Parallel renal and extremity blood supply abnormalities in nonmodulation: responses to ACE inhibition.
The aim of this work was to ascertain, in nonmodulating essential hypertension, whether the abnormality in the renal blood supply is extended to the extremities and showed a similar response to ACE inhibition and whether these abnormalities could be identified in normotensive offspring of hypertensives, as non-modulation is a familial process with genetic underpinnings. We measured forearm vascular blood flow (FBF) and forearm vascular resistance (FVR) by plethysmography and urinary albumin excretion in 20 normotensive without family story of hypertension (NT: 25+/-9 years), 10 modulating offspring of hypertensive parents (MHO: 25+/-6 years), 10 nonmodulating offspring of hypertensive parents (NMHO: 26+/-5 years), 12 modulating essential hypertensives (MHT: 34+/-5 years), and 11 nonmodulating essential hypertensives (NMHT: 32+/-4 years). Measurements were repeated in hypertensives after 3-month treatment with ramipril (5 mg daily). Nonmodulating individuals showed lower maximum FBF (NMHT: 41.96+/-3.3 mL/100 g per minute and NMHO: 35.6+/-9.0 mL/100 g per minute) than modulating subjects (MHT: 57.5+/-10.0 mL/100 g per minute and MHO: 51.8+/-7.0 mL/100 g per minute; P<0.003). Likewise, all nonmodulating subjects showed higher minimum FVR (NMHT: 2.5+/-0.2 AU; NMO: 2.8+/-0.5 AU) than modulating individuals (MHT: 1.9+/-0.5 AU; MHO, 1.8+/-0.3AU; P<0.025). Urinary albumin excretion was higher in NMHT and NMHO than MHT, MHO, and NT (P<0.05). Ramipril increased maximum FBF to 53.8+/-8.0 mL/100 g per minute and reduced minimum FVR to 1.9+/-0.5 AU in NMHT (P<0.01). Likewise, ramipril increased effective renal plasma flow and reduced renal vascular resistance and urinary albumin excretion only in NMHT (P<0.05). These results have shown an early involvement of the peripheral circulation in association with increased urinary albumin excretion not only in essential hypertensives but also in NMHO. The effectiveness of ramipril in reducing minimum FVR and urinary albumin excretion in NMHT also suggests a common mechanism.
Sánchez
Ramiro A
RA
Sección Hipertensión Arterial, Instituto de Cardiología y Cirugía Cardiovascular, Fundación Favaloro, Belgrano 1746, (1093) Buenos Aires, Argentina. rsanchez@ffavaloro.org
Ramos
Felipe
F
Giannone
Carlos
C
Fischer
Patricia
P
Masnatta
Lucas
L
Baglivo
Hugo P
HP
Ramírez
Agustín J
AJ
Hollenberg
Norman K
NK
D000328:Adult; D000419:Albuminuria / Q000175:diagnosis; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D005192:Family Health; D005260:Female; D005542:Forearm / Q000098:blood supply*; D005919:Glomerular Filtration Rate; D006801:Humans; D006973:Hypertension / Q000235:genetics / Q000503:physiopathology*; D008297:Male; D010991:Plethysmography; D017257:Ramipril / Q000494:pharmacology*; D012039:Regional Blood Flow / Q000187:drug effects; D012079:Renal Circulation / Q000187:drug effects*; D012964:Sodium / Q000008:administration & dosage; D014655:Vascular Resistance / Q000187:drug effects
D000806:Angiotensin-Converting Enzyme Inhibitors; D012964:Sodium; D017257:Ramipril