Biomedical subjects

R J Balment

Publications and source records attributed to R J Balment.

At least 73 records · Page 4Linked to original sources

PubMed1993

A novel computer-driven, servo-controlled fluid replacement technique and its application to renal function studies in conscious rats.

1. A new rat model has been developed allowing body fluid status to be accurately controlled and maintained throughout experimentation by computer-driven, servo-controlled replacement of spontaneous urinary fluid losses. 2. Experiments in vitro were performed to test the accuracy of the servo system, and experiments in vivo were carried out to re-assess basic renal function in servo-controlled vasopressin-replete Long Evans and vasopressin-deficient Brattleboro rats. The model was further evaluated in water-diuretic Wistar rats with or without administration of a vasopressin V2-receptor agonist, 1-desamino-8-D-arginine vasopressin. 3. The data gained from the present study indicate the suitability of the servo-controlled replacement system for conscious renal function studies in three different rat strains. Haemodynamic and renal function variables measured were demonstrated to be stable throughout a 5 h experimental procedure and reproducible between repeated experimental occasions over a 14 day post-operative period. 4. Using the servo-control technique, the expected action of 1-desamino-8-D-arginine vasopressin on renal water handling was demonstrated, but the natriuretic effect reported by some workers was not evident. 5. Since the servo-controlled fluid replacement technique maintains many of the inherent differences between vasopressin-replete Long Evans and vasopressin-deficient Brattleboro rats and eliminates the changes in body fluid volume during transition from a diuretic to an antidiuretic state, the model confers an advantage over previously employed constant infusion protocols.

Animals↗

PubMed1993

Arginine vasopressin-induced natriuresis in the anaesthetized rat: involvement of V1 and V2 receptors.

The present study was undertaken to determine the involvement of the two established vasopressin receptor subtypes (V1 and V2) in arginine vasopressin (AVP)-induced natriuresis and also to determine whether changes in mean arterial pressure (MAP) and/or the renally active hormones atrial natriuretic peptide (ANP), angiotensin II (AII) and aldosterone are a prerequisite for the expression of AVP-induced natriuresis. In Sprague-Dawley rats which were anaesthetized with Inactin (5-ethyl-5-(1'-methylpropyl)-2-thiobarbiturate) and infused with 0.077 mol NaCl/l, infusion of 63 fmol AVP/min was found to be natriuretic whereas an approximately equipotent dose of the specific V2 agonist [deamino-cis1,D-Arg8]-vasopressin (dDAVP) did not induce natriuresis. The specific V1 antagonist [beta-mercapto-beta,beta-cyclopenta-methylene-propionyl1,O-Me- Tyr2,Arg8]-vasopressin when administered prior to infusion of 63 fmol AVP/min did not inhibit AVP-induced natriuresis. AVP-induced natriuresis was not accompanied by changes in MAP or in the plasma concentrations of the renally active hormones ANP, AII or aldosterone. These results suggest that neither the V1 nor the V2 receptors subtypes are involved in AVP-induced natriuresis. In addition, it was found that changes in MAP, plasma ANP, AII or aldosterone concentrations were not a prerequisite for AVP-induced natriuresis.

Aldosterone↗

PubMed1993

Patterns of neurohypophysial hormone release during dehydration in the rat.

A study was performed investigating the daily patterns of hormone release accompanying changes in fluid balance in the male rat during 48 h of dehydration. The blood volume decreased by 18%, the largest change occurring during the initial period when the rats showed an effective loss of body sodium. During the second day of dehydration, sodium retention was again seen. Plasma sodium concentrations showed a progressive increase, the total rise being 5-6%; the greatest changes were seen during the dark phases of the cycle which may be due to the nocturnal food intake. Plasma vasopressin and oxytocin concentrations were significantly elevated throughout dehydration to levels which could be reproduced by acutely increasing plasma sodium and decreasing blood volume to the same extent. The observed increases were influenced by the phase of the day-night cycle, being greatest over the dark phases of the cycle. The overall increases were greatest when dehydration commenced at the start of the dark phase. Dehydration initially led to a rise in plasma corticosterone concentrations, whilst plasma concentrations of atrial natriuretic peptide were decreased. Plasma angiotensin II concentrations rose significantly during the later period of sodium retention.

Angiotensin II↗

PubMed1993

The involvement of vasopressin in the renal actions of atrial natriuretic peptide in conscious fluid-balanced rats.

The renal and endocrine actions of atrial natriuretic peptide (ANP) administered at a rate to induce plasma concentrations within the physiological range have been re-examined in conscious rats in which body fluid volume was maintained by infusion of replacement fluid at a rate to match spontaneous urine losses (servo-controlled replacement) throughout experimentation. The involvement of vasopressin in the actions of ANP was assessed by comparing the responses induced in Brattleboro (DI) and Long-Evans (LE) rats. A rate of ANP administration inducing a less than twofold increment in circulating ANP concentration evoked a small but significant diuresis and natriuresis. In contrast to previous studies during which body fluid balance had not been maintained and the response to ANP was transient, renal responses were rapid in onset and sustained over the period of hormone administration. The change in renal excretion occurred without concomitant changes in mean arterial blood pressure, haematocrit or glomerular filtration rate, and without consistent alterations in the circulating concentrations of angiotensin II, vasopressin, aldosterone or corticosterone. Furthermore, although small differences between the two strains in the character of the response could be demonstrated, the evoked response was of similar magnitude in vasopressin-replete and -deficient animals. In summary, in conscious rats in which body fluid volume was maintained, the profile of the diuretic and natriuretic responses evoked by low-rate ANP administration was different from that previously observed in anaesthetized and/or constantly infused preparations; being rapid in onset and sustained.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Acute chloroquine administration increases renal sodium excretion.

