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R J Balment

Publications and source records attributed to R J Balment.

At least 91 records · Page 5Linked to original sources
PubMed1990

Influence of neurohypophysectomy on the renal actions of aldosterone in the adrenalectomized rat.

The influence of aldosterone administration on urine flow, Na+ and K+ excretion was examined in hypotonic saline infused, Inactin anesthetised rats following removal of the adrenals or adrenals and posterior pituitary. Plasma adrenal steroid levels were considerably depressed but still detectable 10-14 days after adrenalectomy. Removal of the posterior pituitary markedly reduced Na+ excretion in adrenalectomized animals implying that Na+ retention following neurohypophysectomy is not dependent on adrenal gland function. In adrenalectomized rats aldosterone administration at 42 pmol/min reduced Na+ excretion and urine flow without significantly changing K+ excretion, though plasma K+ was reduced. In adrenalectomized/neurohypophysectomized rats aldosterone further reduced the already low rate of Na+ excretion and increased K+ excretion, though there was no observable effect on urine flow. The results obtained indicate that the Na(+)-retaining actions of aldosterone are largely independent of posterior pituitary influence. The K(+)-losing action of aldosterone was, however, only observed in animals in which the posterior pituitary was absent.

Adrenal Glands↗
PubMed1989

Steroidogenic role of the caudal neurosecretory system in the flounder, Platichthys flesus.

Transfer of flounders from seawater (SW) to fresh water (FW) resulted in a small reduction in circulating cortisol levels and urophysial protein storage. Transfer of flounders from FW to SW resulted in a larger increase in plasma cortisol and specific urophysial protein storage. Over the first 4 days after transfer from FW to SW there was a positive correlation between the observed changes in urophysial urotensin I (UI) content and plasma cortisol. This apparent steroidogenic effect of UI was supported by the increases in plasma cortisol observed following iv injection of crude flounder urophysial gland extract and synthetic Catostomus commersoni UI. The study supports a contribution of the caudal neurosecretory system to the control of interrenal steroidogenesis as part of the integrated osmoregulatory physiology of euryhaline species like the flounder.

Animals↗
PubMed1989

Endocrines and osmoregulatory mechanisms in the Nile crocodile, Crocodylus niloticus.

The changes in body fluid economy and endocrine status associated with exposure of the Nile crocodile, Crocodylus niloticus, to hypertonic media have been related to the responses to altered renin-angiotensin system (RAS) activity observed in fresh water (FW) animals. Animals held in hypertonic media for 7 days showed a 18.2% body weight loss and raised plasma and urinary sodium, potassium, chloride, and osmotic concentrations. Within 6 hr of return to FW rapid imbibition had largely restored body weight and produced significant plasma dilution. Although plasma sodium, chloride, and osmotic concentrations remained higher than in FW controls, plasma levels of corticosterone, aldosterone, and arginine vasotocin were not significantly altered. Angiotensin I (AI) administration in FW crocodiles stimulated drinking and raised plasma aldosterone levels by comparison with animals given the converting enzyme inhibitor, Captopril, together with AI. The compensatory drinking behaviour exhibited by the Nile crocodile may thus involve the RAS. The RAS also appears to influence interrenal steroidogenesis and thus may afford an integrative role in crocodile fluid management as it does in homeotherms.

Aldosterone↗
PubMed1989

The renin-angiotensin system and vascular and dipsogenic regulation in elasmobranchs.

The role of a renin-angiotensin-like system (RAS) in the regulation of blood pressure and drinking has been investigated in the elasmobranch, Scyliorhinus canicula. Injection of exogenous angiotensin II produced, as expected, a vasopressor response, though injection of the converting enzyme inhibitor, Captopril, alone produced little change in resting blood pressure. Papaverine, a smooth muscle relaxant, reduced blood pressure which completely recovered within 30 min. A subsequent injection of Captopril produced a rapid vasodepressor response with no recovery over 2 hr. The low basal levels of drinking in dogfish were not altered by Captopril injection but angiotensin II-induced increased drinking and papaverine administration resulted in markedly stimulated water intake, which was inhibited by coadministration with Captopril. Captopril inhibition of the recovery in blood pressure and associated dipsogenic response following the papaverine-induced hypotension is consistent with the activation of a RAS-like system in the dogfish. This and other evidence supporting the presence of a RAS-like system in elasmobranchs are discussed in relation to other vertebrates.

