Acute renal haemodynamic and renin‐angiotensin system responses to graded renal artery stenosis in the dog.

Anderson, Warwick P.; Johnston, Colin I.; Korner, Paul I.

doi:10.1113/jphysiol.1979.sp012656

Cited by 42 publications

(42 citation statements)

References 26 publications

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“…The restoration cuts short the initial renal vasodilator response to acute stenosis. The restorative phase involves constriction of the renal vasculature and is prevented by pretreatment with CEI and with Sar 1 , He 8 All, 5 indicating that it is due to the intrarenal constrictor effects of AIL The opposing effects on RBF of the initial vasodilatation and the subsequent All-mediated vasoconstriction are most obvious at the mildest levels of stenosis, where no changes in systemic arterial pressure were detected. Thus, during reduction of renal artery pressure to only 60 mm Hg, RBF first falls slightly as described in detail previously, 6 then returns to control levels over the next few minutes as further renal vasodilation occurs, and finally falls again as renal vascular resistance and renal artery pressure rise.…”

Section: Discussionmentioning

confidence: 99%

“…However, if the renal vasculature was constricted under these circumstances by intrarenal infusion of exogenous All, effective stenosis resistance fell but rose again when All infusion stopped. 5 In the 7-day stenosis experiments, leakage cannot be absolutely excluded, but is unlikely in view of the complete recovery of the saline used to inflate the cuff. Moreover, the pressure in the inflated perivascular cuff is very high (between 700-800 mm Hg) 5 and the inflated cuffs are taut and fairly rigid.…”

Section: Discussionmentioning

confidence: 99%

“…5 In the 7-day stenosis experiments, leakage cannot be absolutely excluded, but is unlikely in view of the complete recovery of the saline used to inflate the cuff. Moreover, the pressure in the inflated perivascular cuff is very high (between 700-800 mm Hg) 5 and the inflated cuffs are taut and fairly rigid. The amount of extra fluid is about 25% greater after repeated reduction to 20 mm Hg in the distal renal artery pressure over the first hour of stenosis than after a single reduction of pressure.…”

Section: Discussionmentioning

confidence: 99%

“…2b). 5 The relationship between renal artery pressure and A PRA at 15 minutes and at 30-45 minutes obtained from the data of individual dogs in the two grades of stenosis was approximately linear ( fig. 2c).…”

Section: Relationship Between Pra and Renal Artery Pressure In Mild Amentioning

confidence: 99%

“…8 Plasma renin activity (PRA) was only transiently elevated. 5 In this present investigation we have studied the relationship between the above renal effects and the development of systemic hypertension in four grades of renal artery stenosis. The results indicate that in the conscious dog it is only with very severe stenosis that restoration of distal renal artery pressure is slow and that systemic hypertension develops.…”

Section: L~*mentioning

confidence: 99%

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Acute angiotensin II-mediated restoration of distal renal artery pressure in renal artery stenosis and its relationship to the development of sustained one-kidney hypertension in conscious dogs.

