Estimating renin participation in hypertension: Superiority of converting enzyme inhibitor over saralasin

Case, David B.; Wallace, John M.; Keim, Hans J.; Weber, Michael A.; Drayer, Jan I.M.; White, Robert P.; Sealey, Jean E.; Laragh, John H.

doi:10.1016/0002-9343(76)90160-1

Cited by 166 publications

(30 citation statements)

References 12 publications

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“…The strong response to ACE inhibition in group 1 could not be explained by differences of sodium excretion, age, or aldosterone concentrations (Tables 1,2). Despite nearly identical baseline renin activities, the responses to ACE inhibition in group 1 are comparable to those in high-renin hypertensive patients described by previous investigators [6,[10][11][12][13]. The slightly elevated aldosterone in group 1 seems to be related to the overall increased renin concentration.…”

Section: Discussionsupporting

confidence: 80%

Renal haemodynamics and organ damage in young hypertensive patients with different plasma renin activities after ACE inhibition

Erley¹,

Holzer²,

Krämer³

et al. 1992

Nephrology Dialysis Transplantation

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Abstract. We describe our observations concerning differences in two groups of young hypertensive patients according to their renin activities after ACE inhibition. Seventeen of these patients (age 26 ±7 years), so far untreated, were investigated prospectively for hormone levels (renin, aldosterone, vasopressin), microalbuminuria, renal haemodynamics (inulin and PAH clearance) and signs of organ damage (echocardiography, fundoscopy). Secondary forms of hypertension were excluded by routine methods, including angiography. We differentiated two groups of young hypertensive patients. Group 1 (n = 9) had a false positive captopril test with elevated renin activities after ACE inhibition with captopril (8.4±5 ng/ml per hour) compared to group 2 (renin activity: 2.2 ± 1.3 ng/ml per hour) or an increase of >400% of renin activity after ACE inhibition. Baseline renin activities and sodium excretion did not differ between the groups. Group 1 also showed significantly greater GFR, FF, and microalbuminuria, as well as signs of organ damage, with left ventricular hypertrophy and hypertensive changes in fundoscopy. There were no differences between the groups concerning mean arterial blood pressure and duration of hypertension. In conclusion, we were able to demonstrate that patients with highly stimulated renin activities showed signs of visceral organ damage and renal hyperfiltration compared to the normal renin activity group after ACE inhibition. Investigations of the reninangiotensin-aldosterone system with ACE inhibitors Correspondence and offprint requests to Christiane M Erley. MD. University of Tuebingen, Medical Section III. Otfned-Muller-Str 10. 7400 Tuebingen. Gcrman>. might constitute a helpful indicator of renal changes and organ damages in young hypertensive patients.

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Section: Discussionsupporting

confidence: 80%

Renal haemodynamics and organ damage in young hypertensive patients with different plasma renin activities after ACE inhibition

Erley¹,

Holzer²,

Krämer³

et al. 1992

Nephrology Dialysis Transplantation

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“…In contrast, with saralasin infusion renin could be implicated in only 10% of these patients. 11 In the light of the present work, the observation that CEI infusion produces no fall in blood pressure in patients with low renin levels and in anephric patients" cannot be interpreted as indicating that CEI modifies blood pressure only by its effect on angiotensin II production.…”

Section: Discussionmentioning

confidence: 52%

“…Another recent paper has demonstrated such a discrepancy, which was attributed to the agonist action of saralasin. 11 Therefore it was concluded that CEI is superior as a scientific tool. Of crucial relevance is the significance of the bradykinin-potentiating action of CEI.…”

mentioning

confidence: 99%

Converting enzyme inhibitor and saralasin infusion in rats. Evidence for an additional vasodepressor property of converting enzyme inhibitor.

