.03, and 0.1 mg·kg–1, respectively; in contrast, DPCPX, when administered intravenously at the same doses, only increased urine flow by 0%, 18%, and 36%. The increases in urine flow induced by intraportal administration of DPCPX were abolished in rats with liver denervation. Intrahepatic infusion of adenosine significantly decreased urine flow and this response was abolished by intraportal administration of DPCPX. Neither intraportal nor intravenous administration of 3,7-dimethyl-1-propargylxanthine, a selective adenosine A2 receptor antagonist, showed significant influence on urine flow. Systemic arterial pressure, renal blood flow and glomerular filtration rate were unaltered by the administration of any of the drugs. In conclusion, intrahepatic adenosine A1 receptors are responsible for the adenosine-mediated hepatorenal reflex that regulates renal water and sodium excretion.

Vasomotor waves of arterial blood pressure after cessation of cardiopulmonary bypass in man

Perfusion ◽  
1990 ◽  
Vol 5 (4) ◽  
pp. 261-266
Author(s):  
V. Vainionpää ◽  
A. Hollme'n ◽  
J. Timisjärvi
Keyword(s):  
Blood Pressure ◽  
Cardiopulmonary Bypass ◽  
Arterial Pressure ◽  
Venous Pressure ◽  
Systemic Arterial Pressure ◽  
Heart Patients ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
The Mean ◽  
Epicardial Pacing

The occurrence of vasomotor waves during cardiopulmonary bypass (CPB) is a recognized phenomenon. The lesser known oscillation of arterial pressure after cessation of CPB was observed in 18 open-heart patients. The duration of an oscillatory wave was 13.5±5.0 seconds, the amplitude 6.1 ±2.6mmNg and the mean arterial pressure 76.5± 10.7mmHg. Inter-and also intraindividual variations in frequency and amplitude of the oscillation, however, did occur. In 13 patients, this oscillation occurred during ventricular epicardial pacing. The oscillation continued until the end of the operation in eight patients; in others, the oscillation was of shorter duration. An oscillation of pulmonary arterial pressure (PAP) was simultaneously observed in nine patients (eight with pacemaker) and central venous pressure (CVP) oscillation in eight patients (all with pacemaker). The duration of a wave was the same as in systemic arterial pressure and the amplitudes were 1.5-3.0mmHg in PAP and 1.0-2.0mmHg in CVP. These arterial vasomotor waves, seen here after CPB, largely resemble those observed during perfusion in man and also the Mayerwaves explored in experimental animals. The pacing rhythm seems to favourthe appearance of those blood pressure oscillations.

Upstream pressure for systemic to pulmonary flow from bronchial circulation in dogs

1987 ◽  
Vol 63 (2) ◽  
pp. 485-491 ◽  
Author(s):  
P. G. Agostoni ◽  
M. E. Deffebach ◽  
W. Kirk ◽  
S. Lakshminarayan ◽  
J. Butler
Keyword(s):  
Arterial Pressure ◽  
Venous Pressure ◽  
Systemic Arterial Pressure ◽  
Driving Pressure ◽  
Upstream Site ◽  
Bronchial Circulation ◽  
Pulmonary Flow ◽  
Upstream Pressure ◽  
Pulmonary Arterial ◽  
Bidirectional Flow

