Circulating plasma prekallikrein and tissue kallikrein in normotensive and hypertensive humans: effects of angiotensin II infusion.
Kinins lower blood pressure but the stimuli leading to kinin generation and their origin are less well known. We administered angiotensin II in graded infusion doses to patients with primary hypertension and normotensive controls to study the effects of on circulating kallikreins. Angiotensin II infusion did not significantly alter plasma prekallikrein or tissue kallikrein levels and the plasma levels and their changes did not correlate with blood pressure levels or changes. In the normotensive group prekallikrein levels and renin activity correlated negatively with urinary sodium and chloride excretion during basal conditions and partially during the infusion. U-tissue kallikrein concentration increased in the normotensive group. Thus, acute elevation of blood pressure induced by angiotensin II does not activate the circulating kallikrein-kinin systems. Data rather indicate that the circulating kallikrein-kinin systems may be related to alterations in volume and sodium balance and that these mechanisms may be altered in primary hypertension.
Ohman
K P
KP
Department of Medicine and Care, Faculty of Health Sciences, University Hospital, Linköping, Sweden.
Karlberg
B E
BE
D000328:Adult; D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000494:pharmacology*; D001794:Blood Pressure / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000503:physiopathology* / Q000652:urine; D007262:Infusions, Intravenous; D007610:Kallikreins / Q000378:metabolism*; D008875:Middle Aged; D011288:Prekallikrein / Q000378:metabolism*; D012016:Reference Values; D012083:Renin / Q000097:blood
D000804:Angiotensin II; D000450:Aldosterone; D011288:Prekallikrein; D007610:Kallikreins; D012083:Renin