Redistribution of regional blood flow following angiotensin-converting enzyme inhibition. Comparison of normal subjects and patients with heart failure. 1984

D P Faxon, and M A Creager, and J L Halperin, and D B Bernard, and T J Ryan

The systemic and regional circulatory effects of angiotensin-converting enzyme inhibition were investigated in 30 normal subjects and in 36 patients with severe congestive heart failure. Regional blood flow was measured in individual patient groups. Cardiac index rose and systemic vascular resistance fell in normal subjects after angiotensin-converting enzyme inhibition. In the patients with heart failure, a similar rise in cardiac index and fall in systemic resistance occurred. In addition, right and left ventricular filling pressures decreased. The fall in systemic vascular resistance correlated with plasma renin activity (r = 0.57, p less than or equal to 0.001). Of the regional circulations investigated in normal subjects, only forearm blood flow increased after angiotensin-converting enzyme inhibition. Although over-all there was no change in renal or coronary blood flow, coronary flow dramatically increased in some patients and the increase in flow correlated with plasma renin activity (r = 0.939, p less than or equal to 0.001). In patients with heart failure, forearm, splanchnic, and coronary flow were unaffected by angiotensin-converting enzyme inhibition, whereas renal blood flow estimated from para-aminohippurate clearance increased 60 percent and accounted for 50 percent of the increase in cardiac output seen in these patients. Thus, redistribution of flow occurs in congestive heart failure with a significant reduction in the fraction flow to the kidneys when compared with normal flow. The contribution of the renin-angiotensin system to the regulation of regional blood flow is different in normal subjects and in patients with heart failure. Angiotensin-converting enzyme inhibition augments skeletal flow in normal subjects whereas it increases renal blood flow in patients with heart failure.

UI MeSH Term Description Entries
D009842 Oligopeptides Peptides composed of between two and twelve amino acids. Oligopeptide
D011392 Proline A non-essential amino acid that is synthesized from GLUTAMIC ACID. It is an essential component of COLLAGEN and is important for proper functioning of joints and tendons. L-Proline,L Proline
D012039 Regional Blood Flow The flow of BLOOD through or around an organ or region of the body. Blood Flow, Regional,Blood Flows, Regional,Flow, Regional Blood,Flows, Regional Blood,Regional Blood Flows
D012079 Renal Circulation The circulation of the BLOOD through the vessels of the KIDNEY. Kidney Circulation,Renal Blood Flow,Circulation, Kidney,Circulation, Renal,Blood Flow, Renal,Flow, Renal Blood
D012083 Renin A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC 3.4.99.19. Angiotensin-Forming Enzyme,Angiotensinogenase,Big Renin,Cryorenin,Inactive Renin,Pre-Prorenin,Preprorenin,Prorenin,Angiotensin Forming Enzyme,Pre Prorenin,Renin, Big,Renin, Inactive
D012084 Renin-Angiotensin System A BLOOD PRESSURE regulating system of interacting components that include RENIN; ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; ANGIOTENSIN I; ANGIOTENSIN II; and angiotensinase. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I. Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II, an extremely powerful vasoconstrictor. Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure. In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney. Angiotensin-converting enzyme also breaks down BRADYKININ, a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM. Renin-Angiotensin-Aldosterone System,Renin Angiotensin Aldosterone System,Renin Angiotensin System,System, Renin-Angiotensin,System, Renin-Angiotensin-Aldosterone
D002216 Captopril A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin. (S)-1-(3-Mercapto-2-methyl-1-oxopropyl)-L-proline,Capoten,Lopirin,SQ-14,225,SQ-14,534,SQ-14225,SQ-14534,SQ 14,225,SQ 14,534,SQ 14225,SQ 14534,SQ14,225,SQ14,534,SQ14225,SQ14534
D002302 Cardiac Output The volume of BLOOD passing through the HEART per unit of time. It is usually expressed as liters (volume) per minute so as not to be confused with STROKE VOLUME (volume per beat). Cardiac Outputs,Output, Cardiac,Outputs, Cardiac
D003326 Coronary Circulation The circulation of blood through the CORONARY VESSELS of the HEART. Circulation, Coronary
D005542 Forearm Part of the upper extremity in humans and primates extending from the ELBOW to the WRIST. Antebrachium,Antebrachiums,Forearms

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