The renin-angiotensin system and the third mechanism of renal blood flow autoregulation

2009 ◽  
Vol 296 (6) ◽  
pp. F1334-F1345 ◽  
Author(s):  
Erdmann Seeliger ◽  
Thomas Wronski ◽  
Mechthild Ladwig ◽  
Leszek Dobrowolski ◽  
Torsten Vogel ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renin Angiotensin System ◽  
Renal Perfusion ◽  
Mirror Image ◽  
Tubuloglomerular Feedback ◽  
Step Response ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Renal Vascular

Autoregulation of renal blood flow comprises three mechanisms: the myogenic response (MR), the tubuloglomerular feedback (TGF), and a third mechanism (3M). The nature of 3M is unknown; it may be related to hypotensive resetting of autoregulation that probably relies on pressure-dependent stimulation of the renin-angiotensin system (RAS). Thus we used a normotensive angiotensin II clamp in anesthetized rats and studied autoregulation 1) by slow ramp-shaped reductions in renal perfusion pressure (RPP) followed by ramp-shaped RPP restorations and 2) by means of the step response technique: after 30 s of either total or partial suprarenal aortic occlusion, a step increase in RPP was made and the response of renal vascular conductance analyzed to assess the mechanisms' strength and initial direction (vasodilation or constriction). The angiotensin clamp abolished the resetting of autoregulation during ramp-shaped RPP changes. Under control conditions, the initial TGF response was dilatory after total occlusions but constrictive after partial occlusions. The initial 3M response presented a mirror image to the TGF: it was constrictive after total but dilatory after partial occlusions. The angiotensin clamp suppressed the TGF and turned the initial 3M response following total occlusions into dilation. We conclude that 1) pressure-dependent RAS stimulation is a major cause behind hypotensive resetting of autoregulation, 2) TGF sensitivity strongly depends on pressure-dependent changes in RAS activity, 3) the 3M is modulated, but not mediated, by the RAS, and 4) the 3M acts as a counterbalance to the TGF and might possibly be related to the recently described connecting tubule glomerular feedback.

Autoregulation of renal blood flow in the puppy

1975 ◽  
Vol 229 (4) ◽  
pp. 983-988 ◽  
Author(s):  
PA Jose ◽  
LM Slotkoff ◽  
S Montgomery ◽  
PL Calcagno ◽  
G Eisner
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Electromagnetic Flowmeter ◽  
Renin Angiotensin System ◽  
Renal Perfusion ◽  
Angiotensin System ◽  
Group Of Seven ◽  
Selective Blockade

The ability of the immature kidney to autoregulate blood flow was investigated. Renal blood flow was measured by electromagnetic flowmeter. In six puppies, selective blockade of the intrarenal effects of angiotensin II (AII) by [1-sarcosine, 8-alanine]angiotensin II (anti-AII) administered into the renal artery did not change renal blood flow. During selective renal AII blockade, intravenous AII raised perfusion pressure from 76 +/- 2 to 100 +/- 6 mmHg. Renal blood flow increased from 1.59 +/- 0.29 to 1.98 +/- 0.59 ml/g kidney per min, but returned to control levels within 40 s in spite of persistent arterial pressure elevation. In another group of seven puppies, renal blood flow remained constant despite reduction of renal perfusion pressure by aortic constriction to 60 mmHg. In two of these seven puppies intrarenal anti-AII did not abolish autoregulation. Autoregulation of renal blood flow occurs in the puppy and is not influenced by inhibition of angiotensin. The renin-angiotensin system does not appear to be involved in the normal regulation of renal blood flow in the puppy.

The step response: a method to characterize mechanisms of renal blood flow autoregulation

2003 ◽  
Vol 285 (4) ◽  
pp. F758-F764 ◽  
Author(s):  
T. Wronski ◽  
E. Seeliger ◽  
P. B. Persson ◽  
C. Forner ◽  
C. Fichtner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Perfusion ◽  
Oscillation Period ◽  
Tubuloglomerular Feedback ◽  
Step Response ◽  
Myogenic Response ◽  
Renal Vasculature ◽  
The Individual ◽  
Reported Data

Response of renal vasculature to changes in renal perfusion pressure (RPP) involves mechanisms with different frequency characteristics. Autoregulation of renal blood flow (RBF) is mediated by the rapid myogenic response, by the slower tubuloglomerular feedback (TGF) mechanism, and, possibly, by an even slower third mechanism. To evaluate the individual contribution of these mechanisms to RBF autoregulation, we analyzed the response of RBF to a step increase in RPP. In anesthetized rats, the suprarenal aorta was occluded for 30 s, and then the occlusion was released to induce a step increase in RPP. Three dampened oscillations were observed; their oscillation periods ranged from 9.5 to 13 s, from 34.2 to 38.6 s, and from 100.5 to 132.2 s, respectively. The two faster oscillations correspond with previously reported data on the myogenic mechanism and the TGF. In accordance, after furosemide, the amplitude of the intermediate oscillation was significantly reduced. Inhibition of nitric oxide synthesis by Nω-nitro-l-arginine methyl ester significantly increased the amplitude of the 10-s oscillation. It is concluded that the parameters of the dampened oscillations induced by the step increase in RPP reflect properties of autoregulatory mechanisms. The oscillation period characterizes the individual mechanism, the dampening is a measure for the stability of the regulation, and the square of the amplitudes characterizes the power of the respective mechanism. In addition to the myogenic response and the TGF, a third rather slow mechanism of RBF autoregulation exists.

