Open AccessDIMINISHED ANGIOTENSIN-II AND INTACT VASOPRESSIN RESPONSE TO HEMORRHAGE IN PORTAL HYPERTENSION
Author(s) -
Yue Wu,
Burns Rc,
Sitzmann Jv
Publication year - 1998
Publication title -
shock
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.095
H-Index - 117
eISSN - 1540-0514
pISSN - 1073-2322
DOI - 10.1097/00024382-199801000-00008
Subject(s) - vasopressin , portal hypertension , splanchnic , medicine , angiotensin ii , endocrinology , renin–angiotensin system , hemodynamics , portal venous pressure , plasma renin activity , aldosterone , splanchnic circulation , arginine , vasodilation , blood pressure , cirrhosis , chemistry , biochemistry , amino acid
Portal hypertension is characterized by splanchnic vasodilation and diminished arterial vasoconstrictor response to hemorrhage. Angiotensin-II and arginine vasopressin are critical modulators of the splanchnic response to hemorrhage in normal animals. We hypothesized that alterations in endogenous renin, angiotensin-II, or arginine vasopressin production or release could contribute to the abnormal response to hemorrhage in portal hypertension. Hemodynamics were studied in normal and portal hypertensive rabbits following either graded isovolumetric or single large volume hemorrhage, followed by reinfusion of blood. Hemodynamic and renin-angiotensin-II, and arginine vasopressin activities were determined. The experiments demonstrated a significantly diminished appearance in angiotensin-II (110.87+/-30 vs. 245+/-51.0 pg/mL) and aldosterone (54.2+/-9.5 vs. 119.4+/-13.5 ng/dL), and plasma renin activity (19.4+/-4.2 vs. 29.1+/-2.8 ng/mL/h) in portal hypertension compared with normal, but an appropriate rise in arginine vasopressin levels following hemorrhage in portal hypertension. These findings suggest a diminished angiotensin-II production or release in portal hypertension, which may mediate the failure of the appropriate splanchnic vasoconstrictive response to hemorrhage.