Angiotensin II↗
PubMed1989

Kappa-opioid-induced changes in renal water and electrolyte management and endocrine secretion.

1. Subcutaneous injection of the kappa-opioid agonist U50,488 into conscious, saline-loaded rats was associated with a diuresis, antinatriuresis and antikaliuresis which lasted for up to 3 h. Plasma renin activity and corticosterone levels were elevated but plasma vasopressin (AVP) and aldosterone levels were unaltered in similarly treated rats. 2. U50,488 administration to adrenal demeddulated rats was not associated with a diuresis but produced an antinatriuresis, though sodium excretion rates were higher in demedullated than in sham-operated animals. Plasma AVP and corticosterone levels were not affected by demeddulation or subsequent U50,488 treatment. Sham-operated, U50-488-treated rats showed the expected increase in plasma corticosterone levels. 3. U50,488 administration resulted in an antidiuresis and an antinatriuresis in AVP-deficient Brattleboro DI rats. 4. When coupled with fasting stress U50,488 administration resulted in similar but attenuated renal responses compared with those observed in unfasted rats. Basal plasma corticosterone levels were elevated in fasted animals and were further increased by U50,488. 5. Both water and electrolyte handling by the kidney are altered by U50,488. The diuretic effects of U50,488 were reversed by adrenal demedullation and in the absence of endogenous AVP, but the antinatriuretic actions were not altered, suggesting that the effects upon renal water and electrolyte excretion may be mediated by separate mechanisms.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1989

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

1. 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.

Aldosterone↗
PubMed1989

Central and peripheral effects of the peptide ANF on renal function and blood pressure in hypertensive rats.

1. The present study assesses renal and blood pressure effects of systemically and intracerebroventricularly (I.C.V.) administered atrial natriuretic factor (ANF) in anaesthetized New Zealand genetically hypertensive (NZGH) rats and their normotensive substrain (NZN). 2. Plasma ANF concentration was significantly raised in NZGH compared with NZN animals. Intravenous ANF administration increased circulating ANF concentration to similar levels in NZGH and NZN rats. Plasma aldosterone concentrations were initially similar in normotensive and hypertensive animals and were reduced markedly by I.V. ANF administration in both groups. 3. Peripheral administration of ANF produced a significant and sustained hypotension during the period of the hormone administration in NZGH animals, while arterial mean blood pressure (MBP) was not altered significantly in NZN rats. Central infusion of ANF produced no change in MBP in either NZGH or NZN animals. There was no detectable change in heart rate during central or peripheral administration of the hormone in either group. 4. By comparison with animals maintained on hormone-free infusate, urine flow changed little over the 80 min period of I.V. ANF infusion in NZGH rats but was markedly increased in NZN animals. Urinary sodium excretion was elevated during ANF infusion in both NZGH and NZN animals. Central infusion of ANF produced a diuresis in NZN rats but a slight reduction in urine flow in NZGH animals, while sodium excretion was not affected in either group. 5. It appears from the present study that central and peripheral ANF effects on renal function and blood pressure differ in hypertensive and normotensive animals. These differences may in part reflect adjustments to long-term elevation in plasma ANF in hypertension and in part are possibly associated with disturbances in related endocrine mechanisms.

Aldosterone↗
PubMed1989

Renal and blood pressure changes in response to vasopressin antagonism in the New Zealand genetically hypertensive rat.

The effects of a mixed pressor and antidiuretic vasopressin antagonist on blood pressure and renal function have been investigated in New Zealand genetically hypertensive and normotensive rats. Vasopressin antagonism was associated with a diuresis, compensatory polydipsia and kaliuresis in both normotensive and hypertensive animals. Hypertensive animals alone exhibited a natriuresis and a fall in systolic blood pressure, which was associated with a reduction in water balance and plasma sodium compared with antagonist-treated normotensive animals. The data suggest that vasopressin may exert a long-term influence on blood pressure through renally rather than vascularly mediated effects.

Animals↗
PubMed1988

Neurohypophysial hormone influence on renal function in the New Zealand genetically hypertensive rat.