RENIN ANGIOTENSIN SYSTEM AND AUTOREGULATION OF RENAL BLOOD FLOW IN THE EXERCISING DOG

1977 ◽  
Vol 9 (1) ◽  
pp. 48
Author(s):  
E. J. Zambraski ◽  
G. F. DIBona ◽  
C. M. Tipton ◽  
Edward J. Zambraski
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

Effect of angiotensin II antagonist infusion on autoregulation of renal blood flow

1976 ◽  
Vol 231 (4) ◽  
pp. 1267-1271 ◽  
Author(s):  
Y Abe ◽  
T Kishimoto ◽  
K Yamamoto
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Renin Angiotensin System ◽  
Pressure Reduction ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Renal Autoregulation ◽  
Angiotensin Ii Antagonist

The role of the renin-angiotensin system in the autoregulation of renal blood flow was examined in the anesthetized dog. The angiotensin II antagonist, [1-sarcosine, 8-isoleucine]angiotensin II, was continuously infused into the renal artery at rates of 1 and 3 mug/min, and renin secretion rate and intrarenal distribution of blood flow as well as total renal blood flow were measured during acute reductions in renal perfusion pressure within and below the range of autoregulation. Renal autoregulation and redistribution of blood flow by pressure reduction were not disturbed by the angiotensin II antagonist. This result does not provide any evidence for a primary role of the renin-angiotensin system in renal autoregulation. Redistribution of blood flow by pressure reduction occurred independently of the renin-angiotensin system. It might depend on the differences in the resting tone among the zones.

Renal hemodynamics in the rat before and during inhibition of angiotensin II

1977 ◽  
Vol 233 (4) ◽  
pp. F290-F297 ◽  
Author(s):  
W. J. Arendshorst ◽  
W. F. Finn
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Renin Angiotensin System ◽  
Renal Hemodynamics ◽  
Dietary Group ◽  
Base Line ◽  
Angiotensin I ◽  
Angiotensin System ◽  
Renin Angiotensin

Renal blood flow (RBF) was measured with a noncannulating electromagnetic flow transducer in anesthetized rats which had been maintained for 3-5 wk on low, normal, or high salt plus deoxycorticosterone diets. After base-line observations, one of two dissimilar inhibitors of the renin-angiotensin system, angiotensin I converting enzyme inhibitor SQ 20881 or the structural analogue [Sar1,Ala8]angiotensin II was administered intravenously. The employed doses of SQ 20881 and [Sar1,Ala8]angiotensin II effectively inhibited the pressor and renal vasoconstrictor responses induced by exogenous angiotensin I and II, respectively, in each dietary group. Both inhibitors vasodilated kidneys in salt-restricted rats; however, neither affected base-line renal hemodynamics in salt-loaded rats. Pressure-flow relationships were evaluated by clamping the aorta to reduce renal perfusion pressure. Renal blood flow was autoregulated between 100 and 140 mmHg with the same efficiency before and during inhibition of angiotensin II in each dietary group. These data indicate that angiotensin II modifies base-line RBF and renal vascular resistance and are consistent with the view that the renin-angiotensin system is not an essential mechanism responsible for autoregulation of RBF in the rat.

Differential renal effects of cyclooxygenase inhibition in sodium-replete and sodium-deprived dog

1980 ◽  
Vol 239 (4) ◽  
pp. F360-F365 ◽  
Author(s):  
M. Cynthia Blasingham ◽  
Alberto Nasjletti
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Renin Angiotensin System ◽  
Receptor Blocker ◽  
Sodium Balance ◽  
Angiotensin System ◽  
Renal Effects ◽  
Renin Angiotensin ◽  
Arterial Blood

We studied the renal effects of the cyclooxygenase inhibitor sodium meclofenamate (M) (5 mg/kg, iv) in the pentobarbital-anesthetized dog that had been maintained on an elevated (100 meq/day) or on a reduced (<5 meq/day) sodium intake, and during the administration of angiotensin II in the sodium-replete dog, or the angiotensin receptor blocker [Sar1–Ala8]angiotensin II in the sodium-deprived dog. In the sodium-replete dog, M did not affect mean arterial blood pressure (MABP), renal blood flow (RBF), glomerular filtration rate (GFR), or urine volume (V), but reduced the urinary excretion of sodium (UNa V) by 47%, and of immunoreactive PGE2 (iPGE2) by 90%. However, in the sodium-replete dog during angiotensin II infusion (3 ng · kg-1 · min-1, iv), M reduced RBF by 35%, GFR by 24%, V by 71%, and iPGE2m by 94%. Similarly, in the sodium-deprived dog M reduced RBF by 34%, GFR by 28%, and iPGE2 excretion by 89%. However, M did not affect RBF or GFR in the sodium-deprived dog during infusion of [Sar1-Ala8]angiotensin II (6 μg · kg-1 · min-1, iv), although iPGE2 excretion was reduced by 84%. This study demonstrates that the effects of M on renal hemodynamics in the dog vary with the state of sodium balance and suggests that a prostaglandin(s) contributes to maintenance of renal blood flow during activation of the renin-angiotensin system. meclofenamate; renal prostaglandins; renin-angiotensin system; receptor blocker; renal hemodynamic and excretory function Submitted on October 17, 1979 Accepted on May 9, 1980

Effects of conjugated oestrogen and droloxifene on the renin-angiotensin system, blood pressure and renal blood flow in postmenopausal women

2004 ◽  
Vol 60 (3) ◽  
pp. 315-321 ◽  
Author(s):  
Ellen W. Seely ◽  
K. Bridget Brosnihan ◽  
Xavier Jeunemaitre ◽  
Kyoko Okamura ◽  
Gordon H. Williams ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Postmenopausal Women ◽  
Renal Blood Flow ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin
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