Search Results
You are looking at 1 - 7 of 7 items for
- Author: J. R. BLAIR-WEST x
- Refine by access: All content x
Search for other papers by PAMELA A. SIMPSON in
Google Scholar
PubMed
Search for other papers by J. R. BLAIR-WEST in
Google Scholar
PubMed
SUMMARY
A renin—angiotensin system was shown to be present in several marsupial species in plasma and homogenates of the renal cortex. Species studied were: Eastern Grey kangaroo (Macropus giganteus), Red kangaroo (Megaleia rufa), common wombat (Vombatus hirsutus), pademelon (Thylogale billardierii), Bennett's wallaby (Wallabia rufogrisea frutica), a quokka (Setonix brachyurus) and a tiger cat (Dasyurus maculatus). Renin-substrate was found in the plasma of the Eastern Grey kangaroo, the Red kangaroo and the wombat. Renin was shown to be present in the plasma of all species by incubation alone or with heterologous marsupial renin-substrate. Plasma renin concentration and renal renin content were estimated by an established method using standard sheep renin-substrate. Plasma renin concentration was high, suggesting that marsupial renins have a high affinity for sheep substrate; renal renin estimates were low relative to eutherian species, suggesting that renal storage may be small. Plasma renin concentration and renal renin levels were proportionately related. Renin levels were consistently lowest in the wombat. Bilateral nephrectomy of an Eastern Grey kangaroo reduced plasma renin concentration to zero and increased renin-substrate concentration eightfold. The angiotensin-like incubation product from Eastern Grey kangaroo renin-substrate did not cross react with antibodies to [5-Ile]-angiotensin I, suggesting that the product has a different sequence of amino acids.
Search for other papers by PAMELA A. SIMPSON in
Google Scholar
PubMed
Search for other papers by J. R. BLAIR-WEST in
Google Scholar
PubMed
SUMMARY
Bilateral nephrectomy of an Eastern Grey kangaroo (Macropus giganteus) increased plasma renin-substrate concentration approximately tenfold when compared with intact kangaroos. A preparation made from this plasma had a renin-substrate concentration of 3000 ng/ml. A pH profile of rate of reaction with pig renin had an optimum at pH 5·39. By comparison, the pH optimum of sheep renin-substrate was pH 6·15. Estimates of plasma renin concentration for kangaroos, wombats and wallabies, using kangaroo renin-substrate or sheep renin-substrate were highly correlated. Results from incubation with sheep renin-substrate were greater and hence indicate the advantage in using this substrate for marsupial renin estimation.
The consistently large difference between sheep and kangaroo renin-substrate when incubated with renin from marsupial and eutherian species appears to be due to a structural difference between the two substrates, probably near the C-terminal end of the angiotensin I molecule.
Search for other papers by R. D. Wright in
Google Scholar
PubMed
Search for other papers by J. R. Blair-West in
Google Scholar
PubMed
Search for other papers by J. F. Nelson in
Google Scholar
PubMed
Search for other papers by G. W. Tregear in
Google Scholar
PubMed
Search for other papers by M. Rosenblatt in
Google Scholar
PubMed
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
Search for other papers by R. D. Wright in
Google Scholar
PubMed
Search for other papers by J. R. Blair-West in
Google Scholar
PubMed
Search for other papers by J. F. Nelson in
Google Scholar
PubMed
Search for other papers by G. W. Tregear in
Google Scholar
PubMed
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.
Search for other papers by J. R. BLAIR-WEST in
Google Scholar
PubMed
Search for other papers by J. P. COGHLAN in
Google Scholar
PubMed
Search for other papers by D. A. DENTON in
Google Scholar
PubMed
Search for other papers by D. T. W. FEI in
Google Scholar
PubMed
Search for other papers by K. J. HARDY in
Google Scholar
PubMed
Search for other papers by B. A. SCOGGINS in
Google Scholar
PubMed
Search for other papers by R. D. WRIGHT in
Google Scholar
PubMed
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.
Search for other papers by J. R. BLAIR-WEST in
Google Scholar
PubMed
Search for other papers by J. P. COGHLAN in
Google Scholar
PubMed
Search for other papers by D. A. DENTON in
Google Scholar
PubMed
Search for other papers by ANGELA P. GIBSON in
Google Scholar
PubMed
Search for other papers by CATHERINE J. ODDIE in
Google Scholar
PubMed
Search for other papers by W. H. SAWYER in
Google Scholar
PubMed
Search for other papers by B. A. SCOGGINS in
Google Scholar
PubMed
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.
Search for other papers by J. R. BLAIR-WEST in
Google Scholar
PubMed
Search for other papers by A. BRODIE in
Google Scholar
PubMed
Search for other papers by J. P. COGHLAN in
Google Scholar
PubMed
Search for other papers by D. A. DENTON in
Google Scholar
PubMed
Search for other papers by C. FLOOD in
Google Scholar
PubMed
Search for other papers by J. R. GODING in
Google Scholar
PubMed
Search for other papers by B. A. SCOGGINS in
Google Scholar
PubMed
Search for other papers by J. F. TAIT in
Google Scholar
PubMed
Search for other papers by S. A. S. TAIT in
Google Scholar
PubMed
Search for other papers by E M. WINTOUR in
Google Scholar
PubMed
Search for other papers by R. D. WRIGHT in
Google Scholar
PubMed
SUMMARY
The effect of sodium depletion on the conversion of corticosterone to aldosterone has been examined in vivo using the adrenal transplants of two sheep. [3H]Corticosterone was infused continuously directly into the adrenal gland via the carotid artery over a period of 30 min. and the total adrenal effluent was collected via the jugular vein in six consecutive 5-min. samples. The conversion of [3H]corticosterone to [3H]aldosterone and the endogenous output of aldosterone was measured in each sample using a double isotope derivative method and the specific activity of the aldosterone calculated. Radioactive conversion of B → aldosterone reached equilibrium within 10 min. of the start of infusion and remained constant over a period of 10–25 min. Aldosterone secretion was also constant during the first 25 min. of infusion.
In the same sheep the mean percentage conversion increased as aldosterone secretion rose over a range of 2–12 μg./hr. With more severe sodium depletion, i.e. with aldosterone secretion rates of 12–16 μg./hr., conversion decreased to that found in the sodium replete state. The specific activity of the aldosterone was constant throughout the mildly deplete range (2–12 μg./hr.) but fell with severe sodium depletion. In the sodium replete range (0–2 μg./hr.) before the introduction of a parotid fistula, the specific activity was the same as in the mildly deplete state. After the introduction of a parotid fistula the specific activity increased as the secretion decreased from 2 to 0 μg.
The validity of the approach and interpretation of the results in terms of the biosynthetic pathways involved are discussed.
