Baroreflex sensitivity and pressor responses in a rat model of uraemia

1985 ◽  
Vol 69 (5) ◽  
pp. 637-640 ◽  
Author(s):  
Alan J. Watson ◽  
Donald Di Pette
Keyword(s):  
Renal Failure ◽  
Angiotensin Ii ◽  
Rat Model ◽  
Arginine Vasopressin ◽  
Baroreflex Sensitivity ◽  
Pressor Response ◽  
Regression Line ◽  
Control Group ◽  
Failure Group ◽  
Pressor Responses

1. Baroreflex sensitivity and pressor responsiveness to exogenous noradrenaline, angiotensin II and arginine vasopressin were determined in a rat model of uraemia. 2. The slope of the regression line relating Δheart rate to Δblood pressure after phenylephrine administration was significantly less in the renal failure group than the normal control group, indicating a reduction of baroreflex sensitivity in the setting of uraemia. 3. The pressor response to noradrenaline and angiotensin II was significantly less in the renal failure group whereas there was no difference in Δblood pressure on administration of arginine vasopressin. 4. It is concluded that diminished baroreflex sensitivity does not contribute to the pathogenesis of hypertension in uraemia by the hypothesized mechanism of allowing the pressor effect of endogenous pressor substances to go unbuffered.

Prolonged inhibition of pressor response to vasopressin by a potent specific antagonist, [1-(β-mercapto-β,β-cyclopentamethylenepropionic acid) 2-(O-methyl)tyrosine]arginine-vasopressin

1981 ◽  
Vol 59 (9) ◽  
pp. 1008-1012 ◽  
Author(s):  
Catherine C. Y. Pang ◽  
Kenneth M. Leighton
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Pressor Response ◽  
Duration Of Action ◽  
Pressor Responses ◽  
Anaesthetized Rats ◽  
Pressor Activity ◽  
Specific Antagonist

The specificity, the potency, and the duration of action of [1-(β-mercapto-β,β-cyclopentamethylenepropionic acid) 2-(O-methyl)tyrosine]arginine-vasopressin [d(CH2)5Tyr(Me)AVP] to antagonize pressor responses to arginine vasopressin (AVP) was examined in pentobarbital-anaesthetized rats. Injection of the compound (4 μg∙kg−1 i.v.) prevented pressor responses to i.v. infusions of supramaximal doses of AVP, but not to i.v. infusions of another peptide, angiotensin II (Ag II). The antagonism of AVP persisted for at least 3 h. Since i.v. injection of the compound in the absence of exogenous administration of AVP did not cause any change in the arterial pressure of rats, it appears that the compound is devoid of agonistic pressor activity. The results show that d(CH2)5Tyr(Me)AVP is a potent and a specific antagonist of pressor responses to AVP.

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.

scholarly journals A Subpressor Dose of Angiotensin II Elevates Blood Pressure in a Normotensive Rat Model by Oxidative Stress

2015 ◽  
pp. 153-159 ◽  
Author(s):  
M. M. GOVENDER ◽  
A. NADAR
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Angiotensin Ii ◽  
Mrna Expression ◽  
Rat Model ◽  
Wistar Rat ◽  
Control Group ◽  
Sod Activity ◽  
Male Wistar Rats ◽  
Experimental Group

Oxidative stress is an imbalance between free radicals and antioxidants, and is an important etiological factor in the development of hypertension. Recent experimental evidence suggests that subpressor doses of angiotensin II elevate oxidative stress and blood pressure. We aimed to investigate the oxidative stress related mechanism by which a subpressor dose of angiotensin II induces hypertension in a normotensive rat model. Normotensive male Wistar rats were infused with a subpressor dose of angiotensin II for 28 days. The control group was sham operated and infused with saline only. Plasma angiotensin II and H2O2 levels, whole-blood glutathione peroxidase, and AT-1a, Cu/Zn SOD, and p22phox mRNA expression in the aorta was assessed. Systolic and diastolic blood pressures were elevated in the experimental group. There was no change in angiotensin II levels, but a significant increase in AT-1a mRNA expression was found in the experimental group. mRNA expression of p22phox was increased significantly and Cu/Zn SOD decreased significantly in the experimental group. There was no significant change to the H2O2 and GPx levels. Angiotensin II manipulates the free radical-antioxidant balance in the vasculature by selectively increasing O2− production and decreasing SOD activity and causes an oxidative stress induced elevation in blood pressure in the Wistar rat.

