Effect of ventilatory rate on renal venous PGE2 and PGF2 alpha efflux in anesthetized dogs

1982 ◽  
Vol 242 (1) ◽  
pp. F38-F45
Author(s):  
A. J. Lonigro ◽  
D. W. Brash ◽  
A. H. Stephenson ◽  
L. J. Heitmann ◽  
R. S. Sprague
Keyword(s):  
Blood Pressure ◽  
Important Determinant ◽  
Venous Blood ◽  
Plasma Renin ◽  
Normal Range ◽  
Arterial Blood ◽  
Ventilatory Rate ◽  
Arterial Ph ◽  
Anesthetized Dogs ◽  
Arterial Plasma

In anesthetized laparotomized male mongrel dogs with ventilatory rate set at 10 breath.min-1, tidal volume was adjusted so that control arterial pH and PCO2 were within the normal range for unanesthetized dogs. Control renal venous PGE2 and PGF2 alpha concentrations were comparable to those of unanesthetized dogs, namely, 57 +/- 10 and 114 +/- 18 pg.ml-1, respectively. In contrast, control arterial plasma renin activity (PRA), 6.6 +/- 1.2 ng.ml-1.h-1, was considerably greater than in unanesthetized dogs. Stepwise increases in ventilatory rate increased renal venous PGE2 and PGF2 alpha to 109 +/- 18 and 205 +/- 41 pg.ml-1, respectively. Hyperventilation reduced PCO2 and increased pH and PRA but had no effect on renal blood flow, arterial blood pressure, or arterial PGE2 and PGF2 alpha concentrations. When the ventilatory rate was returned to control levels, pH, PCO2, PRA, and renal venous PGE2 and PGF2 alpha concentrations returned to control. Ventilatory rate or some consequence of altering ventilatory rate is, therefore, a determinant of renal venous efflux of PGE2 and PGF2 alpha. Moreover, it may be a more important determinant of "resting" concentrations of prostaglandins in renal venous blood than anesthesia, laparotomy, or PRA.

Renal actions of endothelin: interaction with prostacyclin

1990 ◽  
Vol 259 (4) ◽  
pp. F645-F652 ◽  
Author(s):  
S. Y. Chou ◽  
A. Dahhan ◽  
J. G. Porush
Keyword(s):  
Blood Pressure ◽  
Filtration Rate ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Renin Release ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Arterial Plasma ◽  
Prostacyclin Synthesis

The renal actions of endothelin were examined by infusing it intrarenally in anesthetized dogs at 4 ng.min-1.kg-1 without affecting arterial blood pressure or cardiac output. Endothelin infusion caused a transient and significant increase in renal blood flow (RBF) by 13 +/- 2%, followed by large decreases in RBF and glomerular filtration rate (GFR; by 26 +/- 2 and 23 +/- 7%, respectively) but did not alter urine flow rate or absolute sodium excretion. After endothelin infusion, renal venous and arterial plasma 6-ketoprostaglandin F1 alpha increased from 250 +/- 58 and 117 +/- 31 to 1,044 +/- 249 and 617 +/- 211 pg/ml, respectively, and its renal output increased from 339 +/- 99 to 963 +/- 202 pg.min-1.g-1 (P less than 0.01 for all). The renal prostacyclin synthesis was augmented by endothelin without stimulating the renal renin release or norepinephrine output. Inhibition of prostaglandin synthesis with indomethacin partially prevented the early renal vasodilation induced by endothelin, which then caused a more pronounced decline in RBF and GFR (by 65 +/- 7 and 54 +/- 8%, respectively). With suppression of prostacyclin synthesis, inhibition of renin release by endothelin was observed. Thus the vasoconstrictive effects of endothelin on renal hemodynamics are significantly modified by its ability to enhance production of vasodilators, including prostacyclin.

Hemodynamics of central infusion of angiotensin II in normal and sodium-depleted dogs

1979 ◽  
Vol 237 (2) ◽  
pp. H139-H145 ◽  
Author(s):  
K. B. Brosnihan ◽  
G. A. Berti ◽  
C. M. Ferrario
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Intraventricular Administration ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Anesthetized Dogs ◽  
Constant Feature

The intraventricular (IVT) administration of angiotensin II (AII) (100 ng.kg-1.min-1) produced significant elevations of arterial blood pressure in pentobarbital-anesthetized dogs on either normal or sodium-deficient diets. In both groups of dogs the intraventricular administration of AII caused comparable and significant elevations in blood pressure averaging 15 +/- 2 and 17 +/- 4 mmHg, respectively, within 10 min after onset of the infusion. The rises in blood pressure were due to increased peripheral resistance (2.87 +/- 1.20 vs. 1.67 +/- 0.43 units). At the peak of the pressor response bradycardia was a constant feature in sodium-depleted animals, but was not present in the normal ones. In both groups of dogs regional cerebral blood flow (rCBF), determined by the xenon-133 washout method, remained unchanged during the development of the pressor response, and peripheral plasma renin activity failed to increase in response to the central infusion of AII. In conclusion, sodium deprivation appears not to influence the sensitivity of the central AII receptor because comparable pressor responses and hemodynamic changes were obtained following the intraventricular administration of AII in both normal and sodium-depleted dogs.

