Cardiovascular and renal effects of intracerebroventricular angiotensin II in conscious sheep

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Abstract
Effects on systemic and pulmonary haemodynamics, renal electrolyte excretion, and plasma concentration of vasopressin, catecholamines, electrolytes and proteins in response to intracerebroventricular infusions of [Val5]‐angiotensin II (ANG II) at 1, 2 and 4 pmol kg‐1min‐1in isotonic saline for 30 min were studied in conscious sheep (n = 6). Vehicle control infusions were performed in four of the animals. All three doses of ANG II were expected to increase CFS concentration of the peptide above physiological levels. All ANG II infusions were noticed to be dipsogenic, but the animals were not allowed to drink freely until at the end of the experiments (at 120 min post‐infusion).The systemic arterial blood pressure increased significantly only in response to 2 and 4 pmol kg‐1min‐1, concomitant with an increase of the systemic vascular resistance, whereas the cardiac output and heart rate remained unchanged. The central venous pressure increased only after administration of the highest ANG II dose, while pulmonary artery, and capillary wedge pressures were unaffected during all experiments.The plasma protein and K concentration fell in response to ANG II administration. Also here, the effects were significant only at 2 and 4 pmol kg‐1min‐1. The plasma levels of vasopressin, noradrenaline, adrenaline and dopamine did not change significantly in response to any of the infusions.The renal Na excretion increased by 100–400%, but not in a strictly dose‐dependent manner. Much smaller and more variable effects were seen on the renal K excretion.We conclude that: (1) supraphysiological CSF ANG II levels are needed to cause a pressor effect when the peptide is administered via the intracerebroventricular route in conscious sheep; (2) the blood pressure is increased exclusively via peripheral vasoconstriction and; (3) increased vasopressin release does not contribute to the cardiovascular changes. The results also demonstrate that ANG II may cause haemodilution via a central site of action.