ABSTRACT
The purpose of this study was to examine the role of the renin-angiotensin system in mediating the hypertension in response to chronic reductions in uterine perfusion pressure (RUPP) in conscious chronically instrumented pregnant rats. Mean arterial pressure was significantly higher in pregnant rats with chronic RUPP (125+/-3.0 mm Hg, P<0.01, n=12) than in pregnant rats (100+/-2.3 mm Hg, n=17). Plasma renin activity in pregnant rats with chronic RUPP was 17.1+/-2.5 nmol angiotensin I. L(-1). h(-1) compared with 21.9+/-3.5 nmol angiotensin I. L(-1). h(-1) in pregnant rats. Chronic oral administration of a converting-enzyme inhibitor (enalapril, 250 mg/L for 6 days) decreased mean arterial pressure to a similar extent in pregnant rats with chronic RUPP (109+/-4.2 mm Hg, P<0.01, n=9) and in normal pregnant (81+/-1.8 mm Hg, P<0.01, n=9) rats. Blockade of the renin-angiotensin system, however, had no significant effect on the blood pressure response to chronic RUPP as differences were similar in control (Delta25 mm Hg) and converting-enzyme inhibitor-treated (Delta27 mm Hg) groups. These findings suggest that the renin-angiotensin system does not play a major role in mediating the hypertension produced by chronic RUPP in pregnant rats.
Subject(s)
Angiotensin II/antagonists & inhibitors , Hypertension/physiopathology , Uterus/blood supply , Angiotensin II/biosynthesis , Angiotensin-Converting Enzyme Inhibitors/pharmacology , Animals , Animals, Newborn , Blood Pressure/drug effects , Body Weight/drug effects , Enalapril/pharmacology , Female , Hypertension/drug therapy , Pregnancy , Rats , Rats, Sprague-Dawley , Renin/blood , Renin/drug effects , Renin-Angiotensin System/drug effects , Renin-Angiotensin System/physiologyABSTRACT
OBJECTIVE: To inventory the possibilities of tracing relatives of patients with familial hypercholesterolaemia (FH) by means of family tree research and DNA diagnostics. DESIGN: Descriptive. METHOD: Blood from patients with the clinical diagnosis of 'FH' was sent, through one of the lipid outpatient clinics in the country, to the Foundation for Tracing Hereditary Hypercholesterolaemia (StOEH) for DNA examination, to characterize the genetic defect. If a mutation was diagnosed in this index patient, he was invited by telephone by a StOEH staff member to have DNA testing done in relatives (especially those of the first degree). The data were stored in a data base. The analysis concerns the patients approached in 1994-1997, as well as those in whom the serum concentration of LDL cholesterol was also determined in 1993-1995. RESULTS: A total of 3013 persons were approached and examined: 146 index patients and 2867 relatives. The DNA diagnosis of 'FH' was made in 1067 relatives (37.2%), 585 (54.8%) women and 482 (45.2%) men. Of these, 21.2% were younger than 20 years, 37.0% 20-39 years, 26.6% 40-59 years and 15.2% > or = 60 years; 44.1% reported being known with a raised cholesterol level, 29.4% were treated with cholesterol-reducing drugs and 6.1% were suffering from a cardiovascular disease. Of the 990 persons in whom the serum LDL cholesterol level was determined, 325 (32.8%) were carriers of a mutation in the LDL receptor gene. 21.2% Of them had a LDL cholesterol level < P95. In the non-carrier group, 14.6% had a serum LDL cholesterol level > P95. CONCLUSION: Tracing FH patients is feasible in practice and leads to detection of as yet untreated patients.
