Male Wistar rats were anesthetized at 6 weeks of age and a silver clip placed around the renal artery to produce renovascular hypertension. The rats were allowed to grow on a normal sodium diet for the next 6–9 weeks. Using diethyl ether anesthesia, arterial and venous cannulae were placed and the animals allowed to awaken in restraining cages. The group of rats was divided into three groups: awake (n = 7), halothane 1.3 vol% (n = 9), and enflurane 2.2 vol% (n = 8). The protocol consisted of a 1-h control awake period, 1 h of stable anesthesia (one group received no anesthesia), and 30-min iv infusion of saralasin, a competitive inhibitor of angiotensin II. Plasma renin activity (PRA) and plasma catecholamines were measured after 1 h of stable anesthesia and after the saralasin infusion. In additional rats treated identically, radiolabelled microspheres were used to measure cardiac output and regional blood flows during halothane (n = 7) or enflurane (n = 6) anesthesia.Principal responses were as follows: mean arterial pressure (MAP) was 193 · 4 mmHg awake and decreased to 114 · 3 mmHg and 135 · 3 mmHg with halothane and enflurane, respectively. Saralasin decreased MAP in the awake group to 176 · 3 mmHg and to 69 · 3 mmHg and 96 · 5 mmHg with halothane and enflurane, respectively. PRA in the awake rats was 7.24 · 1.3 ng · ml−1· h−1. PRA increased with halothane but decreased with enflurane. Plasma catecholamines were decreased markedly by saralasin and by both anesthetic agents. Cardiac output was normal in awake rats and blood pressure elevation was due to increased peripheral resistance. Both anesthetic agents decreased cardiac output and myocardial blood flow and increased brain blood flow. The authors conclude that the cardiovascular and hormonal responses to halothane and enflurane anesthesia in renovascular hypertensive rats are different than the responses seen in normotensive rats. Such alterations may explain the differences seen in regional blood flow to various organs.