hypertension . Hemodynamic mechanism of blood pressure response to captopril in human malignant

The hemodynamic mechanism of blood pressure response to angiotensin blockade is well established in "benign" but not in human malignant hypertension. We studied the changes in mean arterial pressure (MAP), cardiac index (CI), pulmonary wedge pressure (PWP), and in plasma volume (PV) induced by a single oral dose of captopril (150 mg) in 11 patients with malignant hypertension. Two hours after captopril, MAP fell from 178.5 ± 5.8 to 151.8 ± 7.8 mm Hg (p < 0.001) (X ± SEM) due to a fall in total peripheral resistance (TPR) (from 54.8 ± 6.8 to 46.4 ± 1.6 arbitrary units, p < 0.001). However, there was a simultaneous increase in CI (from 3.29 ± 0.13 to 3.70 ± 0.15 llter/mln/m, p < 0.001), and a decrease in PWP (from 15.3 ± 3.5 to 11.0 ± 2.5 mm Hg, p < 0.001), while PV remained unchanged (from 4.02 ± 0.26 to 4.12 ± 0.12 liters, n.s.). Our data show that, in human malignant hypertension, blood pressure response to captopril is due to a decrease in TPR, but in contrast to benign hypertension, there is also a simultaneous increase in CI. Our results suggest that, in malignant hypertension, potentially high CI levels are artificially normalized by the increased TPR and may be fully disclosed by vasodilation. (Hypertension 5 (supp I): I-53-I-58, 1983)

[1]  J. Rouby,et al.  Resistance to sodium nitroprusside in hypertensive patients , 1982, Critical care medicine.

[2]  O. Kohlmann,et al.  [Treatment of hypertensive crisis with captopril]. , 1981, Arquivos brasileiros de cardiologia.

[3]  J. Laragh,et al.  Acute and Chronic Treatment of Severe and Malignant Hypertension with the Oral Angiotensin‐converting Enzyme Inhibitor Captopril , 1981, Circulation.

[4]  R. Carey,et al.  Acute and chronic effect of captropril in hypertensive patients. , 1980, Hypertension.

[5]  R. Cody,et al.  Hemodynamic and Volume Changes Associated with Captopril , 1980, Hypertension.

[6]  H. Gavras,et al.  Clinical Use of an Orally Acting Converting Enzyme Inhibitor: Captopril , 1980, Hypertension.

[7]  R. Tarazi,et al.  Contrasts and Similarities of Acute Hemodynamic Responses to Specific Antagonism of Angiotensin II ([Sar1, Thr8] A II) and to Inhibition of Converting Enzyme (Captopril) , 1980, Circulation.

[8]  A. Amery,et al.  Haemodynamic effects of captopril in hypertensive patients: comparison with saralasin. , 1979, Clinical science.

[9]  R. Tarazi,et al.  Renin, aldosterone and cardiac decompensation: studies with an oral converting enzyme inhibitor in heart failure. , 1979, The American journal of cardiology.

[10]  E. Sonnenblick,et al.  Treatment of chronic congestive heart failure with captopril, an oral inhibitor of angiotensin-converting enzyme. , 1979, The New England journal of medicine.

[11]  N. Hollenberg,et al.  Converting Enzyme Inhibition in Essential Hypertension: The Hypotensive Response Does Not Reflect Only Reduced Angiotensin II Formation , 1979, Hypertension.

[12]  A. Chobanian,et al.  Converting enzyme inhibition in hypertensive emergencies. , 1979, Annals of internal medicine.

[13]  J. Reid,et al.  The effect of SQ 14225 on baroreceptor reflex sensitivity in conscious normotensive rabbits [proceedings]. , 1978, British journal of pharmacology.

[14]  T. Waldron,et al.  Inhibition of Angiotensin-Converting Enzyme by SQ 14,225 in Anesthetized Dogs: Hernodynamic and Renal Vascular Effects , 1978, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.

[15]  R. Tarazi,et al.  Hemodynamic characteristics in hypertension. , 1978, Herz.

[16]  J. Möhring Pathogenesis of malignant hypertension: experimental evidence from the renal hypertensive rat. , 1975, Clinical nephrology.

[17]  C. Swartz,et al.  Hemodynamics of hypertension in uremia. , 1975, Kidney international. Supplement.

[18]  C. Ferrario,et al.  The unresolved nature of malignant hypertension. , 1974, Acta physiologica latino americana.

[19]  J. Laragh,et al.  Antihypertensive action of propranolol. Specific antirenin responses in high and normal renin forms of essential, renal, renovascular and malignant hypertension. , 1973, The American journal of cardiology.

[20]  A. Schwartz,et al.  Hemodynamics of Hypertension in Chronic End‐Stage Renal Disease , 1972, Circulation.

[21]  G. Shugoll,et al.  Follow-up observations and prognosis in primary myocardial disease. , 1972, Archives of internal medicine.

[22]  M. Neff,et al.  Hemodynamics of Uremic Anemia , 1971, Circulation.

[23]  A. Lever,et al.  Plasma renin concentration in human hypertension. , 1967, American heart journal.

[24]  D. Davies,et al.  Plasma Renin Concentration in Human Hypertension. 1: Relationship Between Renin, Sodium, and Potassium , 1965, British medical journal.

[25]  M. Chrétien,et al.  STUDIES ON THE RENIN-ANGIOTENSIN SYSTEM IN HYPERTENSIVE PATIENTS. , 1964, Canadian Medical Association journal.

[26]  E. A. Stead The role of the cardiac output in the mechanisms of congestive heart failure. , 1949, The American journal of medicine.