Experimental angiotensin II hypertension

1980 ◽  
Vol 239 (3) ◽  
pp. H391-H398 ◽  
Author(s):  
D. B. Young ◽  
R. H. Murray ◽  
R. G. Bengis ◽  
A. K. Markov
Keyword(s):  
Cardiac Output ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Vascular Tone ◽  
Control Level ◽  
Circulatory System ◽  
Question Mark ◽  
Control Value

The mechanisms by which angiotensin II (AII) produces hypertension was studied in a group of 13 large dogs maintained on a Na intake of 200 meq/day. AII was infused at 10 ng x kg-1 x min-1 iv for 8 days. Arterial pressure increased from the control level of 98 +/- 3 to 160 +/- 7 mmHg and cardiac output fell significantly from the control value of 3.4 +/- 0.2 to 2.4 +/- 0.2 and 2.6 +/- 0.1 l/min on the 5th and 8th days of AII infusion. Mean circulatory filling pressure (MCFP) rose from the control mean of 9.5 +/- 0.5 to 11.6 +/- 0.9 (P < 0.05) and 12.6 +/- 0.6 mmHg (P inverted question mark 0.05) on the 5th and 8th day of infusion. On the 1st day of AII infusion, approximately 70 meq Na was retained; this retention persisted until the 4th day, when a marked natriuresis returned the dogs to Na balance. 22Na space increased slightly (P < 0.05) during the early part of the study, but fell back to the control level by the 5th day of infusion. Blood volume was unchanged throughout the study. The marked increase observed in MCFP with unchanged blood volume indicates that the unstressed volume or compliance of the circulatory system must have decreased. In this form of hypertension, the increase in arterial pressure was achieved without volume expansion and cardiac output elevation, but with large initial increases in arterial and venous vascular tone.

Hemodynamics and blood volume in angiotensin II salt-dependent hypertension in dogs

1989 ◽  
Vol 257 (5) ◽  
pp. H1402-H1412 ◽  
Author(s):  
J. E. Krieger ◽  
R. J. Roman ◽  
A. W. Cowley
Keyword(s):  
Cardiac Output ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Salt Intake ◽  
Control Period ◽  
Ang Ii ◽  
Sequential Effects ◽  
High Salt Intake ◽  
Total Body

The sequential effects of an increased daily NaCl intake on hemodynamics, fluid electrolyte balances, and hormonal responses were evaluated in dogs (n = 7) with fixed circulating levels of angiotensin II (ANG II). During the control period, ANG II was infused at 3 ng.kg-1.min-1 while dogs were maintained on an 8 meq NaCl/day diet. Water intake was fixed at 700 ml/day. Continuously recorded (24 h/day) changes of total body weight (TBW) were used as an index of total body water. Cardiac stroke volume and arterial pressure were recorded, and each beat was digitized to provide hourly and 24-h average cardiac output (CO), mean arterial pressure (MAP), and total peripheral resistance (TPR). After three stable control days, daily salt intake was increased to 120 meq for 7 days. TBW increased gradually to 448 +/- 111 g (2.9%, P less than 0.05) above control by day 3. An 11% expansion of blood volume (P less than 0.05) was found (51CR-labeled red blood cells) on day 2 of high NaCl. CO rose 12% and MAP 20% (P less than 0.05) in parallel with TBW by day 4. By day 7, CO remained only 5% elevated, whereas MAP had stabilized at 20% above control levels. TPR remained significantly elevated from days 3 through 7. A positive Na balance averaging 91 +/- 8 meq (P less than 0.05) occurred on day 1. Plasma Na concentration was increased 2-3 meq/l above control throughout the period of high-salt intake. Plasma renin activity and aldosterone levels decreased to nearly undetectable levels, vasopressin rose slightly, and atrial natriuretic peptide levels increased significantly. Dogs maintained at 8 meq/day NaCl during the same infusion of ANG II showed no changes in MAP, CO, TPR, or TBW. In summary, the salt-induced hypertension was consistently related to small but significant fluid retention, blood volume expansion, elevations of cardiac output, and a gradual increase in TPR.

