Angiotensin II Blockade before and after Marked Sodium Depletion in Patients with Hypertension

Vanhoogdalem, P; Donker, A. J. M.; Leenen, F. H.

doi:10.1042/cs0540075

Cited by 10 publications

(18 citation statements)

References 25 publications

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“…ANG II analogues with antagonistic actions, such as [Sar',Ala 8 ] -ANG II (Pals et al, 1971), have provided useful tools to elucidate angiotensin's role 1974;Streeten et al, 1975;Brown et al, 1976;Case et al, 1976;McGregor & Dawes, 1976;Fagard et al, 1977a, b;Noth et al, 1977;Posternak et al, 1977;Fagard et al, 1978c;Van Hoogdalem et al, 1978). However, saralasin possesses intrinsic agonistic angiotensin-like activities on the vascular smooth muscle, on the adrenal gland and possibly on the renal receptors involved in the direct suppression of renin by ANG II (Case et al, 1976;Hollenberg et al, 1976;McGregor & Dawes, 1976;Anderson et al, 1977;Bumpus & Khosla, 1977;Noth et al, 1977;Brown et al, 1978;Fagard et al, 1978a;Williams et al, 1978;Agabiti-Rosei et aI., 1979;Donker et al, 1979;Williams et al, 1979).…”

Section: Discussionmentioning

confidence: 98%

“…It has become clear that saralasin, particularly in sodium-replete conditions, may raise arterial pressure (Streeten et al, 1975;Case et al, 1976;Hollenberg, Williams, Burger, Ishikawa & Adams, 1976;McGregor & Dawes, 1976;Anderson, Streeten & Dalakos, 1977;Fagard et al, 1977a;Noth et al, 1977) and renal vascular resistance (Hollenberg et al, 1976), increase plasma aldosterone levels (Noth et al, 1977;Brown, Tucker, Tue, Wisgerhof & Salassa, 1978;Fagard, Lijnen, Amery & Reybrouck, 1978a;Williams, Hollenberg, Brown & Mershey, 1978;Agabiti-Rosei, Brown, Brown, Fraser, Trust, Lever, Morton & Robertson, 1979;Donker, Van Hoogdalem, Pratt & Leenen, 1979) and possibly suppress renin activity (Hollenberg et al, 1976;McGregor & Dawes, 1976;Noth et al, 1977;Williams et al, 1978). When plasma renin and angiotensin levels rise in response to sodium restriction blood pressure usually falls during saralasin (Brunner et aI., 1974;Streeten et al, 1975;Brown et al, 1976;Case et al, 1976;McGregor & Dawes, 1976;Fagard et al, 1977a;Noth et al, 1977;Posternak et al, 1977;Fagard et al, 1978c;Van Hoogdalem et al, 1978), plasma aldosterone decreases or remains unchanged (Brown et al, 1976;Noth et al, 1977;Brown et al, 1978;Fagard et al, 1978a;Williams et al, 1978;Agabiti-Rosei et al, 1979;Donker et aI., 1979;Williams, Hollenberg, Moore, Swartz & Dluhy, 1979) and ...…”

Section: Introductionmentioning

confidence: 94%

“…The antagonistic properties of angiotensin II (ANG II) analogues, such as [Sar 1,Ala8)ANG II (saralasin) (Pals, Masucci, Sipos & Denning, 1971) have been used to study the physiological (McGregor & Dawes, 1976;Fagard, Amery, Reybrouck, Lijnen, Moerman, Bogaert & De Schaepdryver, 1977b;Noth, Tan & Murrow, 1977' Posternak, Brunner, Gavras & Brunner, 1977Fagard, Amery, Reybrouck, Lijnen, Billiet, Bogaert, Moerman & De Schaepdryver, 1978c) and pathophysiological (Brunner, Gavras, Laragh & Keenan, 1974;Streeten, Freiberg, Anderson & Dalakos, 1975;Brown, Brown, Fraser, Lever, Morton, Robertson, Rosei & Trust, 1976;Case, Wallace, Keirn, Sealy & Laragh, 1976;Fagard, Amery, Lijnen & Reybrouck, 1977a;Van Hoogdalem, Donker & Leenen, 1978) role of ANG II in normo-and hyper-tension. However, saralasin and other analogues are not devoid of intrinsic agonistic angiotensin-like activity (Bumpus & Khosla, 1977) so that caution is required in the interpretation of the results.…”

Section: Introductionmentioning

confidence: 95%

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Angiotensin II and Sodium as Determinants of the Agonistic-Antagonistic Balance of Saralasin's Actions