The acute effects of physiological levels of AVP and oxytocin administration on renal water and sodium handling have been investigated in New Zealand genetically hypertensive and normotensive rats. AVP infusion was associated with an antidiuresis in both normotensive and hypertensive rats and while normotensive rats also displayed a dose-related natriuresis, this was attenuated in hypertensive rats. Oxytocin administration had no effect on urine flow or sodium excretion in normotensive rats, but was associated with an antidiuresis in hypertensive rats. Combined hormone infusion produced a greater reduction in urine flow than following AVP alone in both normotensive and hypertensive groups and was associated with a potentiation of the natriuretic action of AVP in the hypertensive animals. The data suggest that the contribution of oxytocin to renal sodium excretion in hypertensive rats may be suppressed. A compensatory increase in basal AVP secretion in hypertensive rats may overcome their apparent renal insensitivity to AVP, to maintain appropriate sodium excretion. This intriguing disturbance in neurohypophysial function may reflect or possibly contribute to the hypertension of these animals.

Animals↗
PubMed1986

The influence of neurohypophysial hormones on renal function in the acutely hypophysectomized 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.

Animals↗
PubMed1986

A synergistic effect of oxytocin and vasopressin on sodium excretion in the neurohypophysectomized rat.

1. Renal function and the effect of oxytocin and vasopressin replacement have been examined in anaesthetized male neurohypophysectomized rats. 2. Rates of urine flow were higher but sodium excretion markedly lower in neurohypophysectomized rats than in intact animals receiving hypotonic saline infusion (33.8 +/- 2.3 vs. 27.0 +/- 0.7 ml and 472 +/- 84 vs. 1946 +/- 124 mumol respectively for the third to sixth hour of study). 3. In intact animals, mean arterial blood pressure stabilized at 106 mmHg. Haematocrit (46%) remained stable but glomerular filtration rates declined slightly over the 8 h of study to 2.5 +/- 0.2 ml/h. These values in neurohypophysectomized rats did not differ significantly from those in intact rats. 4. Although plasma corticosterone levels (54 +/- 13 ng/ml) did not differ significantly from those in intact rats, neurohypophysectomy was associated with greatly reduced aldosterone concentration (0.12 +/- 0.03 vs. 0.76 +/- 0.04 ng/ml). Trace levels of vasopressin (0.17 +/- 0.03 microunit/ml) were found in neurohypophysectomized rat plasma. 5. Oxytocin administration at 15 microunits/min, which produced plasma hormone levels of 1.62 +/- 0.19 microunit/ml, had no detectable effect on sodium excretion but increased urine flow. Arginine vasopressin administration (12 microunits/min) inducing plasma levels of 1.24 +/- 0.08 microunit/ml, reduced urine flow by 80% and produced a small increase in sodium excretion. 6. Concurrent administration of oxytocin (15 microunits/min) potentiated the natriuretic response to vasopressin (12 microunits/min). Total sodium excretion during the 3 h combined hormone infusion (1256 +/- 149 mumol) greatly exceeded that in animals receiving vasopressin alone (549 +/- 132 mumol) and approached that observed in intact animals (1946 +/- 124 mumol). Combined hormone administration at the lower rate of 5 microunits/min oxytocin and 4 microunits/min vasopressin produced a similar large increment in sodium excretion. 7. It is concluded that replacement of both neurohypophysial hormones, at plasma levels within the physiological range, largely reverses the renal sodium retention of neurohypophysectomized rats, oxytocin considerably potentiating the natriuretic action of vasopressin. This synergism between the two neurohypophysial peptides to promote salt excretion may be an important component of the non-steroidal management of sodium.

Animals↗
PubMed1985

Endogenous renin-angiotensin system and drinking behavior in flounder.

High rates of drinking in seawater-adapted, compared with freshwater (FW)-adapted, flounder were associated with raised plasma chloride and osmotic concentrations. Hypotension in FW-adapted fish, after papaverine administration, gave rise to greatly elevated rates of drinking. This dipsogenic response apparently relied on activation of the endogenous renin-angiotensin system (RAS) and was abolished by simultaneous administration of the converting enzyme inhibitor, captopril. Exogenous angiotensin II was shown to be dipsogenic and vasopressor in the FW-adapted fish. The physiological importance of the activation of the RAS in the control of drinking behavior in euryhaline fish is discussed.

Animals↗
PubMed1985

Renal sodium retention and vasopressin induced kaliuresis in ethanol anaesthetised rats.