Systemic to pulmonary flow from bronchial circulation, important in perfusing potentially ischemic regions distal to pulmonary vascular obstructions, depends on driving pressure between an upstream site in intrathoracic systemic arterial network and pulmonary vascular bed. The reported increase of pulmonary infarctions in heart failure may be due to a reduction of this driving pressure. We measured upstream element for driving pressure for systemic to pulmonary flow from bronchial circulation by raising pulmonary venous pressure (Ppv) until the systemic to pulmonary flow from bronchial circulation ceased. We assumed that this was the same as upstream pressure when there was flow. Systemic to pulmonary flow from bronchial circulation was measured in left lower lobes (LLL) of 21 anesthetized open-chest dogs from volume of blood that overflowed from pump-perfused (90–110 ml/min) pulmonary vascular circuit of LLL and was corrected by any changes of LLL fluid volume (wt). Systemic to pulmonary flow from bronchial circulation upstream pressure was linearly related to systemic arterial pressure (slope = 0.24, R = 0.845). Increasing Ppv caused a progressive reduction of systemic to pulmonary flow from bronchial circulation, which stopped when Ppv was 44 +/- 6 cmH2O and pulmonary arterial pressure was 46 +/- 7 cmH2O. A further increase in Ppv reversed systemic to pulmonary flow from bronchial circulation with blood flowing back into the dog. When net systemic to pulmonary flow from bronchial circulation by the overflow and weight change technique was zero a small bidirectional flow (3.7 +/- 2.9 ml.min-1 X 100 g dry lobe wt-1) was detected by dispersion of tagged red blood cells that had been injected.(ABSTRACT TRUNCATED AT 250 WORDS)

Fetal cardiovascular, endocrine, and fluid responses to atrial natriuretic factor infusion

1989 ◽  
Vol 257 (3) ◽  
pp. R580-R587 ◽  
Author(s):  
R. A. Brace ◽  
L. A. Bayer ◽  
C. Y. Cheung
Keyword(s):  
Arterial Pressure ◽  
Blood Volume ◽  
Atrial Natriuretic Factor ◽  
Venous Pressure ◽  
Plasma Renin ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Fetal Sheep ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The purpose of this study was to determine the effects of atrial natriuretic factor (ANF) in the fetus and to explore the interactions among the fetal cardiovascular, endocrine, and fluid responses to ANF. In 12 chronically catheterized fetal sheep at 130 +/- 1 (SE) days gestation, ANF was infused intravenously for 30 min at 14-300 ng.min-1.kg-1. Fetal arterial plasma ANF concentration increased by 174 to 5,410 pg/ml from a preinfusion value of 163 +/- 13 pg/ml. The clearance of ANF from the circulation was 122 +/- 28 ml.min-1.kg-1 and the half-life was 0.46 +/- 0.07 min. When plasma ANF was greater than 2,000 pg/ml, fetal arterial pressure decreased, venous pressure increased transiently, and heart rate was unchanged. Plasma arginine vasopressin (AVP) concentration and plasma renin activity (PRA) increased with high ANF concentrations, while norepinephrine concentrations were unaffected. Fetal blood volume decreased in all fetuses, and urine flow increased significantly but not in every fetus. Blood and urine osmolalities did not change. On terminating the infusion, venous pressure and urine flow decreased below control, while blood volume and arterial pressure remained reduced. Plasma AVP concentration increased further, and this was accompanied by an increase in urine osmolality. Thus the most consistent effect of ANF in the fetus was a reduction in blood volume, which was independent of urine flow changes. Other cardiovascular, endocrine, and fluid responses to ANF as well as interactions among them appeared to occur largely at supraphysiological concentrations and may be secondary to the changes in blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Disruption of the blood-brain barrier in cerebrum and brain stem during acute hypertension

1986 ◽  
Vol 251 (6) ◽  
pp. H1171-H1175 ◽  
Author(s):  
W. G. Mayhan ◽  
F. M. Faraci ◽  
D. D. Heistad
Keyword(s):  
Arterial Pressure ◽  
Brain Stem ◽  
Blood Brain Barrier ◽  
Venous Pressure ◽  
Fluorescent Microscopy ◽  
Systemic Arterial Pressure ◽  
Brain Barrier ◽  
Acute Hypertension ◽  
Blood Brain ◽  
The Brain

