Changes in Blood Pressure in Relation to Vascular and Plasma Renin after Renin Injection in Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 153s-156s ◽  
Author(s):  
M. Loudon ◽  
R. F. Bing ◽  
J. D. Swales ◽  
H. Thurston
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Plasma Renin ◽  
Aortic Tissue ◽  
Relative Importance ◽  
Bilateral Nephrectomy ◽  
Single Intravenous Injection ◽  
Angiotensin Ii Antagonist ◽  
Renal Origin

1. To assess the relative importance of vascular as opposed to plasma renin, groups of conscious rats received a single intravenous injection of partially purified rat renin 18 h after bilateral nephrectomy. Blood pressure was monitored continuously and plasma and aortic renin concentrations were determined at 1, 3, 6 or 9 h after injection. In separate groups of rats the effect of the competitive angiotensin II antagonist, saralasin, on blood pressure was measured 3 or 6 h after renin injection. 2. Blood pressure remained elevated for up to 6 h after renin injection, returning to normal by 9 h. Saralasin infusion reversed the rise in blood pressure at both 3 and 6 h after injection. 3. Aortic renin concentration followed the pattern of the pressor response whereas plasma renin concentration had returned to subnormal values by 3 h. 4. Circulating renin of renal origin is taken up by aortic tissue. The pressor response to exogenous renin in rats after bilateral nephrectomy is not related to changes in plasma renin but is similar in duration to the persistence of aortic renin-like activity and can be blocked by saralasin at both 3 and 6 h after injection.

Pressor Responsiveness to Angiotensin in Renovascular and Steroid Hypertension

1979 ◽  
Vol 57 (s5) ◽  
pp. 47s-50s ◽  
Author(s):  
E. S. Marks ◽  
H. Thurston ◽  
R. F. Bing ◽  
J. D. Swales
Keyword(s):  
Angiotensin Ii ◽  
Pressor Response ◽  
Plasma Renin ◽  
Receptor Occupancy ◽  
Bilateral Nephrectomy ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Pressor Responses ◽  
Salt Hypertension ◽  
Converting Enzyme Inhibition

1. The pressor response to angiotensin II was reduced in rats with early (<6 weeks) and chronic (>4 months) Goldblatt two-kidney, one-clip hypertension and enhanced in DOCA—salt hypertension. 2. Converting enzyme inhibition with captopril brought the angiotensin pressor response curves into closer proximity although the DOCA hypertensive rats were minimally hyper-responsive and rats with early and chronic renovascular hypertension showed slightly reduced responsiveness. 3. After bilateral nephrectomy the pressor responses to angiotensin were similar. 4. The pressor response to angiotensin II in these animals was inversely related to plasma renin concentration and therefore largely dependent upon receptor occupancy by endogenous angiotensin II. There is no evidence for enhanced pressor responsiveness to angiotensin in either renovascular or DOCA hypertension.

Action of Angiotensin Antagonists and Antiserum upon the Pressor Response to Renin: Further Evidence for the Local Generation of Angiotensin II

1974 ◽  
Vol 46 (2) ◽  
pp. 273-276 ◽  
Author(s):  
H. Thurston ◽  
J. D. Swales
Keyword(s):  
Blood Pressure ◽  
Molecular Weight ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Low Molecular Weight ◽  
Angiotensin Ii Antagonist ◽  
Local Generation

1. Bilaterally nephrectomized rats were infused with a pressor dose of renin. The blood pressure was only partially restored to normal by sufficient angiotensin II antiserum to block the pressor response to exogenous angiotensin II. 2. A reduced pressor response still occurred when animals which had been pretreated with angiotensin II antiserum were infused with renin. 3. Infusion of an angiotensin II antagonist (1-sarcosine-8-alanine angiotensin II) restored the blood pressure of both groups of animals to normal. 4. These observations support the hypothesis that renin generates angiotensin II at a local vascular level. This site is inaccessible to antisera, but accessible to the low-molecular-weight antagonist.

