title: Increased systemic and renal vascular sensitivity to angiotensin II in normotensive men with positive family histories of hypertension.
abstract: Normotensive young men (mean age 36 years) with positive (PFH) (n = 13) and negative (n = 29) family histories of hypertension were investigated in order to study systemic and renal hemodynamics at baseline conditions and during infusion of low doses (0.1 and 0.5 ng/min/kg) of angiotensin II (AII). The control group with negative family histories of hypertension was subdivided into one group matched for body mass index (n = 15) to subjects with PFH, and one lean control group (n = 14). Baseline blood pressure and sodium intake, measured as urinary excretion, were higher in PFH and in matched controls than in the lean control group. At baseline, renal blood flow (para-aminohippurate clearance) did not differ significantly among the three groups, while glomerular filtration rate (inulin clearance) was higher in PFH than in matched controls. Both doses of angiotensin II infusion increased the blood pressure significantly in PFH. In matched controls a small increase in blood pressure was seen with the highest dose only, while no change in blood pressure was observed in the lean control group. In PFH both doses of AII infusion caused diminished renal blood flow (P less than .01) and increased renal vascular resistance (P less than .001). The two control groups remained unchanged with both AII doses. These results could indicate that normotensive subjects with positive family histories of hypertension are characterized by an increased sensitivity to AII in the systemic and renal circulation as compared with subjects with negative family histories of hypertension.
authors.affiliation: Department of Medicine, Sahlgrenska Hospital, Gothenburg, Sweden.
authors.forename: B R
authors.initials: BR
authors.lastname: Widgren
authors.forename: H
authors.initials: H
authors.lastname: Herlitz
authors.forename: M
authors.initials: M
authors.lastname: Aurell
authors.forename: G
authors.initials: G
authors.lastname: Berglund
authors.forename: J
authors.initials: J
authors.lastname: Wikstrand
authors.forename: O K
authors.initials: OK
authors.lastname: Andersson
mesh_terms: D000328:Adult; D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D007668:Kidney / Q000098:blood supply / Q000187:drug effects / Q000502:physiology*; D008297:Male; D009638:Norepinephrine / Q000097:blood; D011188:Potassium / Q000652:urine; D011863:Radioimmunoassay; D012039:Regional Blood Flow / Q000187:drug effects; D012083:Renin / Q000097:blood; D012964:Sodium / Q000652:urine; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology
chemical_list: D000804:Angiotensin II; D000450:Aldosterone; D012964:Sodium; D012083:Renin; D011188:Potassium; D009638:Norepinephrine