The purpose of this study was to examine hemodynamic mechanisms of protection of the blood-brain barrier in the brain stem during acute hypertension. We used a new method to examine the microcirculation of the brain stem. Intravital fluorescent microscopy and fluorescein-labeled dextran were used to evaluate disruption of the blood-brain barrier during acute hypertension in rats. During control conditions, pressure (servo null) in arterioles (60 microns in diameter) was 50 +/- 2% (mean +/- SE) of systemic arterial pressure in the cerebrum and 67 +/- 1% of systemic arterial pressure in the brain stem (P less than 0.05 vs. cerebrum). In the cerebrum, pial venous pressure increased from 7 +/- 1 to 25 +/- 2 mmHg during acute hypertension, and there was marked disruption of the blood-brain barrier in venules (26 +/- 2 leaky sites). In contrast, in the brain stem, pial venous pressure increased from 4 +/- 1 to only 8 +/- 1 mmHg (P less than 0.05 vs. cerebrum), and there was minimal disruption of the blood-brain barrier in venules (1.5 +/- 0.6 leaky sites, P less than 0.05 vs. cerebrum). During acute hypertension, increases in blood flow (microspheres) were less in brain stem than in cerebrum. The findings suggest distribution of vascular resistance differs in the brain stem and cerebrum under control conditions, whereas large arteries account for a greater fraction of resistance in cerebrum; pial venous pressure increases less in brain stem than cerebrum during acute hypertension, so that the blood-brain barrier is protected.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanism of cold diuresis in the rat

1983 ◽  
Vol 244 (2) ◽  
pp. F210-F216 ◽  
Author(s):  
M. L. Morgan ◽  
R. J. Anderson ◽  
M. A. Ellis ◽  
T. Berl
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Hemodynamic Parameters ◽  
Water Excretion ◽  
Urinary Osmolality ◽  
6 Hydroxydopamine ◽  
Renal Water Excretion

The effect of cold exposure (CE) on renal water excretion has not been clearly delineated. Conscious rats were exposed to decreased ambient temperature (15 degrees C). Forty-five minutes of CE resulted in reversible increases in urine flow and decreases in urine osmolality. The diuresis was not due to a diminished response to vasopressin (VP), as the antidiuresis associated with 500 microU of Pitressin given to water-diuresing rats was comparable at 15 and 30 degrees C. To determine whether the diuresis was due to intrarenal factors, glomerular filtration rate, renal blood flow, sodium excretion, and osmolar clearances were measured and found to be equivalent during control and cold conditions. To determine whether the observed diuresis was due to suppression of endogenous VP, VP-free Brattleboro rats undergoing a constant VP infusion were cold exposed. In these rats, CE was not associated with a change in either urine flow or urinary osmolality. This antidiuretic hormone-mediated mechanism was corroborated by a decrease in immunoassayable VP levels. To determine the mechanism whereby CE suppresses endogenous VP, plasma osmolality and hemodynamic parameters were measured. Although CE was not associated with a change in plasma osmolality, it did result in a significant increase in both mean arterial pressure and cardiac index. Pretreatment of rats with 6-hydroxydopamine prevented both the increase in mean arterial pressure and cold diuresis. We conclude that the diuresis observed upon exposure to 15 degrees C results from nonosmotic suppression of endogenous VP, as a consequence of the increase in mean arterial pressure.

Right atrium and renal sodium excretion

1975 ◽  
Vol 228 (1) ◽  
pp. 184-190 ◽  
Author(s):  
SO Stitzer ◽  
RL Malvin
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Right Atrium ◽  
Venous Pressure ◽  
Right Atrial ◽  
Binary Response ◽  
Balloon Inflation ◽  
Water Excretion ◽  
Significant Difference ◽  
The Right

Inflation of a balloon in the right atrium of 13 dogs resulted in salt and water retention not attributable to changes in GFR, RPF, filtration fraction, mean arterial pressure, left atrial pressure, or renal venous pressure. The response to right atrial balloon inflation was compared with the renal effects of constriction of the abdominal aorta above the renal arteries and constriction of the ascending aorta. Neither procedure evoked the same response as balloon inflation. Results suggest that the decrease in mean arterial pressure which accompanies balloon inflation accounts for only part of the decreased salt and water excretion. There was no significant difference between the responses of denervated and intact kidneys to right atrial balloon inflation. A binary response to stretching of the right atrium is suggested, both components apparently involving hormonal mediation.

