title: Effects of ANG-converting enzyme and alpha 1-adrenoceptor inhibition on intrarenal hemodynamics in SHR.
abstract: To investigate the prolonged effects of angiotensin-converting enzyme (ACE) inhibition and alpha 1-adrenoceptor blockade on intrarenal hemodynamics, whole kidney and renal micropuncture studies were performed in male 21-wk-old Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats treated for 3 wk with quinapril (3 mg/kg), terazosin (1 mg/kg), or in their combination (quinapril 1.5 mg/kg and terazosin 0.5 mg/kg). In WKY, only quinapril significantly reduced mean arterial pressure (MAP) associated with reduced afferent arteriolar resistance; there were no other significant changes. In contrast, all treatments similarly decreased MAP in SHR. Quinapril increased renal plasma flow and decreased filtration fraction. With respect to intrarenal hemodynamics, quinapril increased single-nephron plasma flow and reduced glomerular capillary pressure (from 53.1 to 47.8 mmHg; P < 0.01), associated with reduced afferent (from 4.80 to 3.17 10(10)dyn.s.cm-5; P < 0.01) and efferent (from 1.70 to 1.17 10(10)dyn.s.cm-5; P < 0.01) arteriolar resistances, and increased ultrafiltration coefficient (from 0.037 to 0.052 nl.s-1.mmHg-1; P < 0.05). Terazosin only reduced arteriolar resistance. The combined treatment attenuated either agent's independent effects on glomerular hemodynamics. These data demonstrate that prolonged ACE and adrenergic inhibition therapy alone or in combination produce different effects than when given by vein, suggesting that prolonged renopressor system inhibition may be more effective than adrenergic in SHR.
authors.affiliation: Hypertension Research Laboratories, Alton Ochsner Medical Foundation, New Orleans, Louisiana 70121.
authors.forename: A
authors.initials: A
authors.lastname: Numabe
authors.forename: K
authors.initials: K
authors.lastname: Komatsu
authors.forename: E D
authors.initials: ED
authors.lastname: Frohlich
mesh_terms: D058668:Adrenergic alpha-1 Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects; D004347:Drug Interactions; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D007546:Isoquinolines / Q000494:pharmacology*; D007668:Kidney / Q000098:blood supply / Q000187:drug effects / Q000502:physiology*; D007678:Kidney Glomerulus / Q000187:drug effects / Q000502:physiology; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D009399:Nephrons / Q000187:drug effects / Q000502:physiology; D011224:Prazosin / Q000031:analogs & derivatives* / Q000494:pharmacology; D000077583:Quinapril; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology; D012039:Regional Blood Flow / Q000187:drug effects; D012079:Renal Circulation / Q000187:drug effects*; D013045:Species Specificity; D044005:Tetrahydroisoquinolines; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D058668:Adrenergic alpha-1 Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D007546:Isoquinolines; D018340:Receptors, Adrenergic, alpha-1; D044005:Tetrahydroisoquinolines; C041226:Terazosin; D000077583:Quinapril; D011224:Prazosin