Captopril-Induced Functional Renal Insufficiency in Patients with Bilateral Renal-Artery Stenoses or Renal-Artery Stenosis in a Solitary Kidney

Hricik, Donald E.; Browning, Philip J.; Kopelman, Richard I.; Goorno, Warren E.; Madias, Nicolaos E.; Dzau, Victor J.

doi:10.1056/nejm198302173080706

Cited by 642 publications

(174 citation statements)

References 11 publications

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“…The conductance then remained near this level for the remainder of the experiment (for example, it averaged 20.1 ±5.4% below mean prestenosis values on days 21-25 [ Figure l];/?<0.01). In the sham-stenosis group, total peripheral conductance did not change significantly (+1.3±13.5%, NS from pre-sham-stenosis values on days [21][22][23][24][25].…”

Section: Responses To Left Renal Artery Stenosismentioning

confidence: 99%

Development of hypertension from unilateral renal artery stenosis in conscious dogs.

1990

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The renal and systemic changes after stenosis of the left renal artery (n=S) or sham stenosis (n=6) in conscious dogs were studied sequentially over 25 days. Stenosis produced a prompt rise in arterial pressure, which was at all times due to reduced peripheral vascular conductance, with no increase in cardiac output despite initial evidence of mild fluid retention. The decrease in peripheral conductance was attributable to 1) the stenotic kidney (25% of the total and due to the mechanical effect of the stenosis itself), 2) the nonstenotic kidney (about 15% of the total and not caused by angiotensin II), and 3) the nonrenal vasculature (60%). The decrease in conductance in the nonrenal vasculature was due partly to angiotensin II, but there was also a gradually developing non-angiotensin II component Acute administration of captopril caused significantly greater changes in arterial pressure and peripheral conductance throughout the period of stenosis than before stenosis (and greater than in sham-stenosis dogs), indicating that angiotensin II was constricting the peripheral vasculature even when plasma renin levels were no longer elevated. In the stenotic kidneys, captopril produced a fall in renal vascular resistance, but renal blood flow did not rise because there was an approximately equal rise in the resistance of the stenosis. There was no evidence for a role for the autonomic nervous system in the hypertension, as ganglion blockade (pentolinium) had similar hemodynamic effects before and after stenosis. Thus, the hypertension was due at all times to reduced peripheral conductance, with the two kidneys responsible for 40% of this reduced conductance. (Hypertension 1990;16:441-451) U nilateral renal artery stenosis produces hypertension in humans and in experimental animals, including rats (see Reference 1), sheep, 2 and dogs, 3 " 5 provided that the stenosis is severe enough. 4 Evidence from previous experiments suggests that both the renin-angiotensin system and the autonomic nervous system are involved in the development of this two-kidney, one clip (2K 1C) form of hypertension. 8 However, gaining a complete understanding of the early stages of the hypertension has been complicated by the fact that stenosis has, with very few exceptions, been induced during surgery in anesthetized animals. Surgery itself disturbs the renin-angiotensin system, autonomic reflexes, and body fluid homeostasis, 9 the very factors thought to be involved in the initiation and development of hypertension.We recently published a comprehensive analysis of the hemodynamic events involved in the first hour of Received October 11, 1989; accepted in revised form May 25, 1990. this form of renal hypertension in conscious dogs. 10This showed that the initial rise in arterial pressure was due entirely to decreased peripheral vascular conductance (increased resistance) and, remarkably, that the kidneys themselves were responsible for almost half of this fall in conductance. In the case of the stenotic kidney, its conductance was reduced...

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Section: Responses To Left Renal Artery Stenosismentioning

confidence: 99%

Development of hypertension from unilateral renal artery stenosis in conscious dogs.

1990

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“…This angiotensindependent, highly susceptible group is now well characterized, and includes hypovolaemic and hyponatraemic patients as well as patients on high doses of diuretics (Packer et al, 1984). Particularly at risk are patients with severe congestive heart failure (Cleland et al, 1984(Cleland et al, , 1985Mujais et al, 1984) and hypertensive individuals with bilateral renal artery stenosis or stenosis of the artery to a single remaining kidney (Hrick et al, 1983). These are the patients who should start therapy with a low dose of ACE inhibitor under close medical supervision.…”

Section: Undesirable Effectsmentioning

confidence: 99%

Lisinopril: dose‐peak effect relationship in essential hypertension.

