THE EFFECTS OF SAR1ALA8‐ANGIOTENSIN II IN VASOPRESSIN‐TREATED DEHYDRATED SHEEP

Mildly dehydrated conscious Merino ewes were infused with vasopressin (AVP) at 5 mu.min−1 alone and simultaneously with the angiotensin II receptor blocker sar1ala8‐angiotensin II (saralasin) at 15 µg.min−1. AVP was slightly pressor and produced an increase in the calculated total peripheral resistance, and an increase in glomerular filtration rate, urine flow and electrolyte excretion, without a change in total renal plasma flow. These results indicate renal efferent arteriolar vasoconstriction as well as other non‐renal vasoconstriction. Saralasin infusion checked the rise in total peripheral resistance (which continued to increase after saralasin withdrawal), but caused a marked increase in renal vascular resistance resulting in a decrease in renal plasma flow and to a lesser extent in glomerular filtration rate. These results suggest that saralasin was acting as an angiotensin II agonist in the kidney, but as an antagonist elsewhere. Deductions from previous experiments in the literature of the renal function of angiotensin II, based on its supposed inhibition by saralasin, may not be justified

Diagnosis of sodium status in small ruminants

Existing techniques of determining the Na status of ruminants were evaluated in goats and sheep that had widely varying intakes of Na (3-86 mmol/day) and K (20-780 mmol/day). The experiments involved the examination of relationships between Na balance, plasma aldosterone and renin, Na content of faeces and urine, and salivary Na:K ratio in these animals. The variables were measured at monthly intervals for 6 months in goats receiving low or high Na diets, and during 1 month in sheep offered a low Na and low K diet alone or supplemented with 1.5 or 3.0% K. Aldosterone was closely correlated with salivary Na, K and Na:K ratio for both goats and sheep, but there was little relationship indicated between aldosterone and the other variables, either by the raw or logarithmically transformed data. Sodium balance was poorly correlated with all variables, probably because of the unavoidable inaccuracies in measuring Na intake and output. Therefore it was assumed that aldosterone was the best indicator of Na status, since it is the major hormone regulating Na conservation. Stepwise multiple linear regression of all the data with aldosterone as the dependent variable yielded the equation: In (aldosterone) = 5.7-0.87 in (saliva Na:K). Coefficient of multiple determination (R2) was 0.93. In both species aldosterone levels increased markedly when salivary Na:K ratio was less than 4:l. It is concluded that the ratio of Na:K in saliva is a reliable indicator of Na status and a ratio of less than 4 is diagnostic of an incipient Na deficiency

HYPOTENSION‐INDUCED HYPOKALAEMIA IN SHEEP

Plasma K+ was measured in Merino ewes during 50‐90 min periods of hypotension induced by sodium nitroprusside, isoprenaline, verapamil or nifedipine. Doses were adjusted to produce falls in systemic blood pressure of approximately 20 mmHg. All of these drugs caused decreases in plasma K+ which could not be attributed to increased urinary excretion of K+. In all cases plasma renin activity increased during the hypotension. Plasma aldosterone concentration which was measured in some sodium nitroprusside experiments also increased during the hypotension. However, enhancement of the plasma renin activity and plasma aldosterone concentration responses by prior sodium depletion of the sheep by furosemide administration or suppression of the plasma renin activity and plasma aldosterone concentration responses by prior salt loading did not influence the magnitude of the hypotension‐induced hypokalaemia

Changes in the hippocampus induced by glucose in thiamin deficient rats detected by MRI

Using T-2-weighted Magnetic Resonance Imaging (MRI) in a pyrithiamin-treated, thiamin deficient (TD) rat model of Wernicke's encephalopathy (WE), we have observed hyperintensity in the thalamus, hypothalamus, collicular bodies and hippocampus which was enhanced 40 min after a glucose load. Hyperintensity was not evident in these structures in thiamin replete rats receiving glucose nor was it enhanced in TD rats administered 2-deoxyglucose. Residual hyperintensity was still evident in the hippocampus as long as 30 days after thiamin administration and was increased by repeat glucose challenge at that time. These data indicate that the hippocampus is as vulnerable as the thalamus to some persistent pathological change when glucose is metabolised in a state of thiamin deficiency. (C) 1998 Elsevier Science B.V