Effects of serotonin on pulmonary blood volume in the dog

1962 ◽  
Vol 202 (5) ◽  
pp. 957-960 ◽  
Author(s):  
Charles J. McGaff ◽  
William R. Milnor
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Transit Time ◽  
Mean Transit Time ◽  
Dilution Method ◽  
Continuous Intravenous Infusion ◽  
Pulmonary Blood Volume ◽  
Control Value ◽  
Vascular Bed

Changes in pulmonary blood volume produced by continuous intravenous infusion of serotonin (5-hydroxytryptamine) were measured in 16 experiments on ten dogs. Pulmonary mean transit time was measured by the dye dilution method, using consecutive injections into pulmonary artery and left atrium; pulmonary blood volume was calculated by multiplying this mean transit time by the cardiac output. Serotonin lowered pulmonary blood volume by an average of 2.9 ml/kg, or 26% of the control value ( P <0.001). Pulmonary vascular resistance increased 94 ru (resistance units) kg, and systemic vascular resistance fell 294 ru kg, effects similar to those reported by other investigators. The magnitude of the decrease in pulmonary blood volume indicates that a relatively large part of the pulmonary vascular bed is constricted by serotonin, and provides an example of shifting of blood from pulmonic to systemic circuits by reciprocal changes in the distensibility of these beds.

Hemodynamic effects of vasopressin compared with angiotensin II in conscious rats

1987 ◽  
Vol 252 (3) ◽  
pp. H628-H637 ◽  
Author(s):  
J. W. Osborn ◽  
M. M. Skelton ◽  
A. W. Cowley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Fold Increase ◽  
Adrenergic Blockade ◽  
Ganglionic Blockade ◽  
Conscious Rats ◽  
Potent Vasoconstrictor

The mechanisms whereby arginine vasopressin influences hemodynamic and autonomic function were investigated in conscious rats. In normal rats, 60-min intravenous infusions produced dose-related increases of arterial pressure and total peripheral resistance with marked decreases of both heart rate and cardiac output. Cholinergic blockade with methscopolamine attenuated the bradycardia at higher doses of vasopressin, whereby the fall of cardiac output was not affected. beta-Adrenergic blockade with atenolol attenuated the fall of heart rate seen with lower doses of vasopressin but did not prevent the fall of cardiac output. Ganglionic blockade with methscopolamine and hexamethonium resulted in nearly a 60-fold enhancement of vasopressin pressor sensitivity. This was related to a greater rise of peripheral resistance, since the fall of cardiac output was not altered compared with normal rats. Hemodynamic responses to angiotensin II were determined in other groups of conscious, normal rats and rats with ganglionic blockade. Peripheral resistance increased in the normal rats, whereas the related decreases in cardiac output and heart rate were only 30% of the responses seen with equipressor doses of vasopressin. Ganglionic blockade increased pressor activity only two- to eightfold compared with the 60-fold increase observed with vasopressin. We conclude that vasopressin is a more potent vasoconstrictor than angiotensin II, decreases cardiac output independent of neural mechanisms, and results in withdrawal of sympathetic vascular tone to buffer rises of arterial pressure.

Development of chronic perinephritic hypertension in dogs without volume expansion

1977 ◽  
Vol 233 (4) ◽  
pp. F278-F281 ◽  
Author(s):  
R. H. Freeman ◽  
J. O. Davis ◽  
B. E. Watkins
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Volume Expansion ◽  
Left Kidney ◽  
Renal Hypertension ◽  
Control Level ◽  
Whole Body ◽  
Sodium Balance ◽  
Contralateral Kidney ◽  
Experimental Renal Hypertension

The theory of whole body autoregulation to explain the pathogenesis of experimental renal hypertension states that hypertension is initiated in response to an early increase in salt and water retention and a subsequent elevation of the cardiac output. This hypothesis was evaluated in the present study. Dogs (n,5) were made hypertensive by wrapping the left kidney in cellophane and removing the contralateral kidney 3 wk later. One week prior to right nephrectomy, the dogs were volume depleted by placing them on a low sodium intake (less than 3 meq of sodium/day) and giving them a mercurial diuretic for the first 3 days of the diet. This superimposed sodium depletion (negative sodium balance of 137 +/- 17 meq) increased plasma renin activity 3-5 times but did not change arterial pressure or heart rate. Within 2 days after nephrectomy, the mean arterial pressure increased from the control level of 105 +/- 1 to 135 +/- 6 mmHg (P less than 0.005) and pressure remained elevated throughout an additional 4-wk period in which volume depletion was enforced. The present study suggests, therefore, that initial blood volume expansion with such possible consequences as elevated cardiac output are not essential to the pathogenesis of experimental renal hypertension.