The Protective Effect of γ-Glutamyl l-Dopa on the Glycerol Treated Rat Model of Acute Renal Failure

1983 ◽  
Vol 65 (2) ◽  
pp. 159-164 ◽  
Author(s):  
I. F. Casson ◽  
D. A. Clayden ◽  
G. F. Cope ◽  
M. R. Lee
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Protective Effect ◽  
Rat Model ◽  
Fold Increase ◽  
Plasma Creatinine ◽  
Control Group ◽  
Creatinine Excretion ◽  
Urine Creatinine ◽  
Before And After

1. γ-Glutamyl l-dopa, a renal pro-drug for dopamine, was administered to rats before and after injection of glycerol, and to a control group which received water in place of glycerol. A third group of rats was given glycerol but no γ-glutamyl l-dopa. 2. The plasma creatinine in rats given γ-glutamyl l-dopa and glycerol was significantly lower than in rats receiving glycerol alone. 3. The fall in urine creatinine excretion, and polyuria, after glycerol was reduced by γ-glutamyl l-dopa and the natriuresis abolished. 4. γ-Glutamyl l-dopa given alone caused a 4000-fold increase in urine dopamine excretion, associated with a natriuresis. 5. The administration of γ-glutamyl l-dopa reduces the severity of renal failure produced by glycerol.

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.

Evidence that centrally released arginine vasopressin is involved in central pressor action of angiotensin II

1996 ◽  
Vol 270 (1) ◽  
pp. H167-H173 ◽  
Author(s):  
S. Lon ◽  
E. Szczepanska-Sadowska ◽  
M. Szczypaczewska
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Pressor Effect ◽  
Ang Ii ◽  
Central Administration ◽  
Hypotensive Action ◽  
Series Of Experiments

Five series of experiments were performed on conscious trained dogs to find out whether intracranially released arginine vasopressin (AVP) is involved in mediation of central cardiovascular effects of angiotensin II (ANG II). The dogs were implanted with guide tubes leading to the third cerebral ventricle (ICV) and implanted with the intra-arterial catheters. Blood pressure and heart rate were continuously monitored during intracerebroventricular administration of 1) ANG II alone (250 ng), 2) AVP alone (0.01 ng/min during 10 min), 3) ANG II together with AVP, 4) AVP together with AVP V1-receptor antagonist 1(1-mercapto-4-methylcyclohexaneacetic acid)-8-AVP [MeCAAVP, V1ANT,100 ng/min], and 5) ANG II together with V1ANT. The results revealed that 1) ANG II and AVP applied separately elicited significant, long-lasting increases of blood pressure; 2) the maximum pressor effect after ANG II and AVP applied together did not differ from that after separate application of either of these peptides, but the duration of the pressor response was significantly shorter; 3) pretreatment with V1ANT effectively prevented blood pressure increases elicited by central administration of AVP and ANG II; and 4) after blockade of V1 receptors administration of AVP resulted in a significantly delayed decrease of blood pressure below baseline. The results strongly suggest that 1) centrally released AVP mediates the pressor effect of intracerebroventricularly applied ANG II by means of V1 receptors; 2) intracerebroventricularly applied ANG II and AVP interact to activate the mechanism involved in extinction of their pressor effect; and 3) blockade of central V1 receptors uncovers the hypotensive action of centrally applied AVP.

Pressor responses of rats to vasopressin: effect of sodium, angiotensin, and catecholamines

1983 ◽  
Vol 244 (2) ◽  
pp. H253-H258 ◽  
Author(s):  
M. Burnier ◽  
H. R. Brunner
Keyword(s):  
Angiotensin Ii ◽  
Sodium Intake ◽  
Pressor Response ◽  
Response Curves ◽  
Ether Anesthesia ◽  
Spontaneously Hypertensive ◽  
Lysine Vasopressin ◽  
Pressor Responses ◽  
Wistar Kyoto ◽  
The Right

The pressor response to lysine vasopressin was tested in groups of male Wistar, Brattleboro, Wistar-Kyoto, and spontaneously hypertensive rats. Moreover, the influence of sodium intake, angiotensin II, saralasin, captopril, norepinephrine, and isoproterenol on vasopressin pressor responses was evaluated. The right iliac artery and one or both femoral veins of the animals were catheterized under light ether anesthesia. The experiments were carried out following a 2-h stabilization period with the rats awake and semirestrained. Pressor responsiveness was evaluated acutely on the basis of dose-response curves (0.5-4 mU). In the Wistar rats, angiotensin II (10 and 30 ng/min) and isoproterenol (10 ng/min) markedly decreased the response to vasopressin, whereas variations in sodium intake and blood pressure per se did not seem to exert any influence. Norepinephrine (250 ng/min) slightly enhanced the pressor responsiveness to the smaller doses of lysine-vasopressin. Brattleboro rats with congenital diabetes insipidus were less sensitive to vasopressin than the other animals, and neither angiotensin II nor isoproterenol induced any change. In conclusion, the pressor responsiveness to vasopressin can vary considerably depending on several factors. These must be taken into account when evaluating the possible pressor role of vasopressin in experimental and clinical settings.