scholarly journals Role of endothelin receptor subtypes in volume-stimulated ANF secretion

2000 ◽  
Vol 278 (2) ◽  
pp. H493-H499 ◽  
Author(s):  
Alex J. Baertschi ◽  
Thierry Pedrazzini ◽  
Jean-François Aubert ◽  
Angela Roatti ◽  
Richard A. Pence
Keyword(s):  
Arterial Pressure ◽  
Central Venous Pressure ◽  
Receptor Antagonist ◽  
Atrial Natriuretic Factor ◽  
Venous Pressure ◽  
Receptor Subtypes ◽  
Endothelin Receptor ◽  
Central Venous ◽  
Peak Response

The role of endothelin (ET) receptors was tested in volume-stimulated atrial natriuretic factor (ANF) secretion in conscious rats. Mean ANF responses to slow infusions (3 × 3.3 ml/8 min) were dose dependently reduced ( P < 0.05) by bosentan (nonselective ET-receptor antagonist) from 64.1 ± 18.1 (SE) pg/ml (control) to 52.6 ± 16.1 (0.033 mg bosentan/rat), 16.1 ± 7.6 (0.33 mg/rat), and 11.6 ± 6.5 pg/ml (3.3 mg/rat). The ET-A-receptor antagonist BQ-123 (1 mg/rat) had no effect relative to DMSO controls, whereas the putative ET-B antagonist IRL-1038 (0.1 mg/rat) abolished the response. In a second protocol, BQ-123 (≥0.5 mg/rat) nonsignificantly reduced the peak ANF response (106.1 ± 23.0 pg/ml) to 74.0 ± 20.5 pg/ml for slow infusions (3.5 ml/8.5 min) but reduced the peak response (425.3 ± 58.1 pg/ml) for fast infusions (6.6 ml/1 min) by 49.9% ( P < 0.001) and for 340 pmoles ET-1 (328.8 ± 69.5 pg/ml) by 83.5% ( P < 0.0001). BQ-123 abolished the ET-1-induced increase in arterial pressure (21.8 ± 5.2 mmHg at 1 min). Changes in central venous pressure were similar for DMSO and BQ-123 (slow: 0.91 and 1.14 mmHg; fast: 4.50 and 4.13 mmHg). The results suggest 1) ET-B receptors mainly mediate the ANF secretion to slow volume expansions of <1.6%/min; and 2) ET-A receptors mainly mediate the ANF response to acute volume overloads.

Vagally mediated regulation of renal function in conscious primates

1986 ◽  
Vol 250 (4) ◽  
pp. H546-H549
Author(s):  
S. F. Vatner ◽  
W. T. Manders ◽  
D. R. Knight
Keyword(s):  
Renal Function ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Rhesus Monkeys ◽  
Volume Expansion ◽  
Urine Flow ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Water Excretion

The effects of vagal denervation (VD) were examined on responses of Na+ and water excretion to acute volume expansion (18 ml/kg of 6% dextran in saline) in six conscious rhesus monkeys with chronic sinoaortic denervation (SAD). After SAD, volume expansion increased mean arterial pressure (from 95 +/- 6.6 to 119 +/- 7.5 mmHg), right atrial pressure (from 1.3 +/- 0.7 to 5.9 +/- 1.8 mmHg), urine flow (from 0.08 +/- 0.01 to 0.68 +/- 0.20 ml/min), and Na+ excretion (from 1.30 +/- 0.45 to 29.51 +/- 10.40 mueq/min). After VD, volume expansion increased mean arterial and right atrial pressures similarly, but induced significantly lower (P less than 0.05) increases in urine flow (from 0.05 +/- 0.01 to 0.19 +/- 0.03 ml/min) and Na+ excretion (from 0.87 +/- 0.27 to 11.50 +/- 6.13 mueq/min). Thus vagal mechanisms appear to play an important role in mediating excretion of Na+ and water in response to acute volume expansion in the conscious primate.