Hemorrhage during Isoflurane–Nitrous Oxide Anesthesia

2004 ◽  
Vol 100 (4) ◽  
pp. 885-893 ◽  
Author(s):  
Claudia Höhne ◽  
Pia Vogler ◽  
Ilka Frerking ◽  
Roland C. E. Francis ◽  
Erik R. Swenson ◽  
...  
Keyword(s):  
Nitrous Oxide ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Hormonal Regulation ◽  
Receptor Blockade ◽  
Angiotensin Ii Receptor ◽  
Oxide Anesthesia

Background The objective of this study was to determine whether endothelin-A receptor blockade (ETAB) impairs hemodynamic and hormonal regulation compared with controls and angiotensin II receptor blockade (AT1B) during hypotensive hemorrhage in dogs under isoflurane-nitrous oxide anesthesia. Methods Six dogs were studied in four protocols: (1) control experiments (controls); (2) ETA blockade using ABT-627 (ETAB); (3) AT1 blockade using losartan (AT1B); and (4) combined AT1B and ETAB (AT1B + ETAB). After a 30-min awake period, isoflurane-nitrous oxide anesthesia was established (1.3 minimum anesthetic concentration). After 60 min of anesthesia, 20 ml blood/kg body weight was withdrawn within 5 min, and the dogs were observed for another hour. Thereafter, the blood was retransfused, and the dogs were observed for a final hour. Results Anesthesia: Cardiac output decreased in all protocols, whereas mean arterial pressure decreased more in AT1B and AT1B + ETAB than in controls and ETAB. Hemorrhage: After 60 min, cardiac output had decreased less in controls than in all other protocols. Mean arterial pressure decreased more during ETAB than in controls, but most severely during AT1B and AT1B + ETAB. Angiotensin II increased further only in controls and ETAB, whereas vasopressin and catecholamines increased similarly in all protocols. Retransfusion: Mean arterial pressure remained below controls in all protocols but was lowest when the AT1 receptor was blocked. Cardiac output fully recovered in all but the ETAB protocol. Conclusions ETAB impairs long-term hemodynamic regulation after hemorrhage and retransfusion during anesthesia despite an activation of vasoconstrictive hormones. This suggests that endothelins have a role in long-term cardiovascular regulation. AT1B impairs both short- and long-term blood pressure regulation during anesthesia and after hemorrhage.

Hypertension Induced by Prolonged Intracoronary Administration of Dobutamine in Conscious Dogs

1978 ◽  
Vol 54 (2) ◽  
pp. 153-160 ◽  
Author(s):  
J.-F. Liard
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Extracellular Fluid ◽  
Electromagnetic Flowmeter ◽  
Plasma Renin ◽  
Conscious Dogs ◽  
Control Value ◽  
A Value

1. In order to determine if a sustained increase in cardiac output can lead to hypertension, seven conscious dogs were given a continuous infusion of dobutamine, a powerful stimulant of cardiac inotropism, into the left coronary artery for a 7 day period while arterial pressure, cardiac output (electromagnetic flowmeter) and heart rate were measured. 2. The infusion technique (1·5 × 10−8 mol min−1 kg−1, intracoronary) was selected after short-term experiments showed that it increased cardiac output more effectively than intravenous infusion at the same rate. 3. The rise in cardiac output elicited by intracoronary infusion of dobutamine was largest during the first 6 h of the 7 days administration, at which time calculated peripheral resistance was decreased. Subsequently, cardiac output returned progressively toward its control value whereas mean arterial pressure remained elevated (by an average of 20–25 mmHg) and peripheral resistance increased significantly. 4. Measurements of blood and extracellular fluid volumes as well as plasma renin activity indicated that these factors were not involved in the blood pressure increase. 5. When the infusion was ended, arterial pressure fell rapidly but peripheral resistance remained elevated during the first 6 h. Cardiac output fell after 2 and 6 h to a value below that of the pre-infusion control. After 1 day and subsequently, blood pressure became normal, as did the peripheral resistance and cardiac output. 6. Both at the onset and offset transients of this model of hypertension, changes in cardiac output preceded changes in peripheral resistance. These experiments may give experimental support to the concept of cardiogenic hypertension.

