The Response of Blood Pressure to Infusion of Angiotensin II: Relation to Plasma Concentrations of Renin and Angiotensin II

1972 ◽  
Vol 42 (4) ◽  
pp. 489-504 ◽  
Author(s):  
R. H. Chinn ◽  
Gisela Düsterdieck
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Diastolic Pressure ◽  
Pressor Response ◽  
Human Subjects ◽  
Plasma Concentrations ◽  
Negative Relationship ◽  
Straight Line ◽  
Plasma Angiotensin ◽  
Standard Rate

1. In thirty-nine normotensive and hypertensive human subjects plasma concentrations of angiotensin II during pressor infusions of the peptide were significantly related to the concentrations found before infusion began. 2. When mean diastolic pressure before and during lower rates of angiotensin infusion were plotted against concurrent plasma angiotensin II concentrations, a straight-line relationship was observed. This relationship also held for the higher rates of infusion in some subjects. 3. During infusion at a standard rate of 4 ng min−1 kg−1 the rise in plasma angiotensin II concentration varied widely from subject to subject. 4. There was a significant negative relationship between this increase and the threshold of the pressor response to angiotensin. 5. There was a significant positive relationship between the threshold of the pressor response and the basal concentrations of renin and angiotensin II. 6. These results suggest that angiotensin normally present in blood lies within or close to a range capable of affecting blood pressure.

Nonadrenergic noncholinergic autonomic mediation of pressor response to feeding in lambs

1993 ◽  
Vol 265 (3) ◽  
pp. R530-R536 ◽  
Author(s):  
S. A. Jones ◽  
B. L. Langille ◽  
S. Frise ◽  
S. L. Adamson
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Adrenergic Blockade ◽  
Arterial Blood ◽  
Plasma Angiotensin ◽  
Muscarinic Cholinergic ◽  
Alpha Beta

We examined factors mediating a 70% increase in arterial blood pressure that occurs during feeding in newborn lambs. We report that the increase in blood pressure during feeding was significantly reduced (to approximately 50%) and delayed in onset by combined alpha- and beta-adrenergic blockade. Plasma angiotensin and vasopressin levels did not increase significantly during feeding, nor was the pressor response to feeding attenuated while using captopril to block the production of angiotensin II. Adrenalectomy or muscarinic cholinergic blockade with atropine was also unsuccessful in attenuating the pressor response to feeding. We demonstrated that the component of the pressor response to feeding that was insensitive to alpha, beta, and muscarinic blockade was mediated by the autonomic nervous system because it was completely eliminated by ganglionic blockade with hexamethonium. Thus nonadrenergic noncholinergic autonomic mechanisms mediate approximately half the pressor response to feeding in lambs.

Effects of the angiotensin II receptor antagonist Losartan (DuP 753/MK 954) on arterial blood pressure, heart rate, plasma concentrations of angiotensin II and renin and the pressor response to infused angiotensin II in the salt-deplete dog

1992 ◽  
Vol 83 (5) ◽  
pp. 549-556 ◽  
Author(s):  
R. J. MacFadyen ◽  
M. Tree ◽  
A. F. Lever ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Pressor Response ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Plasma Angiotensin