Thurston¹,

Swales²

1978

Circulation Research

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SUMMARY Converting enzyme inhibitor (CEI) produced a greater fall in blood pressure (BP) than the competitive antagonist of angiotensin II, sarcosine-alanine angiotensin II (saralasin), when administered to saltdepleted rats; there was no difference in BP response in salt-loaded rats. Thus, two widely used methods of inhibiting the renin-angiotensin system give discrepant effects. The renin-angiotensin system was blocked in anesthetized rats by an infusion of saralasin, and then a bolus injection of CEI was given. A further significant fall in blood pressure occurred in salt-depleted rats (-45.7 ± 6.8 mm Hg; mean ± SE). There was only a small change in blood pressure of salt-loaded rats (-11.2 ± 3.1 mm Hg) and no change in blood pressure of salt-depleted rats 1 hour after bilateral nephrectomy. Saralasin infusion after CEI did not influence BP. Bradykinin infusion potentiated the depressor effect of CEI in bilaterally nephrectomized rats. Renin infusion restored the depressor response of nephrectomized rats to saralasin, but administration of CEI then caused no further fall in BP. BP of saralasin-infused rats with Goldblatt two-kidney hypertension given CEI fell by 11.1 ± 5 . 4 mm Hg; after dietetic salt depletion, BP fell by 20.5 ± 9.9 mm Hg with CEI. Bilateral nephrectomy abolished this response to CEI. Hence, CEI has a significant vasodepressor action in addition to inhibition of angiotensin II production. Since it can be restored in nephrectomized animals by bradykinin infusion, the component of the vasodepressor action of CEI which cannot be blocked by saralasin may be identical with its bradykinin-potentiating action. If so, changes in the renal kallikrein bradykinin system may have an important role in BP control in response to changes in sodium balance and in hypertension.

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“…18 We observed that administration of both blockers resulted in almost no blood pressure reduction in the lesioned groups, compared to the appropriate controls both when AV3V lesion preceded or followed AV38 AND RENIN-ANGIOTENSIN SYSTEM INTERACTION/A/arso/i et al…”

Section: Discussionmentioning

confidence: 78%

Anteroventral third ventricle and renin-angiotensin system interaction in the two-kidney, one clip hypertensive rat.

Marson¹,

Saragoça²,

Ribeiro³

et al. 1983

Hypertension

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SUMMARY To test the peripheral mechanisms of prevention and reversal of two-kidney, one clip (2K1C) hypertension in the rat by lesion of the anteroventral third ventricle (AV3V) region, we studied blood pressure responses in rats to AV3V lesion produced before (n = 8) or after (n = 8) clipping the left renal artery. Two groups of sham-lesioned, clipped rats (n = 9 each) served as controls. At the end of the experiments, saralasin and captopril were given to evaluate the angiotensin-dependent component of blood pressure. To study the influence of the procedures on plasma renin activity (PRA), two parallel groups of rats (n = 26 and 24, respectively) were submitted to similar surgical protocols. We observed that increases in blood pressure were significantly smaller in the previously lesioned compared to previously sham-lesioned animals (ABP = 21.5 ± 3.7 vs 32.9 ± 2.5 mm Hg, p < 0.01); also, AV3V lesion almost completely reversed hypertension (BP from 167.5 ± 2.9 to 136.0 ± 4 . 1 mm Hg, p < 0.001), which was not observed in the sham-lesioned animals (BP from 172.0 ± 2.8 to 168 ± 2.7 mm Hg, NS).Saralasin produced a significantly smaller decrease in BP in the lesioned animals compared to those with sham lesions during both prevention and reversal experiments. Similar results were observed with captopril. Previous AV3V lesion did not significantly affect PRA with clipping of the renal artery, but AV3V destruction after hypertension had been established resulted in significantly lower PRA compared to sham-lesioned animals (4.58 ± 0.72 vs 8.38 ± 1.79, respectively, p < 0.001). It is concluded that, besides being an important central site of angiotensin action, the AV3V area is also important in the pathophysiology of 2K1C hypertension because it acts in the regulation of the peripheral production and action of angiotensin II in this model. 1 "* Those models in which the renin-angiotensin system plays a central pathophysiologic role are especially susceptible to prevention or reversal by discrete lesions of the AV3V region.5 " 6Interruption of a central action of peripherally gener-

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Estimating renin participation in hypertension: Superiority of converting enzyme inhibitor over saralasin

Cited by 166 publications

References 12 publications

Renal haemodynamics and organ damage in young hypertensive patients with different plasma renin activities after ACE inhibition

Renal haemodynamics and organ damage in young hypertensive patients with different plasma renin activities after ACE inhibition

Converting enzyme inhibitor and saralasin infusion in rats. Evidence for an additional vasodepressor property of converting enzyme inhibitor.

Anteroventral third ventricle and renin-angiotensin system interaction in the two-kidney, one clip hypertensive rat.

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