Adrenocortical Function in the Brattleboro Rat*

Milne, Catherine M.; Balment, R. J.; Henderson, Ian; Mosley, W.; Jones, Ian

doi:10.1111/j.1749-6632.1982.tb37431.x

Cited by 33 publications

(27 citation statements)

References 20 publications

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“…Inter-and intra-assay coefficients of variation were 10 1 % (n = 30) and 13 6 % (n = 10), respectively. Plasma aldosterone levels were also determined by radioimmunoassay following initial separation from other steroids by LH 20 chromatography (Milne, Balment, Henderson, Mosley & Chester-Jones, 1982). Inter-and intra-assay coefficients of variation were 12 7 % (n = 42) and 14 4 % (n = 1O), respectively.…”

Section: Measurement Of Electrolytesmentioning

confidence: 99%

Interaction of aldosterone and oxytocin to influence renal sodium excretion in rats

Musabayane¹,

Ndhlovu²,

Ml³

et al. 1994

Experimental Physiology

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SUMMARYThe possibility of an interaction between oxytocin and aldosterone to influence renal Na+ excretion was investigated in Inactin-anaesthetized male Sprague-Dawley rats. Endogenous plasma concentrations of aldosterone were suppressed by either adrenalectomy or bicarbonate infusion. The effects of 2 h intravenous administration of oxytocin (0-04 pmol/min) and/or aldosterone (42 pmol/min) on renal Na+ handling were studied in 0077 M NaCl-infused adrenalectomized (Adx) rats and groups of intact animals that were infused with 0 077 M NaHCO3. Aldosterone alone significantly (P < 0 01) reduced Na+ excretion from pretreatment peak value of 5 0 + 1 0 to 1 5 + 0 4 flmol/min in Adx animals (n = 8) and 9 2 + 1 2 to 5 2 + 12 ,umol/min in NaHCO3-infused rats (n = 8) by 2 h after the start of administration. However, combined administration of aldosterone and oxytocin was associated with a significantly (P < 0 01) increased Na+ excretion rate from a peak pretreatment value of 68 + 07 ,tmol/min to a peak value of 11 5 ±1 ,amol/min by 1 h 40 min after the start of treatment in Adx rats (n = 7). In bicarbonate-infused rats (n = 8) Na+ excretion rose within 20 min of the start of treatment from a pretreatment peak of 9 0 + 0 8 ,tmol/min to a peak value of 13 5 + 0 8 ,tmol/min in response to combined hormone administration. In conclusion, we have shown that concomitant administration of aldosterone and oxytocin increased the rate of excretion of Na+ in two different preparations, which supports the idea of an interaction between the steroid and oxytocin to promote Na+ loss.

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Section: Measurement Of Electrolytesmentioning

confidence: 99%

Interaction of aldosterone and oxytocin to influence renal sodium excretion in rats

Musabayane¹,

Ndhlovu²,

Ml³

et al. 1994

Experimental Physiology

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“…However, circulating aldosterone levels in NZGH rats were not significantly different from those in normotensive animals in this study. Quantitatively, the levels of aldosterone in NZN and NZGH rats were much higher than those currently and previously measured in this laboratory for Sprague-Dawley, Long-Evans and Brattleboro rats (Milne et al 1982). This elevation appears to represent a strain difference and is not related to the expression of hypertension.…”

Section: Discussionmentioning

confidence: 68%

“…Plasma aldosterone was measured by radioimmunoassay following initial separation from other steroids by LH20 chromatography (Milne, Balment, Henderson, Mosley & Chester-Jones, 1982). Inter-and intra-assay coefficients of variation were 12-7 % (n = 42) and 14'4 % (n = 10) respectively.…”

Section: Aldosterone and Corticosterone Radioimmunoamsaysmentioning

confidence: 99%

Blood pressure and renal function in a novel vasopressin‐deficient, genetically hypertensive rat strain.