1. The blood pressure, heart rate, hormonal and pressor responses to constant rate infusion of various doses of the angiotensin (type 1) receptor antagonist Losartan (DuP 753/MK 954) were studied in the conscious salt-deplete dog. 2. Doses in the range 0.1–3 μmin−1 kg−1 caused no change in blood pressure, heart rate or pressor response to angiotensin II (54 ng min−1kg−1), and a dose of 10 μgmin−1 kg−1 had no effect on blood pressure, but caused a small fall in the pressor response to angiotensin II. Infusion of Losartan at 30 μmin−1 kg−1 for 3 h caused a fall in mean blood arterial pressure from baseline (110.9 ± 11.2 to 95.0 ± 12.8 mmHg) and a rise in heart rate (from 84.6 ± 15.1 to 103 ± 15.2 beats/min). Baseline plasma angiotensin II (42.5 ± 11.8 pg/ml) and renin (64.5 ± 92.7 μ-units/ml) concentrations were already elevated in response to salt depletion and rose significantly after Losartan infusion to reach a plateau by 70 min. The rise in mean arterial blood pressure after a test infusion of angiotensin II (35.3 ± 11.6 mmHg) was reduced at 15 min (11.8 ± 6.8 mmHg) by Losartan and fell progressively with continued infusion (3 h, 4.3 ± 3.3 mmHg). The peak plasma angiotensin II concentration during infusion of angiotensin II was unaffected by Losartan, but the rise in plasma angiotensin II concentration during infusion was reduced because of the elevated background concentration. Noradrenaline infusion caused a dose-related rise in mean blood arterial pressure (1000 ngmin−1kg−1, +19.9 ± 8 mmHg; 2000ngmin−1 kg−1, +52.8 ± 13.9 mmHg) with a fall in heart rate (1000 ng min−1 kg−1, −27.9 ± 11.5 beats/min; 2000 ng min−1 kg−1, −31.2 ± 17.3 beats/min). During Losartan infusion the 1000 but not the 2000 ng min−1 kg−1 noradrenaline infusion caused a greater rise in mean arterial blood pressure and a greater fall in heart rate. The fall in heart rate tended to decrease with continued infusion of Losartan. Plasma catecholamine concentrations were unaffected by Losartan. In a further study, higher doses of Losartan (100, 300 and 1000 μg min−1 kg−1; 30 min) produced greater falls in mean arterial blood pressure also with a rise in heart rate and complete blockade of the pressor effect of infused angiotensin II. Some animals became disturbed at the highest dose. 3. Losartan produces rapid dose-related falls in blood pressure and a rise in heart rate and renin release with elevation of plasma angiotensin II. Pressor responses to angiotensin II are reduced at intermediate doses and are eliminated at high doses. Losartan does not appear to inhibit angiotensin II clearance from the plasma and may in some way increase it.

Brain Angiotensin II Stimulates Release of Pituitary Hormones, Plasma Catecholamines and Increases Blood Pressure in Dogs

1980 ◽  
Vol 59 (s6) ◽  
pp. 53s-56s ◽  
Author(s):  
B. A. Schölkens ◽  
W. Jung ◽  
W. Rascher ◽  
A. Schömig ◽  
D. Ganten
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Antidiuretic Hormone ◽  
Pressor Response ◽  
Plasma Concentrations ◽  
Plasma Catecholamines ◽  
Pressure Effects ◽  
Conscious Dogs ◽  
Arterial Blood

1. The mechanisms of central angiotensin II blood pressure effects in conscious dogs on normal or sodium-deficient diets were examined. 2. The biosynthesis of brain angiotensin II in cerebrospinal fluid from its local precursor angiotensinogen was induced in vivo by injection of 0.5 unit of hog kidney renin through a chronically implanted cannula into the third brain ventricle in conscious dogs. 3. Intracerebroventricular administration of renin induced an increase of arterial blood pressure and a marked drinking response under both dietary regimens. Sodium restriction had no effect on the magnitude of the central angiotensin pressor response. 4. Plasma concentrations of renin and angiotensin II decreased, and plasma antidiuretic hormone, noradrenaline, adrenaline and corticosterone increased, in both groups of dogs. 5. Simultaneous intraventricular administrations of captopril with renin inhibited the central renin effects. Intracerebroventricular injections of [Sar1, Val5, Ala8] angiotensin II alone increased plasma renin and angiotensin II concentrations. 6. It is concluded that endogenous brain angiotensin II participates in central mechanisms of blood pressure regulation by the stimulation of the release of antidiuretic hormone, adrenocorticotrophic hormone, adrenaline and noradrenaline.