Enhancement of the Antihypertensive Effect of Hydrochlorothiazide in Dogs after Suppression of Renin Release by Beta-Adrenergic Blockade

1975 ◽  
Vol 48 (2) ◽  
pp. 147-151
Author(s):  
C. S. Sweet ◽  
M. Mandradjieff
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Antihypertensive Effect ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Antihypertensive Activity ◽  
Adrenergic Blockade ◽  
Arterial Blood

1. Renal hypertensive dogs were treated with hydrochlorothiazide (8−2 μmol/kg or 33 μmol/kg daily for 7 days), or timolol (4.6 μmol/kg daily for 4 days), a potent β-adrenergic blocking agent, or combinations of these drugs). Changes in mean arterial blood pressure and plasma renin activity were measured over the treatment period. 2. Neither drug significantly lowered arterial blood pressure when administered alone. Plasma renin activity, which did not change during treatment with timolol, was substantially elevated during treatment with hydrochlorothiazide. 3. When timolol was administered concomitantly with hydrochlorothiazide, plasma renin activity was suppressed and blood pressure was significantly lowered. 4. These observations suggest that compensatory activation of the renin-angiotensin system limits the antihypertensive activity of hydrochlorothiazide in renal hypertensive dogs and suppression of diuretic-induced renin release by timolol unmasks the antihypertensive effect of the diuretic.

scholarly journals Salt sensitivity of blood pressure in NKCC1-deficient mice

2008 ◽  
Vol 295 (4) ◽  
pp. F1230-F1238 ◽  
Author(s):  
Soo Mi Kim ◽  
Christoph Eisner ◽  
Robert Faulhaber-Walter ◽  
Diane Mizel ◽  
Susan M. Wall ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Wheel Running ◽  
Plasma Renin ◽  
Pressure Change ◽  
Standard Diet ◽  
Wild Type ◽  
Vascular Effects ◽  
Arterial Blood ◽  
Deficient Mice

NKCC1 is a widely expressed isoform of the Na-2Cl-K cotransporter that mediates several direct and indirect vascular effects and regulates expression and release of renin. In this study, we used NKCC1-deficient (NKCC1−/−) and wild-type (WT) mice to assess day/night differences of blood pressure (BP), locomotor activity, and renin release and to study the effects of high (8%) or low (0.03%) dietary NaCl intake on BP, activity, and the renin/aldosterone system. On a standard diet, 24-h mean arterial blood pressure (MAP) and heart rate determined by radiotelemetry, and their day/night differences, were not different in NKCC1−/− and WT mice. Spontaneous and wheel-running activities in the active night phase were lower in NKCC1−/− than WT mice. In NKCC1−/− mice on a high-NaCl diet, MAP increased by 10 mmHg in the night without changes in heart rate. In contrast, there was no salt-dependent blood pressure change in WT mice. MAP reductions by hydralazine (1 mg/kg) or isoproterenol (10 μg/mouse) were significantly greater in NKCC1−/− than WT mice. Plasma renin (PRC; ng ANG I·ml−1·h−1) and aldosterone (aldo; pg/ml) concentrations were higher in NKCC1−/− than WT mice (PRC: 3,745 ± 377 vs. 1,245 ± 364; aldo: 763 ± 136 vs. 327 ± 98). Hyperreninism and hyperaldosteronism were found in NKCC1−/− mice during both day and night. High Na suppressed PRC and aldosterone in both NKCC1−/− and WT mice, whereas a low-Na diet increased PRC and aldosterone in WT but not NKCC1−/− mice. We conclude that 24-h MAP and MAP circadian rhythms do not differ between NKCC1−/− and WT mice on a standard diet, probably reflecting a balance between anti- and prohypertensive factors, but that blood pressure of NKCC1−/− mice is more sensitive to increases and decreases of Na intake.

scholarly journals Evaluation of the Accuracy of the Delta Life DL 1000 Oscillometric Monitor for Blood Pressure Measurement in Anesthetized Dogs of Different Weight Ranges

2020 ◽  
Vol 48 ◽  
Author(s):  
Bárbara Silva Correia ◽  
Eduardo Raposo Monteiro ◽  
João Victor Barbieri Ferronatto ◽  
Luciana Branquinho Queiroga ◽  
José Ricardo Herrera Becerra
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Pressure Measurement ◽  
Elective Surgery ◽  
Blood Pressure Measurement ◽  
Measurement Data ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Group 2 ◽  
Group 1

