TY - JOUR
T1 - Role of renal kallikrein in modulating the antihypertensive effect of a single oral dose of captopril in normal- and low-renin essential hypertensives
AU - Madeddu, Paolo
AU - Oppos, Mario
AU - Rubattu, Speranza
AU - Dessi’-Fulgheri, Paolo
AU - Glorioso, Nicola
AU - Soro, Aldo
AU - Rappelli, Alessandro
PY - 1987
Y1 - 1987
N2 - The antihypertensive efficacy of angiotensin converting enzyme (ACE) inhibitors may result from the blockade of angiotensin II formation but also, theoretically, from the inhibition of kinin breakdown. To test whether a blunted activity of the kallikrein-kinin system might account for the failure of ACE inhibitors in lowering blood pressure (BP) in patients in whom the renin-angiotensin system (RAS) is not enhanced, 31 essential hypertensives with normal or low plasma renin activity (PRA) were evaluated before and after a single oral dose (50 mg) of captopril. A significant fall, in both systolic and diastolic BP, was obtained in the subgroup of patients who were classified as ‘normal- kallikrein hypertensives’ according to whether their pretreatment urinary kallikrein excretion was within the normal range, while no significant change in BP was observed in ‘low-kallikrein hypertensives’. Furthermore, the mean percentage fall in mean BP, throughout the 2 h following captopril administration, was significantly related to the basal value of urinary kallikrein excretion (r = 0.47, P <0.05) in all the patients. Our results suggest that blunted activity of the kallikrein system might be responsible for failure of captopril to lower BP in some hypertensive patients.
AB - The antihypertensive efficacy of angiotensin converting enzyme (ACE) inhibitors may result from the blockade of angiotensin II formation but also, theoretically, from the inhibition of kinin breakdown. To test whether a blunted activity of the kallikrein-kinin system might account for the failure of ACE inhibitors in lowering blood pressure (BP) in patients in whom the renin-angiotensin system (RAS) is not enhanced, 31 essential hypertensives with normal or low plasma renin activity (PRA) were evaluated before and after a single oral dose (50 mg) of captopril. A significant fall, in both systolic and diastolic BP, was obtained in the subgroup of patients who were classified as ‘normal- kallikrein hypertensives’ according to whether their pretreatment urinary kallikrein excretion was within the normal range, while no significant change in BP was observed in ‘low-kallikrein hypertensives’. Furthermore, the mean percentage fall in mean BP, throughout the 2 h following captopril administration, was significantly related to the basal value of urinary kallikrein excretion (r = 0.47, P <0.05) in all the patients. Our results suggest that blunted activity of the kallikrein system might be responsible for failure of captopril to lower BP in some hypertensive patients.
KW - ACE inhibitors
KW - Kallikrein
KW - Renin
UR - http://www.scopus.com/inward/record.url?scp=0023622548&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0023622548&partnerID=8YFLogxK
M3 - Article
C2 - 3323316
AN - SCOPUS:0023622548
VL - 5
SP - 645
EP - 648
JO - Journal of Hypertension
JF - Journal of Hypertension
SN - 0263-6352
IS - 6
ER -