Anderson¹,

Korner²,

Johnston³

1979

Hypertension

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SUMMARYThe effects of graded renal artery stenosis on renal and systemic hemodynamics and plasma renin activity (PRA) were studied in conscious, chronically instrumented dogs. In mild and moderate stenosis (following rapid reduction in distal renal artery pressure to 60 or 40 mm Hg) there was initial vasodilatibn followed by prompt restoration within 5-30 minutes of renal artery pressure and vascular resistance; changes in mean aortic pressure (MAP) were minimal. Both A PRA and A renal artery pressure were reciprocally related, the relationship reflecting renal "barostat" control of renin secretion in the conscious dog. Pretreatment with converting enzyme inhibitor before induction of stenosis prevented restoration of renal artery pressure during stenosis. With more severe stenosis, after lowering renal artery pressure to 20 mm Hg, the latter took 2 to 3 days to become fully restored. The MAP rose 18.2 ± 2.5 by the end of 30 minutes but had declined to control by the second or third day. The A PRA during the first hour of stenosis was greater than accounted for by the fall in renal artery pressure, but by Days 2-7 PRA appeared to be predominantly under renal "barostat" control.With even more severe stenosis, systemic MAP remained elevated and after 7 days was 39 ± 14 mm Hg above control levels; PRA also stayed above control levels despite restoration of renal artery pressure, suggesting that it was controlled by factors additional to the "barostat" mechanism. The rise in renal artery pressure was now mainly determined by the increase in systemic MAP. Renal "barostat"-mediated increase in renin-angiotensin activity appears to be the main mechanism that restores renal artery pressure with mild stenosis, while in severe stenosis this is accomplished by development of systemic hypertension. Young and colleagues 1 have suggested that an appropriate hydraulic model is a nonlinear stenosis resistance in series with the resistance of the distal vascular bed. To achieve a given pressure drop experimentally across a stenosis, a greater reduction in vessel diameter will be required when the distal vascular bed is constricted than when it is dilated. There has been relatively little analysis of the hemodynamic events following acute renal artery stenosis in conscious animals, since this requires instrumented preparations in which arterial pressures and renal blood flow can be measured simultaneously and continuously. We have recently performed such an analysis in conscious dogs and have found that immediately upon induction of stenosis there was renal vasodilatation which was followed within minutes by angiotensin II-mediated restoration of renal vascular resistance and renal artery pressure.8 Plasma renin activity (PRA) was only transiently elevated. 5In this present investigation we have studied the relationship between the above renal effects and the development of systemic hypertension in four grades of renal artery stenosis. The results indicate that in the conscious dog it is only with very severe stenosis that restor...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Relationship Between Pra and Renal Artery Pressure In Mild Amentioning

confidence: 99%

Section: L~*mentioning

confidence: 99%

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Acute angiotensin II-mediated restoration of distal renal artery pressure in renal artery stenosis and its relationship to the development of sustained one-kidney hypertension in conscious dogs.

Anderson¹,

Korner²,

Johnston³

1979

Hypertension

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Blood Flow, Oxygenation, and Oxidative Stress in the Post-stenotic Kidney

Evans

O’Connor

2014

Renal Vascular Disease

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Renal ischemia, hypoxia and oxidative stress progress together over the course of renovascular disease, and thus appear to operate in a vicious pathological triangle. Renal ischemia is initially driven by the mechanical effect of the stenosis, and maintained in the medium term chiefl y by activation of the systemic and intrarenal renin-angiotensin systems. In the longer term, ischemia is exacerbated by infl ammation, fi brosis and microvascular rarefaction, at least partly driven by signaling cascades initiated by oxidative stress and tissue hypoxia. Oxidative stress in renovascular disease is initially driven by activation of the renin-angiotensin system, but other factors, such as the pro-oxidant effects of uremic toxins, likely also contribute in the longer term. Oxidative stress drives ischemia by the direct vasoconstrictor effects of reactive oxygen species such as superoxide, and through reduced bioavailability of the vasodilator nitric oxide. This microvascular dysfunction appears to be a major driver of microvascular remodeling and rarefaction. Ischemia drives tissue hypoxia by reducing oxygen delivery to tissue. Oxidative stress and the resultant reduction in nitric oxide bioavailability also promote hypoxia by reducing the efficiency of oxygen utilization in mitochondria. Reduced glomerular fi ltration leads to reduced renal oxygen consumption, so provides some protection against the development of tissue hypoxia, at least in mild or early stage renovascular disease. But, eventually, homeostasis of tissue oxygenation cannot be maintained, and tissue hypoxia ensues.

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Atherosclerotic Renovascular Disease

Leeuw

Tsioufis

2020

Secondary Hypertension

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Acute renal haemodynamic and renin‐angiotensin system responses to graded renal artery stenosis in the dog.

Cited by 42 publications

References 26 publications

Acute angiotensin II-mediated restoration of distal renal artery pressure in renal artery stenosis and its relationship to the development of sustained one-kidney hypertension in conscious dogs.

Acute angiotensin II-mediated restoration of distal renal artery pressure in renal artery stenosis and its relationship to the development of sustained one-kidney hypertension in conscious dogs.

Blood Flow, Oxygenation, and Oxidative Stress in the Post-stenotic Kidney

Atherosclerotic Renovascular Disease

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