Female Wistar rats were infused intravenously with 5% dextrose for 3 days, then with angiotensin II (ANG II) in 5% dextrose at 20 ng . kg-1 . min-1 for 7 days, and finally with dextrose for 2.5 days. ANG II raised mean arterial pressure (MAP) gradually; by the 7th day it was 49.7 mmHg higher than during the dextrose control period in the same rats. Control rats were infused with dextrose for 12.5 days; MAP did not change. Plasma ANG II concentration was measured during infusion. In hypertensive rats on the 7th day of ANG II infusion, it was six times higher than in control rats infused with dextrose. Changes of blood pressure and plasma ANG II concentration were compared in further rats infused with much larger doses of ANG II. Rats receiving 270 ng . kg-1 . min-1 for 1 h had an almost maximal direct pressor response, MAP rising 45.3 mmHg and plasma ANG II rising 32-fold compared with controls. Thus, infusion of ANG II at low dose without direct pressor effect gradually raises blood pressure to a level similar to the maximum direct pressor effect produced by larger doses of ANG II. Sodium balance and food and water intakes were also measured and did not change during prolonged infusion of ANG II at 20 ng . kg-1 . min-1. Thus, the slow pressure effect of ANG II develops at a lower and more nearly physiological plasma concentration of the peptide than do the direct pressor effect and the effects on drinking, eating, and urinary sodium excretion.

Oxygen consumption and delivery (defined as the product of cardiac output, haemoglobin concentration and arterial oxygen saturation) and haemodynamic variables were examined in the conscious resting rat throughout the day and after the expansion of body fluid volumes. Cardiac output was measured in arbitrary units by electromagnetic flowmetry and oxygen consumption by respirometry. The variability of blood pressure in the basal state was significantly less than that of cardiac output. Oxygen consumption was significantly correlated with cardiac output and oxygen delivery. In studies undertaken throughout the day, both oxygen consumption and delivery fell in the afternoon and there was evidence that the relationship between these two variables was curvi- rather than recti-linear. During oral sodium chloride administration for 7 days, blood pressure rose and some evidence was found for an alteration in the relationship between oxygen consumption and delivery, with an excess of delivery relative to consumption, particularly on the first day of salt loading. Intravenous injection of sodium chloride solution (0.171 mol/l) did not alter the relationship between oxygen consumption and delivery. Expansion of blood volume, while the packed cell volume was maintained nearly constant, raised oxygen delivery transiently and evidence was obtained that the relationship between oxygen consumption and delivery was altered, with oxygen delivery rising relatively more than oxygen consumption. The findings are discussed in relation to the autoregulatory hypothesis of circulatory control and for the role of autoregulation in hypertensive states. The importance of relating oxygen delivery to metabolic requirements in studies of the role of autoregulation is emphasized.

Medical Research Society 2 5~ 65 mmm up o m 25 HTDROXTPITANI~Q D ow CALCIUM ABSORPIION AND PLASMA 1,25 DIdEDXY-VITAMIN D IN CORTICOSTEROD -Ell m S Q . TAYLOR AND J. STORER FreHospital, 1Jewcaatle Upon b e , and lQtc Hineral Yetabolism Unit, General Infirmary,Leeds Corticosteroid treated subjects with spinal OsteopOrOEds have calcium malabsorption and low 1,25 dihydroryrritamin D (1,25(0HJ2D) levels, wherean those without osteoporosis are nolmal i n Science 62, 4 1 p . ) . Ye report here the effect on 1,25[OH),D levels and calcium absorption of oral 25 @droqvvitamin D 25 jag daily given t o 13 osteoporotics(B) and 11 non-osteoporotics (no-) on lomptenn prednisolone. me groups w e r e of similar age (62.8 + 2.65 (SE) vs 59.1 2 2.91 yrn respectively, diflerence H.S.), had been on preduisolone f o r similar periods of time ourrently receiving-similar doses (8.2 5 2.31 vs 7 . 5 9 0.95 ag/&aY, H.S.). 250HD3 treatment was given for 3-12 months (6.92 f 0.87 vs 6 . 0 2 0.73 &ha N.S.). h t i n g radiocalcimn absorption y88 a a s m before and on treatment. Initial and treated 25OHD levels were similar in each group (8, 89.3 f 10.3 aud 182.5 + 11.3 hmol/l p