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R. D. Wright, J. R. Blair-West, J. F. Nelson, G. W. Tregear, and M. Rosenblatt


Infusion of bovine parathyroid hormone (bPTH) preparations into the arterial blood supply of the vascularly isolated parotid gland in anaesthetized sheep increases salivary phosphate concentration and gland blood flow rate with rapid onset and offset of action. These responses have been used as a bioassay for PTH and PTH analogues and for assessing the properties of an in-vitro inhibitory analogue [Nle-8, Nle-18, Tyr-34]bPTH-(3–34)amide. [Nle-8, Nle-18, Tyr-34]bPTH-(1–34)amide at 10− 9 to 10 −8 mol/l was four to five times more potent than bPTH(1–34) on both salivary phosphate and blood flow assays. Human PTH(1–34) was not significantly more potent than bPTH(1–34). The [Nle-8, Nle-18, Tyr-34]bPTH-(3–34)amide analogue had very slight agonist activity at 3 × 10−7 mol/l and at a 100:1 ratio of analogue to PTH it completely inhibited the action of bPTH(1–34) on phosphate secretion and gland blood flow. It caused partial inhibition at 10:1 and had no evident effect at 1:1. These results differ from previous in-vitro results and indicate that the preparation may be valuable for evaluation of agonist and antagonist analogues of PTH. The vascularly isolated parotid gland of the sheep permits repeated random testing of analogues in a control–test–control sequence and the results indicate high sensitivity to PTH in a rapidly reactive invivo system with two responding parameters.

J. Endocr. (1984) 102, 375–379

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R. D. Wright, J. R. Blair-West, J. F. Nelson, and G. W. Tregear

Administration of bovine parathyroid hormone (PTH) preparations increased the phosphate concentration in the parotid saliva of sheep. Data on the site of action of PTH (1–84) were obtained by (a) equimolar infusions of PTH (1–84) and (1–34) directly into the arterial blood supply of the vascularly isolated parotid gland in anaesthetized sheep, (b) intravenous infusion of PTH (1–84) at a similar rate and (c) intra-arterial infusion of PTH (1–84) with complete drainage of the venous effluent from the gland during the infusion. Results showed substantial time– and dose–response identity of the two peptides, at 10−9 to 4 × 10−9 mol/l in arterial blood, in raising salivary phosphate concentration. The effect of PTH (1–84) was not due to recirculated fragments because the response was obtained when recirculation was prevented by complete venous drainage and little or no response occurred when the same infusion was given i.v.

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L R Ranganath, J A Christofides, J W Wright, and V Marks


Oestrogen replacement therapy has been shown to protect postmenopausal women from ischaemic heart disease, strokes and hypertension. The mechanism of protection conferred by oestrogen, although partly attributable to changes in serum lipoproteins, is not fully understood. The present study was undertaken to assess the effect of hormone replacement therapy on the composition of platelet membrane fatty acids in postmenopausal women. These were analysed by gas-liquid chromatography before and six weeks after continuous conjugated equine oestrogen therapy (0·625 mg daily) combined with cyclical therapy with 75 μg l-norgestrel from day 17 to 28 of a 28-day cycle. Each subject acted as her own control. The principal findings of the study were that, following treatment, there was a 16·2% reduction in platelet membrane polyunsaturated fatty acids (P<0·001), an increase of 9·1 and 7·1% in saturated fatty acids and monounsaturated fatty acids respectively (P<0·001) and a 17·8% reduction in arachidonic acid (P<0·003). There was no correlation between changes in membrane fatty acids and serum lipoproteins. This suggests that the changes in membrane composition noted in this study may be a primary effect of hormone replacement therapy, especially oestrogen.

Journal of Endocrinology (1996) 148, 207–212

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Comparisons of aldosterone responses to [des-Asp1]-angiotensin II and angiotensin II, often at single dose levels, have shown a wide range of potency ratios. Therefore four-point dose–response comparisons were performed in sodium-replete sheep, using i.v. infusion rates of angiotension II and angiotensin II amide that reproduced the physiological range of blood concentration of angiotensin II for sheep. Angiotensin III was infused i.v. at the same rates. Effects on arterial blood pressure, cortisol secretion rate, adrenal blood flow and plasma levels of Na+ and K+ were also compared. The potency ratio, angiotensin III: angiotensin II amide, was 0·87 for actual aldosterone secretion rate and 0·90 for the calculated increase in aldosterone secretion. For angiotensin III: angiotensin II the ratios were 0·80 and 0·91 respectively. These ratios were not significantly different from 1·00 but the tendency for angiotensin II to be slightly more potent was probably due to a contribution from derived angiotensin III during infusion of angiotensin II. Angiotensin II or angiotensin II amide was ∼ four times as potent as angiotensin III in raising arterial blood pressure. Cortisol secretion rate was slightly but significantly increased by all peptides at the higher infusion rates. Infusions had no effect on adrenal blood flow or plasma levels of Na + but raised plasma levels of K + slightly. These results confirm the conclusion from adrenal arterial infusion experiments that angiotensin II and III are almost equipotent in stimulating aldosterone secretion in sheep.