Ashton

Balment

1989

The Journal of Physiology

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SUMMARY1. Hereditary hypothalamic diabetes insipidus was introduced into the New Zealand genetically hypertensive (NZGH) rat and its normotensive substrain (NZN) by cross-breeding males with female Brattleboro diabetes insipidus (DI) rats.2. Selective breeding of the resultant DI/hypertensive (DI/H) rats on the basis of maximum systolic blood pressure and vasopressin deficiency produced animals in the F6 generation with blood pressures at 10 weeks of age higher than in DI/ normotensive rats (DI/N), but much lower than in age-matched NZGH animals. Age-matched NZN and DI/N rats had comparable blood pressures.3. Fluid turnover was far greater in DI/N and DI/H rats than in NZN and NZGH rats. Although comparable in DI/N and NZN rats, water balance (intake -urinary loss) was reduced in DI/H rats by comparison with NZGH rats.4. Sodium balance was lower in DI/N rats compared with NZN rats but did not differ between DI/H and NZGH animals. Both DI groups had lower potassium balances.5. Basal plasma vasopressin was elevated in NZGH rats compared with NZN rats, while vasopressin was undetectable in DI animals. Plasma aldosterone levels did not differ between groups, but corticosterone was lower in DI/N and DI/H rats by comparison with NZN and NZGH rats.6. Replacement of vasopressin to achieve physiological plasma hormone levels restored normal fluid management in DI animals and was associated with a modest increase in systolic blood pressure in DI/N animals, compared with sham-treated rats. A much larger increase in blood pressure was observed in AVP-treated DI/H animals, but blood pressure remained below that in NZGH rats.7. It is apparent that vasopressin may contribute to the hypertension of the NZGH rat and that it may be required from an early age. The mode of this contribution is unclear, but abnormal renal responses have been identified.

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“…Excluding these possibilities, the prolonged pressor response to vasopressin in the Brattleboro DI rats could be due to either (a) the differential clearance of vasopressin in the two strains or (b) changes in the number or distribution of receptors for vasopressin or (c) different post receptor regulation. Since there are various other differences (probably related to the absence of vasopressin) between the Brattleboro DI rat and rats of the parent Long Evans strain, such as lower plasma levels of aldosterone and corticosterone (Milne et al, 1982), and angiotensin II (Mohring et al, 1974), there could be other factors involved in the differential pressor response to vasopressin. The present study was not designed to identify the mechanism by which the pressor effect of this peptide is prolonged, and this remains to be investigated.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular interactions between vasopressin, angiotensin and noradrenaline in the Brattleboro rat

Laycock

Lightman

1989

British J Pharmacology

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The cardiovascular effects of bolus intravenous injections of vasopressin, angiotensin II and noradrenaline were studied in 6-hydroxydopamine pretreated, anaesthetized Brattleboro rats with hereditary diabetes insipidus and normal rats of the parent Long Evans strain. 2 Pretreatment with 6-hydroxydopamine did not significantly affect control values for mean arterial blood pressure, cardiac output or total peripheral resistance in either Brattleboro or Long Evans rats but the pressor response to haemorrhage was reduced in both strains compared to the control animals. 3 The pressor responses of the untreated Brattleboro rats to 250 mu kg-vasopressin were significantly greater and more prolonged than in control rats of the Long Evans strain. 4 Pretreatment with 6-hydroxydopamine significantly enhanced the peak pressor response to vasopressin, but not to angiotensin II (1 Mg kg-1), in Brattleboro and Long Evans rats. 5 Pretreatment with 6-hydroxydopamine resulted in an enhanced pressor response to 1 pg kg-' noradrenaline in both Brattleboro and Long Evans rats, but the effect was significantly greater in the vasopressin-deficient animals. 6 These results indicate differences in the pressor responsiveness of Brattleboro rats to vasopressin and noradrenaline, but not to angiotensin II, compared with control Long Evans rats and provide evidence for important interactions between the sympathetic nervous system and these pressor hormones.

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Adrenocortical Function in the Brattleboro Rat*

Cited by 33 publications

References 20 publications

Interaction of aldosterone and oxytocin to influence renal sodium excretion in rats

Interaction of aldosterone and oxytocin to influence renal sodium excretion in rats

Blood pressure and renal function in a novel vasopressin‐deficient, genetically hypertensive rat strain.

Cardiovascular interactions between vasopressin, angiotensin and noradrenaline in the Brattleboro rat

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