Background: Arterial blood pressure is one of the most commonly variables monitored during anesthetic procedures in veterinary patients. The most reliable method for measuring arterial blood pressure in dogs and cats is the direct (invasive) method. However, the oscillometric method is less complex and more practical for clinical routine in small animals. Nevertheless, oscillometric monitors present great variability in accuracy. The present study aimed to determine the accuracy of the Delta Life DL 1000 oscillometric monitor for measurement of systolic, mean and diastolic blood pressures (SAP, MAP and DAP, respectively) in anesthetized dogs of different weight ranges.Materials, Methods & Results: This study was approved by the Institutional Ethics Committee of Animal Use. Fifteen female dogs of different breeds, weighing 11.6 ± 10.0 kg and with a mean age of 48 ± 51 months were used. All animals were scheduled for elective surgery under general anesthesia in the Institution Veterinary Hospital. Dogs were anesthetized with morphine, propofol and isoflurane and had one 20 or 22 gauge catheter introduced into the dorsal pedal artery for continuous, invasive monitoring of SAP, MAP and DAP. A blood pressure cuff was positioned over the middle third of the radius and connected to Delta Life DL 1000 monitor. Oscillometric readings of SAP, MAP and DAP were registered every 5 minutes, and invasive values were simultaneously recorded. Values obtained with both methods were compared (invasive versus oscillometric) by use of the Bland Altman method to determine the bias, standard deviation of bias and 95% limits of agreement. The percentages of errors between the methods within 10 mmHg and within 20 mmHg were calculated. The results obtained were compared with the criteria from the American College of Veterinary Internal Medicine (ACVIM) for validation of indirect methods of arterial blood pressure measurement. Data were stratified into two groups according to the weight: < 10 kg (Group 1; n = 9); and ≥ 10 kg (Group 2; n = 6). In Group 1, 119 paired measurements were obtained, four of which classified as hypotension (SAP < 90 mmHg), 98 as normotension (SAP from 90 to 140mmHg) and 17 as hypertension (SAP > 140 mmHg). Bias (± SD) values in Group 1 were as follows: SAP, 5.2 ± 18.1 mmHg; MAP, -3.4 ± 17.2 mmHg; and DAP, 12.0 ± 17.5 mmHg. The percentages of errors within 10 mmHg were 40.3% for SAP; 45.4% for MAP and 28.6% for DAP. The percentages of errors within 20 mmHg were 72.3% for SAP, 84.0% for MAP and 68.1% for DAP. In Group 2, 66 paired measurements were obtained, nine of which classified as hypotension, 56 as normotension and one as hypertension. Bias (± SD) in Group 2 were as follows: SAP, 13.6 ± 14.3 mmHg; MAP, -1.1 ± 13.5 mmHg; and DAP, 8.2 ± 16.0 mmHg. The percentages of errors within 10 mmHg were 33.3% for SAP, 77.3% for MAP and 33.3% for DAP. The percentages of errors within 20 mmHg were 65.1% for SAP, 92.4% for MAP and 83.4% for DAP.Discussion: Based on the results of this study and reference criteria from the ACVIM, the Delta Life DL 1000 monitor had a poor accuracy for SAP, MAP and DAP and did not meet the criteria from the ACVIM in anesthetized dogs under 10 kg. Measurements of MAP in dogs ≥ 10 kg met the ACVIM criteria, but measurements of SAP and DAP did not. Based on the findings in this study, the DL 1000 oscillometric monitor is not recommended for blood pressure measurement in anesthetized dogs < 10 kg. In dogs ≥ 10 kg, measurements of MAP yielded acceptable values, but SAP and DAP measurements did not.

Pharmacological and genetic evidence that cathepsin B is not the physiological activator of rodent prorenin

2010 ◽  
Vol 391 (12) ◽  
Author(s):  
M. David Percival ◽  
Sylvie Toulmond ◽  
Nathalie Coulombe ◽  
Wanda Cromlish ◽  
Sylvie Desmarais ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Cathepsin B ◽  
Plasma Renin ◽  
Renin Activity ◽  
Spontaneously Hypertensive ◽  
Protein Levels ◽  
Arterial Blood ◽  
Gene Compensation

Abstract Renin is the first enzyme in the renin-angiotensin-aldosterone system which is the principal regulator of blood pressure and hydroelectrolyte balance. Previous studies suggest that cathepsin B is the activator of the prorenin zymogen. Here, we show no difference in plasma renin activity, or mean arterial blood pressure between wild-type and cathepsin B knockout mice. To account for potential gene compensation, a potent, selective, reversible cathepsin B inhibitor was developed to determine the role of cathepsin B on prorenin processing in rats. Pharmacological inhibition of cathepsin B in spontaneously hypertensive and double transgenic rats did not result in a reduction in renal mature renin protein levels or plasma renin activity. We conclude that cathepsin B does not play a significant role in this process in rodents.

