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Search for other papers by J. H. Shand in
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Search for other papers by D. W. West in
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ABSTRACT
Rats in mid-lactation were treated, for 2 days, with anti-rat GH serum (anti-rGH) and/or bromocriptine before microsomes were prepared from the freeze-clamped mammary glands. The effects of these anti-hormone treatments on the concentrations of microsomal cholesterol and cholesterol esters and on the activities of acyl-CoA:cholesterol acyltransferase (ACAT), neutral cholesterol ester hydrolase and 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoA reductase) were measured. HMG-CoA reductase was determined in microsomes prepared in both the presence and absence of phosphatase inhibitors to determine the expressed and total activities respectively.
Anti-rGH reduced HMG-CoA reductase and increased microsomal cholesterol and cholesterol esters. Bromocriptine reduced HMG-CoA reductase but increased all of the other parameters. The results indicate that the initial stage in the stimulation of milk secretion involves a decrease in the activity of ACAT and that the phosphorylation level of HMG-CoA reductase is modulated by both prolactin and GH acting in opposition.
Journal of Endocrinology (1991) 128, 287–295
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Lactating rats were treated for 48 h with bromocriptine (to inhibit prolactin release) or bromocriptine together with an antiserum to rat GH. Animals given the combined treatment were also supplemented concurrently with bovine GH (bGH) or human insulin-like growth factor-I (hIGF-I). The effects of these treatments on the activities of 3-methyl-3-glutaryl-CoA reductase (HMG-CoA reductase), acyl-CoA:cholesterol acyltransferase (ACAT) and neutral cholesteryl ester hydrolase (CEH) and on the microsomal concentrations of non-esterified and esterified cholesterol were measured.
Lack of prolactin decreased HMG-CoA reductase but did not affect ACAT, neutral CEH or the concentrations of microsomal cholesterol or cholesteryl esters. In the absence of both hormones, an even greater reduction in HMG-CoA reductase together with increases in ACAT, neutral CEH and both of the microsomal sterols were observed. Concurrent supplementation with either bGH or hIGF-I wholly or partially prevented the effects on HMG-CoA reductase but only bGH was active against the increase in ACAT. Neither bGH nor hIGF-I could prevent the effects of the anti-hormone treatment on neutral CEH, and the changes in ACAT and CEH activities were broadly reflected in the microsomal sterol concentrations.
The results indicate that the cessation of lactation brings about rapid changes in the activities of the enzymes involved in cholesterol metabolism within the mammary gland with a definite switch from synthesis to storage. Supplementation with bGH alone was sufficient to maintain cholesterol synthesis at control levels and could also significantly inhibit storage of the sterol as its ester. In the absence of GH, hIGF-I partially supported cholesterol synthesis but had no effect on its conversion to the ester. On a whole-tissue basis, enzyme activities could be correlated with the physiological effects of the anti-hormone treatments.
Journal of Endocrinology (1997) 152, 447–454
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ABSTRACT
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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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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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.
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Plasma renin activity (PRA) and blood aldosterone and deoxycorticosterone levels were measured in Australian lungfish. Plasma renin activity was depressed after intravenous infusions of iso-osmotic (0·6%) NaCl but not after hypo-osmotic (0·3%) infusions. The presence of PRA in this fish is consistent with prior reports of renal renin activity in other sarcopterygian fishes. The results of the infusion experiments suggest that a fall in plasma osmolality or electrolyte concentrations may oppose the reduction in renin release in response to volume expansion.
Aldosterone and deoxycorticosterone were identified in the blood of Neoceratodus. The concentrations of both appeared higher in females than in males. Infusions of [5-valine]-angiotensin II amide for 2–4 h at rates known to increase blood pressure in this species did not alter blood aldosterone concentrations. This negative finding may suggest that the renin/angiotensin system is not involved in aldosterone regulation in Neoceratodus or that angiotensin receptors involved in regulation of steroidogenesis have a greater specificity for endogenous angiotensin than do vascular receptors.