Renal electrolyte excretion has been examined in water loaded ethanol anaesthetised rats receiving continuous iv saline (0.077 M NaCl) infusion. These animals exhibited very low rates of Na+, K+ and Cl- excretion by comparison with Inactin anaesthetised rats. Water loaded Inactin anaesthetised rats also showed a degree of Na retention but both Na+ and K+ excretory rates were higher than in ethanol anaesthetised animals. Plasma aldosterone levels did not differ between ethanol and Inactin anaesthetised groups. Vasopressin administration did not effect Na+ but potentiated K+ excretion in ethanol anaesthetised animals. This contrasted with the potent natriuretic and weak kaliuretic action of vasopressin in water loaded Inactin anaesthetised rats. The significance of abnormal renal electrolyte handling and the marked kaliuretic effect of vasopressin to the use of ethanol anaesthetised animals for vasopressin bioassay is discussed.

Aldosterone↗
PubMed1984

Natriuretic response of the rat to plasma concentrations of arginine vasopressin within the physiological range.

The relationship of plasma vasopressin concentrations in the physiological range to renal electrolyte excretion was investigated. Unanaesthetized rats, when normally hydrated, were found to have a plasma vasopressin concentration of 1.13 +/- 0.15 mu u./ml. 16 h water deprivation raised this to 1.98 +/- 0.21 mu u./ml. Inactin-anaesthetized rats infused with 0.45% NaCl had a plasma vasopressin concentration of 1.19 +/- 0.18 mu u./ml. Administration of synthetic arginine vasopressin at 6 and 24 mu u./min raised plasma vasopressin levels to 1.88 +/- 0.17 and 4.26 +/- 0.43 microunits./ml respectively. In addition to the expected antidiuresis, vasopressin at a rate of 6 microunits./min also produced a highly significant increase in Na+ excretion from 8.9 +/- 0.6 to 10.5 +/- 0.6 mumol/min and Cl- excretion from 9.1 +/- 0.7 to 10.5 +/- 0.7 mumol/min. At 24 microunits./min it produced larger increases in Na+ and Cl- excretion. Inactin-anaesthetized hypophysectomized rats infused with 0.45% NaCl had a plasma vasopressin concentration of only 0.17 +/- 0.04 microunits./ml. Administration of vasopressin at 6 and 24 microunits./ml raised plasma vasopressin levels in these animals to 0.63 +/- 0.17 and 2.20 +/- 0.11 microunits./ml respectively. 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. 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.

Animals↗
PubMed1983

The renin-angiotensin system and drinking in the euryhaline flounder, Platichthys flesus.

Drinking behaviour and its possible regulation by the renin-angiotensin system (RAS) has been examined in the euryhaline flounder. Fluid intake was greater in seawater (SW)-adapted than freshwater (FW)-adapted fish, the latter having significantly lower plasma sodium, chloride, and osmotic concentrations. Oesophageal cannulation in SW-adapted fish resulted in further elevation of drinking rates, which increased proportionally with progressive body water loss as measured by the fall in body weight and rise in plasma tonicity. The influence of the RAS on drinking in SW-adapted fish was examined in animals with an intact gastrointestinal tract. Fluid intake fell markedly following administration of the converting enzyme inhibitor, Captopril. Infusions of angiotensin I (AI) and angiotensin II (AII) induced dose-related increments in the rate of drinking. The increased drinking in response to AI was inhibited, however, by the simultaneous administration of Captopril. The results are consistent with the presence in the flounder of the major elements of the RAS, including AI, AII, and a converting enzyme-like substance. The RAS appears to play an important regulatory role in the adaptative drinking behaviour associated with migration of euryhaline teleosts between FW and SW.

Adaptation, Physiological↗
PubMed1983

Oxytocin and renal function in the rat; an investigation of a possible proximal site of action.

Direct measurements of proximal tubular fluid reabsorption have been employed to examine the possible renal site of action of oxytocin. In whole kidney studies the natriuresis and chloriuresis, which occurred during the period of oxytocin infusion, did not coincide with the associated diuresis. The latter reached a peak 10-20 min after hormone administration has ceased. The separation in the saliuretic and diuretic responses underlines the apparent independence of these actions of oxytocin on the renal handling of water and electrolytes. The disturbances in renal function were not related to any change in glomerular filtration rate (gfr) and an examination of single nephron function failed to detect any significant effect of oxytocin on proximal tubular reabsorption. The renal actions of oxytocin would therefore appear to emanate from altered tubular rather than glomerular function, though the present study provides no support for a proximal site of action.

Animals↗