Change in the Renin Dependency of Blood Pressure Induced by Volume Depletion and/or Propranolol Therapy in Hypertensive Patients

1976 ◽  
Vol 51 (s3) ◽  
pp. 189s-192s
Author(s):  
G. G. Geyskes ◽  
P. Boer ◽  
J. Vos ◽  
E. J. Dorhout Mees
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin ◽  
Special Importance ◽  
Volume Depletion ◽  
Blood Pressure Elevation ◽  
Hypertensive Patients ◽  
Angiotensin Ii Antagonist ◽  
Different Types ◽  
Propranolol Therapy

1. Plasma renin activity (PRA) and renin dependency of the blood pressure was analysed in ten patients with various forms of hypertension before and during treatment with volume depletion and/or propranolol. Renin dependency was tested by infusion of the specific competitive angiotensin II antagonist Sar1-Ala8-angiotensin II (P113). 2. The P113-induced fall of the blood pressure did correlate with the log PRA (r = 0·888, P < 0001). This correlation was found irrespective of different types of hypertension and treatment schedules. 3. During volume depletion, PRA was stimulated and renin dependency of the blood pressure increased. Propranolol therapy suppressed PRA during normovolaemia as well as during volume depletion, and this was accompanied by a decrease of the renin dependency. 4. No indication was found that a given PRA is of special importance for blood pressure elevation in different patients. 5. Suppression of PRA by propranolol is one of the anti-hypertensive mechanisms of this drug.

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.

Effect of enalapril (MK-421), an orally active angiotensin I converting enzyme inhibitor, on blood pressure, active and inactive plasma renin, urinary prostaglandin E2, and kallikrein excretion in conscious rats

1984 ◽  
Vol 62 (1) ◽  
pp. 116-123 ◽  
Author(s):  
Ernesto L. Schiffrin ◽  
Jolanta Gutkowska ◽  
Gaétan Thibault ◽  
Jacques Genest
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Ace Inhibition ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin I Converting Enzyme

The angiotensin I converting enzyme (ACE) inhibitor enalapril (MK-421), at a dose of 1 mg/kg or more by gavage twice daily, effectively inhibited the pressor response to angiotensin I for more than 12 h and less than 24 h. Plasma renin activity (PRA) did not change after 2 or 4 days of treatment at 1 mg/kg twice daily despite effective ACE inhibition, whereas it rose significantly at 10 mg/kg twice daily. Blood pressure fell significantly and heart rate increased in rats treated with 10 mg/kg of enalapril twice daily, a response which was abolished by concomitant angiotensin II infusion. However, infusion of angiotensin II did not prevent the rise in plasma renin. Enalapril treatment did not change urinary immunorcactive prostaglandin E2 (PGE2) excretion and indomethacin did not modify plasma renin activity of enalapril-treated rats. Propranolol significantly reduced the rise in plasma renin in rats receiving enalapril. None of these findings could be explained by changes in the ratio of active and inactive renin. Water diuresis, without natriuresis and with a decrease in potassium urinary excretion, occurred with the higher dose of enalapril. Enalapril did not potentiate the elevation of PRA in two-kidney one-clip Goldblatt hypertensive rats. In conclusion, enalapril produced renin secretion, which was in part β-adrenergically mediated. The negative short feedback loop of angiotensin II and prostaglandins did not appear to be involved. A vasodilator effect, apparently independent of ACE inhibition, was found in intact conscious sodium-replete rats.

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.

L-arginine analogues inhibit aldosterone secretion in rats

1995 ◽  
Vol 268 (5) ◽  
pp. R1137-R1142 ◽  
Author(s):  
J. C. Simmons ◽  
R. H. Freeman
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Methyl Ester ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Bilateral Nephrectomy ◽  
Aldosterone Secretion ◽  
Series Of Experiments

L-Arginine analogues, e.g., NG-nitro-L-arginine methyl ester (L-NAME), increase arterial pressure and suppress renin release in the rat. On the basis of these observations, it was hypothesized that L-arginine analogues also would attenuate aldosterone secretion. This hypothesis was tested in anesthetized rats treated with L-NAME or NG-nitro-L-arginine (L-NNA, 185 mumol/kg ip). The aldosterone secretion rate, plasma renin activity, and adrenal blood flow were attenuated in rats treated with L-NAME and L-NNA compared with control animals. Similar experiments were performed in anephric rats to examine the effects of L-NAME on aldosterone secretion independent of the circulating reninangiotensin system. The administration of L-NAME reduced adrenal blood flow but failed to reduce aldosterone secretion in these anephric rats. Bilateral nephrectomy reduced plasma renin activity essentially to undetectable levels in these animals. In a third series of experiments, two groups of anephric rats were infused with angiotensin II (3 micrograms/kg body wt iv) to provide a stimulus for aldosterone secretion. Aldosterone secretion and adrenal blood flow were markedly reduced in angiotensin II-infused rats pretreated with L-NAME compared with the control anephric animals infused with angiotensin II. Overall these results suggest that L-arginine analogues attenuate aldosterone secretion by inhibiting the adrenal steroidogenic effects of endogenous or exogenous angiotensin II and/or by reducing plasma levels of renin/angiotensin.

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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