Effect of Acute Vasopressin Infusion on Blood Pressure and Plasma Angiotensin II in Normotensive and DOC A—Salt Hypertensive Rats

1982 ◽  
Vol 62 (2) ◽  
pp. 143-149 ◽  
Author(s):  
J. J. Morton ◽  
C. Garcia Del Rio ◽  
Maria J. Hughes
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Concentrations ◽  
Hypertensive Rats ◽  
Short Term ◽  
Response Curves ◽  
Plasma Vasopressin ◽  
Salt Hypertension ◽  
Plasma Angiotensin ◽  
Basal Plasma

1. Arginine vasopressin was infused at 0.5, 2, 6, 18 or 54 ng min−1 kg−1 for 1 h into normal, sham-operated and DOCA—salt hypertensive rats. Complete vasopressin/blood pressure dose—response curves were constructed from circulating plasma vasopressin concentrations measured at the end of each infusion. 2. DOCA—salt hypertensive rats had a higher basal plasma vasopressin concentration (11.1 ± sd 3.7 fmol/ml) than either the normal (3.9 ± 2.3, P < 0.01) or the sham-operated rats (4.5 ± 2.4, P < 0.01). 3. The DOCA—salt hypertensive rats did not have any detectable enhancement of pressor sensitivity, compared with either of the two normotensive groups. 4. There was no significant increase in blood pressure in either the normal rats or sham-operated rats until vasopressin was infused at 2 ng min−1 kg−1, when the plasma concentration was between 30 and 40 fmol/ml. 5. Subpressor infusion of vasopressin in the normal and sham-operated rats, which gave plasma concentrations of 22–23 fmol/ml, completely suppressed plasma angiotensin II to levels similar to the basal values found in the DOCA—salt hypertensive rats (10.5 ± 2.3, 14.5 ± 4.5 and 8.0 ± 1.6 fmol/ml respectively). 6. These findings suggest that the mechanism of vasopressin involvement in DOCA—salt hypertension is as yet unclear, that short-term changes in vasopressin concentration appear unimportant in the regulation of normal blood pressure, that small physiological changes of vasopressin in normal rats may be important in the regulation of renin secretion, and that the increase in vasopressin concentration seen in DOCA—salt hypertension may contribute to the suppression of renin and angiotensin II in this state.

scholarly journals Blood pressure level and laboratory indicators of disease severity in patients with arterial hypertension and COVID-19

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
K Popov ◽  
A Novitskiy ◽  
Y Shvarts
Keyword(s):  
Blood Pressure ◽  
Multivariate Analysis ◽  
Arterial Hypertension ◽  
Negative Correlation ◽  
Diastolic Pressure ◽  
Negative Relationship ◽  
Laboratory Parameters ◽  
Acute Period ◽  
Nonparametric Correlation ◽  
The Relationship

Abstract Funding Acknowledgements Type of funding sources: None. Background. Many patients with COVID-19 suffer from arterial hypertension and have marked variations in blood pressure (BP) during the acute period of infection. The reasons for such changes are poorly understood. Purpose. To assess the relationship between the level of BP and the severity of changes in the main clinical and laboratory parameters in patients with arterial hypertension and with a moderate course of COVID-19 at the stage of the height of the disease. Materials and methods. The study included 86 hospitalized patients with verified coronavirus disease of moderate severity: 46 of them were male, the median age was 65 years. Patients received adequate hypertension therapy for a long time. After hospitalization, treatment was adjusted if necessary. The level of laboratory parameters in the acute period of the disease was determined, including the electrolytes, C-reactive protein (CRP), albumin, ferritin, general blood test, etc. BP measured daily. The relationship between laboratory parameters and BP level was evaluated by nonparametric correlation using the Spearman coefficient and multivariate analysis based on the "generalized nonlinear model". Results. In 67.44% of patients with hypertension, an elevated BP level (&gt;140/90) was observed against the background of moderate COVID-19. There was a significant negative correlation between the levels of CRP and BP throughout the stay in the hospital, the most significant is the 5th day of hospitalization. At the same time, a slightly stronger relationship is observed with diastolic BP (r = -0.4425) than with systolic BP (r = -0.3525). A similar trend is observed in all BP measurements. Besides, a negative correlation was found between potassium levels and BP values. The strongest association of potassium levels is with systolic BP on the day of hospitalization (r = -0.4850) and diastolic pressure on the 1st day of hospitalization (r = -0.3561). Multivariate analysis confirmed independent and reliable "influence" of CRP (p = 0.00018) and potassium (p = 0.03921) as independent predictors of diastolic pressure. Conclusions. Most patients with hypertension and moderate COVID-19 have elevated BP levels. There is a statistically significant negative relationship between the values of BP and levels of CRP and potassium. The obtained data may correspond to the existing hypothesis about the significant role of the kinin–kallikrein system in the pathogenesis of COVID-19.