Cirillo

Gómez

Salonen

et al. 1988

Brit J Clinical Pharma

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3 Lisinopril 10 and 20 mg day-' produced similar peak antihypertensive effects which were greater than that produced by 2.5 mg day-1, but less than that of 80 mg day-'. If the incidence of first-dose symptomatic hypotension is related to the peak effect, then an initial lisinopril dose of 20 mg should not pose any greater risk than a 10 mg dose. 4 The magnitude of antihypertensive response at 24 h postdrug appeared to be dose related across the 2.5 to 80 mg day-' range.

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“…However, in patients receiving ACE inhibitors, this compensatory response would not be expected to occur, suggesting that in acceleratedmalignant hypertension, blockade of the reninangiotensin system might lead to a deterioration of renal function. In previous reports (26,28,29), azotemia induced by captopril was reversible after withdrawal of the agent. This suggests that a marked decrease in efferent arteriolar tone induced by ACE inhibitors would result in a reduction of glomerular filtration rate in patients with acceleratedmalignant hypertension.…”

Section: Discussionmentioning

confidence: 75%

“…However, contrary to our expectations, in our preliminary experiments, the addition of an ACE inhibitor to a calcium antagonist resulted in a gradual deterioration of renal function. An association between ACE inhibitor therapy and acute renal deterioration has been noted in bilateral renal diseases that are characterized by prominent renovascular involvement (26). In this study, we did not recommend renal angiography because of the risk of contrast exposure during the malignant phase; however, when renal arterial stenosis was strongly suspected, investigations for renovascular hypertension were carried out using ultrasonography and magnetic resonance imaging angiography.…”

Section: Discussionmentioning

confidence: 97%

Nifedipine and Arotinolol in Combination for Accelerated-Malignant Hypertension: Results of One Year Follow-Up.

et al. 1999

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The effects of a combined therapy with a calcium channel antagonist and a$-blocker in patients with accelerated-malignant hypertension on blood pressure and renal function were examined. Thirteen patients presented with the clinical features of malignant hypertension (diastolic blood pressure >130 mmHg, retinal damage and progressive renal failure) at our hospital, over the 3 yr period from 1995 to 1997. These patients were treated with both a calcium antagonist, 60-80 mg/d dose of long acting nifedipine, and an a/9-blocker, 20 mg/d dose of arotinolol, for over 12 mo. At admission, the average blood pressure of the patients was 233 ± 8/144 ± 3 mmHg. The level of serum creatinine in these patients was 6.2 ± 1.0 mg/dl. Intermittent hemodialysis therapy was introduced in 7 patients. Three days after treatment, blood pressure decreased to 162 ± 4/ 102 ± 4 mmHg. A month later, blood pressure decreased to 148 ± 3/89 ± 2 mmHg and serum creatinine levels were 3.6 ± 0.4 mg/dl. Renal function in these patients improved, and they completely recovered from renal dysfunction, allowing withdrawal of haemodialysis therapy. One year later, the blood pressure in all of these patients was well controlled and no further renal deterioration was observed, except in one patient. Despite the reduction in blood pressure, one patient was on hemodialysis three times a week after 8 mo of treatment. From these finding, it is concluded that combination therapy with a calcium antagonist and ai9-blocker is effective in both the reduction of highly elevated blood pressure and protection of the kidneys, resulting in amelioration of accelerated-malignant hypertension. (Hypertens Res 1999; 22: 75-'80)

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Captopril-Induced Functional Renal Insufficiency in Patients with Bilateral Renal-Artery Stenoses or Renal-Artery Stenosis in a Solitary Kidney

Cited by 642 publications

References 11 publications

Development of hypertension from unilateral renal artery stenosis in conscious dogs.

Development of hypertension from unilateral renal artery stenosis in conscious dogs.

Lisinopril: dose‐peak effect relationship in essential hypertension.

Nifedipine and Arotinolol in Combination for Accelerated-Malignant Hypertension: Results of One Year Follow-Up.

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