Pressor effect of arginine vasopressin in progressive autonomic failure

1986 ◽  
Vol 71 (2) ◽  
pp. 173-178 ◽  
Author(s):  
T. D. M. Williams ◽  
D. DaCosta ◽  
C. J. Mathias ◽  
R. Bannister ◽  
S. L. Lightman
Keyword(s):  
Blood Pressure ◽  
Arginine Vasopressin ◽  
Autonomic Failure ◽  
Pressor Response ◽  
Normal Subjects ◽  
Pressor Effect ◽  
Normal Volunteers ◽  
Pressor Responses ◽  
Transient Bradycardia ◽  
Related Increase

1. The blood pressure (BP) and heart rate (HR) responses to 5 min incremental intravenous infusions of noradrenaline (NA) and arginine vasopressin (AVP) were investigated both in patients with progressive autonomic failure (PAF) and in normal volunteers. 2. Stepwise infusion of NA at rates of 300–3000 pmol min−1 kg−1 produced a bradycardia and a dose related increase in BP in normal subjects. In subjects with PAF there was no significant HR response but the dose-BP response was shifted to the left with significant pressor responses at infusion rates of 60–300 pmol min−1 kg−1. 3. Stepwise infusion of AVP at 0.2–5.0 pmol min−1 kg−1 caused transient bradycardia but no pressor response in seven normal volunteers. Further increases in AVP infusion in three other subjects achieved plasma AVP levels as high as 3000–4000 pmol/l, and still no significant pressor response was observed. 4. Stepwise infusion of AVP at 0.05–2.0 pmol min−1 kg−1 in the eight subjects with PAF resulted in a pressor response without any change in HR. During this infusion plasma AVP increased from 0.8 ± 0.2 (mean ± se) to 30 ± 2 pmol/l. A significant pressor response was already apparent at a plasma AVP level of 5.5 ± 1.8 pmol/l.

scholarly journals Attenuation of pressor responses to norepinephrine and pitressin and potentiation of pressor response to angiotensin II by captopril in human subjects.

Hypertension ◽  
1982 ◽  
Vol 4 (3) ◽  
pp. 444-451 ◽  
Author(s):  
Y Imai ◽  
K Abe ◽  
M Seino ◽  
T Haruyama ◽  
J Tajima ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Pressor Response ◽  
Human Subjects ◽  
Pressor Responses

Renal water excretion before and after remission of nephrotic syndrome: Relationship between free water clearance and kidney function, arginine vasopressin, angiotensin II and aldosterone in plasma before and after oral water loading

1986 ◽  
Vol 71 (1) ◽  
pp. 97-104 ◽  
Author(s):  
E. B. Pedersen ◽  
H. Danielsen ◽  
S. S. Sørensen ◽  
B. Jespersen
Keyword(s):  
Nephrotic Syndrome ◽  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Free Water ◽  
Control Group ◽  
Ang Ii ◽  
Free Water Clearance ◽  
Water Load ◽  
Control Subjects ◽  
Before And After

1. An oral water load of 20 ml/kg body wt. was given to eight patients with nephrotic syndrome before and after remission of the syndrome, and to 13 healthy control subjects. Urine volume (D), free water clearance (Cwater), plasma concentrations of arginine vasopressin (AVP), angiotensin II (ANG II) and aldosterone (Aldo), were determined before and three times during the first 4 h after loading. 2. D and Cwater increased to a significantly lower level (P < 0.01) after water loading in patients with nephrotic syndrome than in control subjects, but D and Cwater were normal after remission of the syndrome. The maximum increase in Cwater (ΔCwater max.) was 1.07 ml/min (median) before remission and 7.93 ml/min after, compared with 8.01 ml/min in the control group. 3. Creatinine clearance (Ccr) increased significantly after remission (63 ml/min to 88 ml/min, P < 0.01), and the fractional excretion of sodium was enhanced. AVP was higher in the nephrotic syndrome both before (2.9 pmol/l) and after remission (2.9 pmol/l) compared with the control group (1.8 pmol/l). ANG II and Aldo did not change after remission and remained at the same level as in the control group. 4. The elevation in ΔCwatermax after remission was accompanied by an increase in Ccr in all patients and ΔCwatermax. and Ccr were significantly correlated (ρ = 0.600, n = 16, P < 0.05). No relationship was found between the change in ΔCwater max. and ANG II and Aldo. 5. AVP was significantly suppressed in patients with nephrotic syndrome before remission, but not after remission nor in control subjects, so that although AVP did not differ in nephrotic patients before and after remission, AVP cannot be excluded as a contributory factor to the reduction in Cwater in the nephrotic syndrome. 6. It is concluded that patients with nephrotic syndrome excrete an oral water load slower than control subjects and that the excretion rate is normal after remission of the syndrome. It is suggested that the normalization of Cwater may be attributed to an increase in glomerular filtration rate or a decrease in proximal tubular sodium reabsorption, although a possible role for AVP has not been excluded.

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