Comparison of fast and slow pressor effects of angiotensin II in the conscious rat

1981 ◽  
Vol 241 (3) ◽  
pp. H381-H388 ◽  
Author(s):  
A. J. Brown ◽  
J. Casals-Stenzel ◽  
S. Gofford ◽  
A. F. Lever ◽  
J. J. Morton
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Control Period ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Pressor Effect ◽  
Ang Ii ◽  
Conscious Rat ◽  
Female Wistar Rats

Female Wistar rats were infused intravenously with 5% dextrose for 3 days, then with angiotensin II (ANG II) in 5% dextrose at 20 ng . kg-1 . min-1 for 7 days, and finally with dextrose for 2.5 days. ANG II raised mean arterial pressure (MAP) gradually; by the 7th day it was 49.7 mmHg higher than during the dextrose control period in the same rats. Control rats were infused with dextrose for 12.5 days; MAP did not change. Plasma ANG II concentration was measured during infusion. In hypertensive rats on the 7th day of ANG II infusion, it was six times higher than in control rats infused with dextrose. Changes of blood pressure and plasma ANG II concentration were compared in further rats infused with much larger doses of ANG II. Rats receiving 270 ng . kg-1 . min-1 for 1 h had an almost maximal direct pressor response, MAP rising 45.3 mmHg and plasma ANG II rising 32-fold compared with controls. Thus, infusion of ANG II at low dose without direct pressor effect gradually raises blood pressure to a level similar to the maximum direct pressor effect produced by larger doses of ANG II. Sodium balance and food and water intakes were also measured and did not change during prolonged infusion of ANG II at 20 ng . kg-1 . min-1. Thus, the slow pressure effect of ANG II develops at a lower and more nearly physiological plasma concentration of the peptide than do the direct pressor effect and the effects on drinking, eating, and urinary sodium excretion.

scholarly journals R-PEP-27, a Potent Renin Inhibitor, Decreases Plasma Angiotensin II and Blood Pressure in Normal Volunteers

1994 ◽  
Vol 7 (4 Pt 1) ◽  
pp. 295-301 ◽  
Author(s):  
R. M. Zusman ◽  
K. Y. Hui ◽  
J. Nussberger ◽  
D. M. Christensen ◽  
J. Higgins ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Renin Inhibitor ◽  
Normal Volunteers ◽  
Plasma Angiotensin

Metabolic clearance of angiotensin II in pregnant and nonpregnant sheep

1985 ◽  
Vol 249 (1) ◽  
pp. E49-E55 ◽  
Author(s):  
R. P. Naden ◽  
S. Coultrup ◽  
B. S. Arant ◽  
C. R. Rosenfeld
Keyword(s):  
Angiotensin Ii ◽  
Pressor Response ◽  
Plasma Concentrations ◽  
Metabolic Clearance ◽  
Ang Ii ◽  
Pressor Responses ◽  
Pregnant Sheep ◽  
Vascular Responsiveness ◽  
Arterial Plasma ◽  
In Pregnancy

