SUMMARY1. The present study investigates the nature and magnitude of the renal response to plasma levels of oxytocin which might be induced by salt loading.2. Increased plasma osmolality induced by loading with NaCl is an effective stimulus for oxytocin release in the unanaesthetized male rat. Plasma oxytocin concentration was positively correlated (r = 0.77) with plasma osmolality. Plasma oxytocin (,uu./ml.) = 0 37 x (plasma osmolality (m-osmole/kg) -297).3. In anaesthetized Long Evans rats intra-atrial administration of oxytocin at rates of 0*05 and 0.15 m-u./ml. produced plasma hormone concentrations (5 + 1 and 16 + 2 ,uu./ml. respectively) within the range induced by salt loading. 6. Plasma ocytocin levels similar to those induced by severe dehydration or salt loading are effective in increasing renal Na+ and Cl-excretion and urine flow. These effects on water and electrolyte excretion appear to be independent of each other and both may be modified by the presence or absence of vasopressin.7. This study provides no evidence for a major role for oxytocin in the day to day regulation of salt or water balance under conditions of normal hydration in the male rat.
1. Renal function and the effect of neurohypophysial hormone replacement was investigated in anaesthetized, acutely hypophysectomized, male rats. 2. Although urine production was only slightly lower over the 8 h post-operative study period in hypophysectomized rats, sodium excretion was greatly depressed reaching only 3.5 +/- 1.4 mumol/min compared with a peak of 13.2 +/- 1.0 mumol/min in intact animals. 3. In association with a decline in mean arterial blood pressure, glomerular filtration rate in hypophysectomized rats fell to 2.1 +/- 0.2 ml/min 8 h after operation by comparison with a mean rate in intact rats of 3.2 +/- 0.2 ml/min. 4. Plasma corticosterone levels were much lower in hypophysectomized (4 +/- 2 ng/ml) than in intact (36 +/- 4 ng/ml) rats, plasma aldosterone was reduced to a lesser extent (0.41 +/- 0.08 compared with 0.76 +/- 0.04 ng/ml). While oxytocin was not detectable in hypophysectomized rat plasma, trace levels of vasopressin (0.16 +/- 0.04 mu u./ml) were found. In intact unanaesthetized rats basal plasma levels of oxytocin were 0.32 +/- 0.13 mu u./ml and vasopressin were 0.85 +/- 0.19 mu u./ml. 5. Administration of oxytocin at 150 mu u./min, which produced plasma hormone levels (24.0 +/- 2.5 mu u./ml) greatly in excess of basal concentrations, increased renal sodium excretion but did not alter urine flow. Oxytocin administration at the lower rate of 15 mu u./min producing plasma hormone levels of 2.60 +/- 0.1 mu u./ml, did not alter renal sodium excretion. 6. Arginine vasopressin administered at 12 mu u./min induced plasma hormone levels of 1.54 +/- 0.09 mu u./ml and produced a large antidiuresis and small increase in the rate of sodium excretion. 7. The natriuretic response to vasopressin was potentiated by concurrent administration of oxytocin at 15 mu u./min. The peak sodium excretion of 5.8 +/- 1.0 mumol/min, however, remained well below that seen in intact rats. 8. It is concluded that, as restoration of posterior pituitary hormones at or above the physiological range only partially restored sodium excretion, the absence of anterior pituitary factors may also contribute directly or indirectly to the renal sodium retention of the hypophysectomized rat.
SUMMARY1. The relationship of plasma vasopressin concentrations in the physiological range to renal electrolyte excretion was investigated.2. Unanaesthetized rats, when normally hydrated, were found to have a plasma vasopressin concentration of 113 + 015 ,su./ml. 16 h water deprivation raised this to 1P98+0-21 ,su./ml.3. Inactin-anaesthetized rats infused with 0 45 % NaCl had a plasma vasopressin concentration of 1 19 + 0418 su./ml. Administration of synthetic arginine vasopressin at 6 and 24 ,uu./min raised plasma vasopressin levels to 1P88+0-17 and 4-26 + 0 43 ,uu./ml respectively.4. In addition to the expected antidiuresis, vasopressin at a rate of 6 ,uu./min also produced a highly significant increase in Na+ excretion from 89 + 06 to 10-5+0-6/imol/min and Cl-excretion from 9-1+0-7 to 105+07j7mol/min. At 24 ,uu./min it produced larger increases in Na+ and Cl-excretion.5. Inactin-anaesthetized hypophysectomized rats infused with 0 45 % NaCl had a plasma vasopressin concentration of only 017+004 #zu./ml. Administration of vasopressin at 6 and 24 #su./min raised plasma vasopressin levels in these animals to 0-63 + 0-17 and 2-20 + 0-11 su./ml respectively. 6. Hypophysectomized rats failed to exhibit a natriuresis in response to the lower dose of vasopressin, despite exhibiting an undiminished antidiuresis. The failure of the natriuresis may be related to the lower plasma vasopressin concentration achieved.7. It is concluded that in the rat plasma vasopressin concentrations within the physiological range do influence Na+ and Cl-excretion by the kidney as well as controlling urine flow rate.
Abstract. Renal water and electrolyte handling and related plasma hormone levels were measured in male and female New Zealand genetically hypertensive and normotensive rats, in an attempt to etablish any potentially important sex-related differences in these parameters. Male hypertensive rats had higher blood pressure than female hypertensive rats, but normotensive rats showed no such sex difference. Both groups of males had higher fluid turnover rates than respective females, and this was associated with raised plasma vasopressin in hypertensive males. Female hypertensive rats excreted more sodium, potassium and chloride in association with lower plasma aldosterone and higher corticosterone levels compared with the other groups. Plasma electrolytes did not differ between the four groups, but plasma osmolality was higher in hypertensive than normotensive rats of both sexes. A higher rate of electrolyte loss and lower fluid turnover in association with reduced plasma vasopressin may contribute to the lower blood pressure of female compared with male hypertensive rats.
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