1981

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1. To study which factors determine the balance between the antagonistic and agonistic effects of the angiotensin II analogue [Sar 1,Ala8)angiotensinII (saralasin) in man, saralasin was infused in subjects on a 'normal' sodium intake (group 1) and during sodium restriction with appropriately elevated plasma angiotensin II levels (group 2), and in sodiumrestricted subjects in whom plasma angiotensin II was suppressed by converting-enzyme inhibition with captopril (group 3).2. The saralasin-induced increase of plasma aldosterone concentration in group 1 was different (P < 0·()()5) from the decrease in group 2, whereas saralasin produced a significant increase of plasma aldosterone in group 3. For the three groups combined the changes of plasma aldosterone were significantly related to control angiotensin II levels, but not to the 24 h .ur~ary sodium excretion. The data suggest that It IS the rise of angiotensin II in response to the sodium restriction and not the sodium restriction per se that is associated with the antagonistic action of saralasin on the adrenal receptors.3. On average mean intra-arterial pressure at 30 min was not affected by saralasin in group I, had decreased in group 2 and increased (P < 0·001) by 4·4 mmHg in group 3. Overall the changes of arterial pressure were significantly related to control angiotensinII, but not to the 24 h sodium excretion, suggesting that the angiotensin II levels predominantly determine the agonisticCorrespondence: Dr R. Fagard, Cardiopulmonair Laboratorium, Inwendige Geneeskunde, Aca~emisch Ziekenhuis Pellenberg, B-3041 Pellenberg, Belgium.antagonistic balance of saralasin's actions on arterial pressure. 4. Although saralasin did not affect plasma renin activity in group I, plasma renin rose in group 2 and was reduced by 40% (P < O·()()I)in group 3. For the three groups together the changes of plasma renin activity were significantly related to the changes of mean arterial pressure both on single and multiple regression analyses. The changes of pressure 'explain', however, only a fraction of the changes of plasma renin' it is suggested that saralasin has an agonistic effect on the renal.receptor~invo~ved!n the direct suppression of renm by angiotensinII m low-sodium, low-angiotensin conditions and that an antagonistic effect may contribute to the saralasin-induced rise of renin during sodium restriction with appropriate angiotensin II levels.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 95%

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Angiotensin II and Sodium as Determinants of the Agonistic-Antagonistic Balance of Saralasin's Actions

1981

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“…* The significant influence of initial PRA on depressor responses to CEI in coarcted and control dogs conforms to previously reported findings in normotensive and hypertensive subjects for both CEI and All antagonists. 10 " 17 We are unaware of comparably analyzed data with which to compare our finding of an independent initial-pressure influence on CEI depressor responses.…”

Section: Discussionmentioning

confidence: 99%

Acute responses to arterial pressure and plasma renin activity to converting enzyme inhibition (SQ 20,881) in serially studied dogs with neonatally-induced coarctation hypertension.

Bagby¹

1982

Hypertension

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propriately "normal" (i.e., nonsuppressed) plasma renin activity (PRA) and normal renal function. 1 The abnormal renin/volume relationship in coarcted dogs is demonstrable at normal, low, and high steady-state sodium intakes.3 These observations are compatible with the hypothesis that coarctation hypertension is a renin-mediated process, initiated by balanced underperfusion of total renal mass via transient reninangiotensin excess, the latter generating volume expansion sufficient to normalize renal perfusion and thus PRA at a new steady state. 1To further assess the role of the renin-angiotensin system in coarctation hypertension, we serially examined acute arterial pressure and PRA responses to converting-enzyme inhibitor (CEI; SQ 20,881) in the same dogs during normal and low sodium intake. Concurrent study of littermate controls permitted quantitative analysis of normal CEI responses and comparision with results in coarcted dogs.

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“…However, in diuretic-and/or vasodilator-treated hypertension the elevated BP can become largely dependent on the renin-angiotensin system in many patients (for example , Pettinger et al 1973;Gavras et al, 1977;Hoogdalem et al, 1978). Blockade of renin release in these groups of patients offers a major antihypertensive mechanism.…”

Section: Possible Clinical Implicationsmentioning

confidence: 99%

Possible significance of the pharmacological differentiation of beta‐ blockers for therapy of hypertension.

Leenen¹

1979

Brit J Clinical Pharma

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1 Cardioselective and non-selective P-blockers affect to a different degree several aspects of the circulatory homeostasis. The evidence available in this regard has been evaluated and the possible clinical importance of these differences has been discussed.2 Venous return is partly regulated by P-receptors (possibly of the f2 type) in the venous resistance vessels. Differences in blockade of venous return by the two classes of P-blockers may, therefore, influence the degree of increase in left ventricular size, left ventricular end diastolic BPs and stroke volume during P-blockade.3 At the first part of the dose-response curve, non-selective f-blockers seem to block more effectively renin release than cardioselective P-blockers. 4 The direction and the extent to which P-blockers 'directly' affect total peripheral resistance (TPR), is determined by the resultant of the degree of decrease in TPR by blockade of renin release and the extent of the increase in TPR by blockade of the P2-receptors in the arteriolar wall.5 The clinical relevance of these differences could be that especially in the low doses range non-selective P-blockers may be more 'safe' in patients with compromised cardiac function and may be more appropriate for the therapy of high renin hypertension than cardioselective blockers, whereas the latter may be more appropriate for the majority of hypertensive patients who have lowto normal renin hypertension.

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Angiotensin II Blockade before and after Marked Sodium Depletion in Patients with Hypertension

Cited by 10 publications

References 25 publications

Angiotensin II and Sodium as Determinants of the Agonistic-Antagonistic Balance of Saralasin's Actions

Angiotensin II and Sodium as Determinants of the Agonistic-Antagonistic Balance of Saralasin's Actions

Acute responses to arterial pressure and plasma renin activity to converting enzyme inhibition (SQ 20,881) in serially studied dogs with neonatally-induced coarctation hypertension.

Possible significance of the pharmacological differentiation of beta‐ blockers for therapy of hypertension.

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