Reduced vascular responsiveness to infused angiotensin II (ANG II) has been observed during pregnancy. It has been proposed that infusions produce lower circulating concentrations of ANG II in pregnancy, due to an increase in the metabolic clearance rate of ANG II (MCRangii). We have evaluated the MCRangii and the arterial plasma concentrations of ANG II during constant infusions of 1.15 micrograms ANG II/min into chronically instrumented pregnant (n = 6) and nonpregnant (n = 9) sheep. Although the pressor responses were significantly less in the pregnant than in the nonpregnant sheep (17.5 +/- 0.5 vs. 34.9 +/- 3.2 mmHg, P less than 0.001), the values for MCRangii were not different: 56.2 +/- 6.3 ml X min-1 X kg-1 in nonpregnant and 55.9 +/- 4.3 ml X min-1 X kg-1 in pregnant sheep. The steady-state plasma ANG II concentrations during the infusions were slightly less in pregnant than in nonpregnant sheep (388 +/- 36 vs. 454 +/- 36 pg/ml); however, this difference would be responsible for only a 2-mmHg reduction in the pressor response. We conclude that the reduced pressor response to infused ANG II in pregnancy is not due to an increase in MCRangii nor to lower plasma ANG II concentrations.

Abstract P041: Proximal Tubule-specific Deletion Of Angiotensin Ii Type 1a Receptors In The Kidney Lowers Basal Blood Pressure And Attenuates Angiotensin Ii-induced Hypertension By Increasing Glomerular Filtration And The Pressure-natriuresis Response

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Xiao C Li ◽  
Ana P Leite ◽  
Liang Zhang ◽  
Jia L Zhuo
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Pressor Response ◽  
Control Group ◽  
Ang Ii ◽  
Induced Hypertension ◽  
Basal Blood Pressure ◽  
Pressure Natriuresis ◽  
Specific Deletion

The present study tested the hypothesis that intratubular angiotensin II (Ang II) and AT 1a receptors in the proximal tubules of the kidney plays an important role in basal blood pressure control and in the development of Ang II-induced hypertension. Mutant mice with proximal tubule-specific deletion of AT 1a receptors in the kidney, PT- Agtr1a -/- , were generated to test the hypothesis. Eight groups (n=7-12 per group) of adult male wild-type (WT) and PT- Agtr1a -/- mice were infused with or without Ang II for 2 weeks (1.5 mg/kg, i.p.). Basal systolic, diastolic, and mean arterial pressures were ~13 ± 3 mmHg lower in PT- Agtr1a -/- than WT mice ( P <0.01). Basal glomerular filtration rate (GFR), as measured using transdermal FITC-sinistrin, was significantly higher in PT- Agtr1a -/- mice (WT: 160.4 ± 7.0 μl/min vs. PT- Agtr1a -/- : 186.0 ± 6.0 μl/min, P <0.05). Basal 24 h urinary Na + excretion (U Na V) was significantly higher in PT- Agtr1a -/- than WT mice ( P <0.01). In response to Ang II infusion, both WT and PT- Agtr1a -/- mice developed hypertension, and the magnitude of the pressor response to Ang II was similar in WT (Δ43 ± 3 mmHg, P <0.01) and PT- Agtr1a -/- mice (Δ39 ± 5 mmHg, P <0.01). However, the absolute blood pressure level was still 16 ± 3 mmHg lower in PT- Agtr1a -/- mice ( P <0.01). Ang II significantly decreased GFR to 132.2 ± 7.0 μl/min in WT mice ( P <0.01), and to 129.4 ± 18.6 μl/min in PT- Agtr1a -/- mice ( P <0.01), respectively. In WT mice, U Na V increased from 139.3 ± 22.3 μmol/24 h in the control group to 196.4 ± 29.6 μmol/24 h in the Ang II-infused group ( P <0.01). In PT- Agtr1a -/- mice, U Na V increased from 172.0 ± 10.2 μmol/24 h in the control group to 264.7 ± 35.4 μmol/24 h in the Ang II-infused group ( P <0.01). The pressor response to Ang II was attenuated, while the natriuretic response was augmented by losartan in WT and PT- Agtr1a -/- mice ( P <0.01). Finally, proximal tubule-specific deletion of AT 1a receptors significantly augmented the pressure-natriuresis response and natriuretic responses to acute saline infusion ( P <0.01) or a 2% high salt diet ( P <0.01). We concluded that deletion of AT 1a receptors selectively in the proximal tubules lowers basal blood pressure and attenuates Ang II-induced hypertension by increasing GFR and promoting the natriuretic response in PT- Agtr1a -/- mice.

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