Cardioaccelerator action of angiotensin

1962 ◽  
Vol 202 (2) ◽  
pp. 237-240 ◽  
Author(s):  
S. D. Nishith ◽  
L. D. Davis ◽  
W. B. Youmans
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Abdominal Aorta ◽  
Intravenous Infusion ◽  
Control Level ◽  
Arterial Blood ◽  
Initial Decrease ◽  
Slow Intravenous Infusion

Effects of synthetic angiotensin II on heart rate and blood pressure were determined in dogs under the influence of morphine (3 mg/kg) and chloralose (90 mg/kg). Angiotensin in total doses of 2.5–20 µg, rapidly injected intravenously in intact dogs, caused an initial decrease in heart rate followed by a rise above the control level, despite the continued elevation of arterial blood pressure. When the degree of rise in arterial pressure was buffered by a mechanical compensator connected with the abdominal aorta, rapid intravenous angiotensin injection produced no initial cardioinhibitory phase, and the magnitude of the accleration of heart rate was much greater than in the unbuffered animal. Slow intravenous infusion of angiotensin in some cases caused only a rise in heart rate. In sinoaortic denervated animals both blood pressure and heart rate were greatly increased when a total dose of 10 µg angiotensin was rapidly injected intravenously. Thus, it is demonstrated that the cardioinhibitory response to angiotensin depends largely or exclusively on reflex effects from sinoaortic pressoreceptors, and that angiotensin has a strong cardioaccelerator action which is exerted through the efferent nerves to the heart.

scholarly journals Do alterations in pulmonary vascular tone result in changes in central blood volumes? An experimental study

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Jaap Jan Vos ◽  
J. K. Götz Wietasch ◽  
Andreas Hoeft ◽  
Thomas W. L. Scheeren
Keyword(s):  
Cardiac Output ◽  
Right Ventricular ◽  
Blood Volume ◽  
Vascular Tone ◽  
Left Ventricular ◽  
Cardiac Preload ◽  
Circulating Blood Volume ◽  
Ventricular Afterload ◽  
Spontaneously Breathing ◽  
Blood Volumes

Abstract Background The effects of selective pulmonary vascular tone alterations on cardiac preload have not been previously examined. Therefore, we evaluated whether changing pulmonary vascular tone either by hypoxia or the inhalation of aerosolized prostacyclin (PGI2) altered intrathoracic or pulmonary blood volume (ITBV, PBV, respectively), both as surrogate for left ventricular preload. Additionally, the mean systemic filling pressure analogue (Pmsa) and pressure for venous return (Pvr) were calculated as surrogate of right ventricular preload. Methods In a randomized controlled animal study in 6 spontaneously breathing dogs, pulmonary vascular tone was increased by controlled moderate hypoxia (FiO2 about 0.10) and decreased by aerosolized PGI2. Also, inhalation of PGI2 was instituted to induce pulmonary vasodilation during normoxia and hypoxia. PBV, ITBV and circulating blood volume (Vdcirc) were measured using transpulmonary thermo-dye dilution. Pmsa and Pvr were calculated post hoc. Either the Wilcoxon-signed rank test or Friedman ANOVA test was performed. Results During hypoxia, mean pulmonary artery pressure (PAP) increased from median [IQR] 12 [8–15] to 19 [17–25] mmHg (p < 0.05). ITBV, PBV and their ratio with Vdcirc remained unaltered, which was also true for Pmsa, Pvr and cardiac output. PGI2 co-inhalation during hypoxia normalized mean PAP to 13 (12–16) mmHg (p < 0.05), but left cardiac preload surrogates unaltered. PGI2 inhalation during normoxia further decreased mean PAP to 10 (9–13) mmHg (p < 0.05) without changing any of the other investigated hemodynamic variables. Conclusions In spontaneously breathing dogs, changes in pulmonary vascular tone altered PAP but had no effect on cardiac output, central blood volumes or their relation to circulating blood volume, nor on Pmsa and Pvr. These observations suggest that cardiac preload is preserved despite substantial alterations in right ventricular afterload.

