The effects of the angiotensin II antagonist saralasin on blood pressure and plasma aldosterone in man in relation to the prevailing plasma angiotensin II concentration. 1976

J J Brown, and W C Brown, and R Fraser, and A F Lever, and J J Morton, and J I Robertson, and E A Rosei, and P M Trust

The effect of saralasin in lowering blood pressure and plasma aldosterone concentration in normal subjects, both sodium-replete and sodium-deplete, and in patients with various forms of hypertension, is closely related to the basal plasma angiotensin II concentration. These findings confirm and extend earlier studies of angiotensin II/arterial pressure and angiotensin II/aldosterone dose-response curves. They also emphasize the importance of the renin-angiotensin system in the control of aldosterone in sodium depletion and in renal hypertension.

UI MeSH Term Description Entries
D006973 Hypertension Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more. Blood Pressure, High,Blood Pressures, High,High Blood Pressure,High Blood Pressures
D007676 Kidney Failure, Chronic The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION. ESRD,End-Stage Renal Disease,Renal Disease, End-Stage,Renal Failure, Chronic,Renal Failure, End-Stage,Chronic Kidney Failure,End-Stage Kidney Disease,Chronic Renal Failure,Disease, End-Stage Kidney,Disease, End-Stage Renal,End Stage Kidney Disease,End Stage Renal Disease,End-Stage Renal Failure,Kidney Disease, End-Stage,Renal Disease, End Stage,Renal Failure, End Stage
D008297 Male Males
D012078 Renal Artery Obstruction Narrowing or occlusion of the RENAL ARTERY or arteries. It is due usually to ATHEROSCLEROSIS; FIBROMUSCULAR DYSPLASIA; THROMBOSIS; EMBOLISM, or external pressure. The reduced renal perfusion can lead to renovascular hypertension (HYPERTENSION, RENOVASCULAR). Renal Artery Stenosis,Obstruction, Renal Artery,Obstructions, Renal Artery,Renal Artery Obstructions,Renal Artery Stenoses,Stenoses, Renal Artery,Stenosis, Renal Artery
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
D001794 Blood Pressure PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS. Systolic Pressure,Diastolic Pressure,Pulse Pressure,Pressure, Blood,Pressure, Diastolic,Pressure, Pulse,Pressure, Systolic,Pressures, Systolic
D004032 Diet Regular course of eating and drinking adopted by a person or animal. Diets
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D006929 Hyperaldosteronism A condition caused by the overproduction of ALDOSTERONE. It is characterized by sodium retention and potassium excretion with resultant HYPERTENSION and HYPOKALEMIA. Aldosteronism,Conn Syndrome,Conn's Syndrome,Primary Hyperaldosteronism,Conns Syndrome,Hyperaldosteronism, Primary,Syndrome, Conn,Syndrome, Conn's
D000450 Aldosterone A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium. Aldosterone, (+-)-Isomer,Aldosterone, (11 beta,17 alpha)-Isomer

Related Publications

J J Brown, and W C Brown, and R Fraser, and A F Lever, and J J Morton, and J I Robertson, and E A Rosei, and P M Trust
November 1979, Nihon Jinzo Gakkai shi,
J J Brown, and W C Brown, and R Fraser, and A F Lever, and J J Morton, and J I Robertson, and E A Rosei, and P M Trust
February 1978, Clinical nephrology,
J J Brown, and W C Brown, and R Fraser, and A F Lever, and J J Morton, and J I Robertson, and E A Rosei, and P M Trust
June 1976, Circulation research,
J J Brown, and W C Brown, and R Fraser, and A F Lever, and J J Morton, and J I Robertson, and E A Rosei, and P M Trust
October 1979, Endocrinologia japonica,
J J Brown, and W C Brown, and R Fraser, and A F Lever, and J J Morton, and J I Robertson, and E A Rosei, and P M Trust
December 1976, Schweizerische medizinische Wochenschrift,
J J Brown, and W C Brown, and R Fraser, and A F Lever, and J J Morton, and J I Robertson, and E A Rosei, and P M Trust
January 1979, Acta medica Scandinavica,
J J Brown, and W C Brown, and R Fraser, and A F Lever, and J J Morton, and J I Robertson, and E A Rosei, and P M Trust
June 1990, American journal of hypertension,
J J Brown, and W C Brown, and R Fraser, and A F Lever, and J J Morton, and J I Robertson, and E A Rosei, and P M Trust
January 1981, Developmental pharmacology and therapeutics,
J J Brown, and W C Brown, and R Fraser, and A F Lever, and J J Morton, and J I Robertson, and E A Rosei, and P M Trust
April 1983, Clinical science (London, England : 1979),
J J Brown, and W C Brown, and R Fraser, and A F Lever, and J J Morton, and J I Robertson, and E A Rosei, and P M Trust
January 1979, Arzneimittel-Forschung,
Copied contents to your clipboard!