Diurnal rhythms in fetal urine flow, vascular pressures, and heart rate in sheep

1991 ◽  
Vol 261 (4) ◽  
pp. R1015-R1021 ◽  
Author(s):  
R. A. Brace ◽  
T. R. Moore
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Flow Rate ◽  
Venous Pressure ◽  
Maximum Amplitude ◽  
Diurnal Variations ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Diurnal Rhythms ◽  
Fetal Urine

Conflicting indirect data exist as to whether diurnal variations occur in fetal urine flow rate. In addition, the extent of diurnal rhythms in fetal venous pressure or arterial pressure is unknown, although 24-h rhythms do exist in fetal heart rate. In the present study, we used on-line computer techniques to continuously monitor these variables in chronically catheterized ovine fetuses. Fetal urine flow rate and vascular pressures were successfully recorded in 6 of 11 animals over a 24-h period on 21 days out of a total of 45 days of monitoring. We found highly significant diurnal variations in fetal urine flow rate (P less than 10(-6). Hourly means displayed a maximum at 2130 h and a minimum at 1330 h with a maximum amplitude of 28 +/- 5% of the 24-h mean. A secondary maximum (at 0630 h) and minimum (at 0330 h) of smaller amplitude also occurred. There were simultaneous and highly significant (P less than 0.0001) diurnal rhythms in fetal arterial pressure (+/- 2%), venous pressure (+/- 7%), and heart rate (+/- 5%). The maxima in arterial pressure and heart rate occurred within 1 h of the maximum in urine flow, while venous pressure changes were opposite those in arterial pressure. Hourly mean urine flow correlated significantly with arterial pressure but not venous pressure or heart rate, suggesting that the observed 24-h variations in fetal urine flow rate may be partially mediated by a pressure diuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

GABAergic effects on the depressor responses elicited by stimulation of central nucleus of the amygdala

1999 ◽  
Vol 276 (1) ◽  
pp. H242-H247 ◽  
Author(s):  
John Ciriello ◽  
Stefanie Roder
Keyword(s):  
Arterial Pressure ◽  
Receptor Antagonist ◽  
Wistar Rats ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
The Other ◽  
Central Nucleus ◽  
Male Wistar Rats ◽  
The Mean ◽  
Stimulation Of

GABAergic inputs have been demonstrated in the central nucleus of the amygdala (ACe). However, the contribution of these inhibitory inputs to the cardiovascular responses elicited from the ACe is not known. Experiments were done in chloralose-anesthetized, paralyzed, and artificially ventilated male Wistar rats to investigate the effects of microinjections of GABA, the selective GABAA-receptor antagonist bicuculline, or the GABAB-receptor antagonist phaclofen, in the ACe on the mean arterial pressure (MAP) and heart rate (HR) responses elicited byl-glutamate (Glu) stimulation of the ACe. Microinjections of Glu in the ACe elicited decreases in MAP (−13.7 ± 1.6 mmHg) and HR (−5.3 ± 1.9 beats/min). The MAP and HR responses elicited by Glu stimulation of the ACe were significantly reduced (89%) by the prior microinjection of GABA in the same ACe site. In addition, at some sites in the ACe at which microinjection of Glu did not elicit depressor responses, Glu injections in the presence of phaclofen elicited decreases in MAP (−9.5 ± 1.0 mmHg) and variable changes in HR. On the other hand, the magnitude of the depressor responses elicited during stimulation of the ACe site in the presence of bicuculline was significantly attenuated (60%), whereas phaclofen had no effect on the magnitude of the depressor responses elicited by Glu stimulation of the ACe. These data suggest that GABAergic mechanisms in the ACe alter the excitability of ACe neurons involved in mediating changes in systemic arterial pressure and HR.

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