Cardiovascular response to blood loss during high intracranial pressure

1995 ◽  
Vol 83 (6) ◽  
pp. 1067-1071 ◽  
Author(s):  
Ole J. Kirkeby ◽  
Ingunn R. Rise ◽  
Lars Nordsletten ◽  
Sigmund Skjeldal ◽  
Cecilie Risøe
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Intracranial Pressure ◽  
Blood Loss ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Cardiovascular Response ◽  
Tissue Blood Flow ◽  
Content Type ◽  
Arterial Bleeding

✓ The authors hypothesized that the combination of hemorrhage and increased intracranial pressure (ICP) has deleterious effects on cardiovascular function. The effect of blood loss during normal and increased ICP was studied in eight pigs. The mean arterial pressure (MAP), pulmonary arterial pressure, pulmonary capillary wedge pressure, cardiac output, and cerebrospinal fluid (CSF) pressure were measured. The regional tissue blood flow was determined with radioactive microspheres labeled with four different nuclides. High ICP (80% of MAP) was induced by infusion of artificial CSF into the cisterna magna. The response to rapid arterial bleeding of 25% of blood volume was measured. The decrease in blood flow to the intestine, skeletal muscle, and the kidneys after blood loss was significantly greater during high ICP. The decrease in blood flow to the spleen and pancreas tended to be greater during high ICP, whereas the changes in blood flow to the liver, adrenal glands, and heart muscle showed no such tendency. The fall in cardiac output and heart stroke volume after blood loss were more pronounced when the ICP was high, and the increase in systemic vascular resistance was considerably greater. These observations suggest that during high ICP the physiological protective mechanisms against blood loss are impaired in the systemic circulation, and a loss of 25% of the blood volume, normally well compensated for, may induce a state of shock.

ANG II prolongs splanchnic nerve-mediated inhibition of duodenal mucosal alkaline secretion in the rat

1997 ◽  
Vol 273 (3) ◽  
pp. R942-R946 ◽  
Author(s):  
B. Johansson ◽  
M. Holm ◽  
L. Chen ◽  
A. Pettersson ◽  
C. Jonson ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Control Level ◽  
Renin Angiotensin System ◽  
Splanchnic Nerve ◽  
Total Blood ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Alkaline Secretion

Hypovolemia inhibits duodenal mucosal alkaline (HCO-3) secretion by activation of sympathoadrenergic nerves. A possible involvement of the renin-angiotensin system was investigated. Experiments were performed on chloralose-anesthetized rats. The mucosal alkaline output by a duodenal segment was measured using in situ pH-stat titration equipment. A modest hypovolemia was induced by bleeding the animals approximately 10% of the total blood volume. This procedure decreased duodenal mucosal alkaline secretion to a sustained level of approximately 50% of baseline and reduced mean arterial pressure by approximately 20 mmHg. Intravenous pretreatment with the angiotensin-converting enzyme (ACE) inhibitor enalaprilate (0.7 mg/kg) or the angiotensin II-receptor antagonist losartan (10 mg/kg) altered the response to hypovolemia to a transient one, and alkaline secretion returned to the control level within 40-50 min. When exogenous angiotensin II was administered intravenously (0.25 and 0.75 microgram.kg-1.h-1), a hypovolemia-induced sustained depression of the secretion was observed even during ACE inhibition. Direct electrical stimulation (3 Hz, 5 V, 5 ms, bilaterally) of the peripheral splanchnic nerves decreased duodenal mucosal alkaline secretion to approximately 60% of the control level and increased mean arterial pressure by approximately 20 mmHg. However, in enalaprilate-pretreated animals, the inhibition of alkaline secretion due to splanchnic nerve stimulation was transient, a response that became sustained on angiotensin II substitution. These results suggest that the renin-angiotensin system prolongs the sympathoadrenergic inhibition of duodenal mucosal alkaline secretion and that angiotensin II, in this regard, acts mainly on the peripheral sympathetic efferents.

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