The Generation of Kinins in the Blood of Dogs during Hypotension Due to Haemorrhage

1970 ◽  
Vol 39 (3) ◽  
pp. 349-365 ◽  
Author(s):  
H. E. Berry ◽  
J. G. Collier ◽  
J. R. Vane
Keyword(s):  
Blood Pressure ◽  
Time Course ◽  
Venous Pressure ◽  
Venous Blood ◽  
Systemic Circulation ◽  
Substantial Effect ◽  
Mixed Venous Blood ◽  
Shed Blood ◽  
Arterial Blood ◽  
Organ Technique

1. Circulating kinins were detected and continuously assayed during hypotension due to haemorrhage in dogs, using the blood-bathed organ technique and isolated strips of cat jejunum as the assay tissue. 2. In arterial blood kinin concentrations of 1–5 ng/ml were attained after a hypotension of 35–65 mmHg had been maintained for 10–190 min. When portal venous blood was simultaneously assayed kinins appeared earlier and in concentrations 1–2 ng/ml higher than in arterial blood. No differences in time course of kinin generation or in concentration were found when mixed venous blood and arterial blood were compared. In those instances in which the blood pressure was restored to normal by returning the shed blood, kinin formation stopped. 3. Kinin generation was due to the presence in the circulation of a kinin-forming enzyme, such as kallikrein. When kallikrein was infused into the portal vein, it was partially inactivated by the liver. 4. Prolonged intravenous infusions of kallikrein (20–60 mu kg−1 min−1) generated kinins in the circulation in concentrations (1–5 ng/ml) which were well maintained throughout the infusion, demonstrating that kinin generation is not limited by depletion of the precursor kininogen; nevertheless, the effects of kallikrein infusions on the blood pressure and central venous pressure waned. 5. It is concluded that in hypotension due to haemorrhage, an active kallikrein appears in the portal circulation. Delay in the appearance of kallikrein in the systemic circulation may be due to the kallikrein inactivating mechanism of the liver. This inactivating mechanism may fail during shock. Kinins are generated in amounts sufficient to have a substantial effect on the circulation and an influence on the course of events in shock.

The use of propofol as an induction agent for halothane and isoflurane anesthesia in dogs

1998 ◽  
Vol 34 (1) ◽  
pp. 84-91 ◽  
Author(s):  
A Bufalari ◽  
SM Miller ◽  
C Giannoni ◽  
CE Short
Keyword(s):  
Blood Pressure ◽  
Wave Activity ◽  
Simultaneous Increase ◽  
Induction Agent ◽  
Total Amplitude ◽  
Brain Wave ◽  
Isoflurane Anesthesia ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Brain Wave Activity

Cardiovascular, pulmonary, and quantitative electroencephalographic parameters were assessed in 12 anesthetized dogs to determine the compatibility of the injectable anesthetic propofol with halothane and isoflurane. No cases of apnea were observed during induction of anesthesia. An adequate level of anesthesia was established in each protocol as judged by both the lack of response to mechanical noxious stimuli (i.e., tail clamping) and evidence of reduction in total amplitude of brain wave activity. The initial propofol-mediated decrease in arterial blood pressure continued during either halothane (52.4%) or isoflurane (38%) anesthesia without a simultaneous increase in heart rate. The results of this study suggest that propofol, in combination with inhalant agents, can be used effectively and safely for canine anesthesia in veterinary practice.

Plasma renin activity responses to graded decreases in renal perfusion pressure in fetal and newborn lambs

1992 ◽  
Vol 262 (3) ◽  
pp. R524-R529 ◽  
Author(s):  
N. D. Binder ◽  
D. F. Anderson
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Activity ◽  
Renal Perfusion Pressure ◽  
Arterial Blood ◽  
The Right ◽  
The Relationship

We examined the relationship between acute reductions in renal perfusion pressure, as approximated by femoral arterial blood pressure, and plasma renin activity in the uninephrectomized fetal lamb. Renal perfusion pressure was reduced and maintained at a constant value by controlled partial occlusion of the aorta above the renal artery. After 15 min of reduced blood pressure, blood samples were taken for determination of plasma renin activity. This protocol was performed 22 times in 11 fetal lambs. Additionally, three of the fetuses were delivered by cesarean section and studied as newborns for the first week of life. In the fetus, there was a linear relationship between log plasma renin activity and femoral arterial blood pressure (P less than 0.01). After birth, the relationship still existed, although it was shifted to the right (P less than 0.0001). We conclude that there is a significant relationship between plasma renin activity and renal perfusion pressure in the fetal lamb, and as early as 1 day after birth, this relationship shifts to the right in the newborn lamb.

Sign in / Sign up

Export Citation Format

Share Document