The effect of a 2-hour intravenous chloroquine infusion (0.015, 0.030 and 1.25 micrograms min-1) on renal fluid and electrolyte handling was investigated in the saline infused, Inactin anaesthetized rat. Blood pressure and glomerular filtration rate were not affected by chloroquine administration, remaining around 128 mmHg and 2.4 ml min-1, respectively throughout the 5-hour post-equilibration period. Chloroquine produced an increase in Na+ and Cl- excretion without affecting the urine flow. By 1 hour after the start of treatment (0.03 micrograms chloroquine min-1) the Na+ excretion rate had increased to 14.5 +/- 2.1 mumol min-1 (n = 6), and was significantly (P < 0.01) greater than in control animals (8.6 +/- 1.0 mumol min-1) at the corresponding time. Parallel but lesser increases in Cl- excretion rates were also observed. The plasma aldosterone and corticosterone levels following either 10, 30 or 120 minutes infusion of chloroquine at 0.03 micrograms min-1 did not differ statistically from each other or from control values. It is concluded that acute chloroquine administration induces an increase in Na+ excretion. The mechanism of this natriuresis cannot be established from the present study, but is likely to involve altered tubular handling of Na+.

Aldosterone↗

PubMed1992

Renal, cardiovascular and endocrine effects of centrally administered galanin in the anaesthetised rat.

Several studies implicate galanin as a central neuromodulator with an ability to influence hypothalamic and pituitary secretion. Central galanin content is also sensitive to the state of body hydration. Cardiovascular, renal and peripheral endocrine changes evoked by intracerebroventricular administration of galanin have been examined in the anaesthetized rat. Central galanin infusion consistently induced a transitory diuresis, the increase in urine flow being associated with a reduction in urine osmolality. There was no demonstrable change in plasma vasopressin concentration at the end of a 40 min galanin infusion. However, plasma aldosterone and corticosterone concentrations were significantly reduced by comparison with time-matched vehicle infused controls. There were no clear changes in renal electrolyte excretion or in heart rate or mean arterial blood pressure during the study period. The findings of this study support a participatory role for galanin in body fluid homeostasis, though the mechanisms responsible for mediating its central action on urine production remain unclear.

Animals↗

PubMed1992

Purification and characterization of urotensin II and parvalbumin from an elasmobranch fish, Scyliorhinus canicula (common dogfish).

The caudal portion of the spinal cord of elasmobranch fish incorporates a diffuse neuroendocrine system. Using an antiserum raised against urotensin II from a teleost fish (goby) to facilitate purification, a peptide structurally related to urotensin II was isolated in pure form from an extract of neuroendocrine tissue from the spinal cord of the European common dogfish, Scyliorhinus canicula. The primary structure of the peptide was established as: Asn-Asn-Phe-Ser-Asp-Cys-Phe-Trp-Lys-Tyr-Cys-Val. The amino acid sequence was confirmed by chemical synthesis. A comparison of this sequence with those of the known teleost urotensin II peptides shows that the cyclic region of the molecule has been fully conserved between species and suggests that the presence of an acidic residue at position 5 and a hydrophobic residue at position 12 are important features for the biological activity of the peptide. The dogfish spinal cord extract also contained a high concentration of the calcium-binding protein, parvalbumin and the amino acid sequence at its NH2 terminus [residues (1-50)] was determined.

Amino Acid Sequence↗

PubMed1992

The effect of chronic and acute changes in plasma composition on vasopressin secretion and cerebrospinal fluid in the rat.

The effects of chronic and acute changes in plasma composition on the osmolality and sodium concentration of cerebrospinal fluid and plasma vasopressin (AVP) concentration have been examined. Chronic elevation of plasma osmolality in three strains of genetically AVP-deficient rats (Brattleboro and New Zealand hypertensive and normotensive Brattleboro) was associated with increased cerebrospinal fluid osmolality by comparison with AVP-replete controls (Long Evans and New Zealand genetically hypertensive and normotensive rats). The linear correlation between plasma and cerebrospinal fluid osmolality did not reflect a similar relationship between plasma and cerebrospinal fluid sodium concentration. Hypertensive animals exhibited a threefold higher plasma AVP concentration in association with significantly elevated cerebrospinal fluid osmolality by comparison with normotensive controls. Although ip hypertonic saline injection elicited parallel increases in plasma and cerebrospinal fluid osmolality and sodium concentration in both hypertensive and normotensive rats, only in the normotensives did this result in an increase in plasma AVP concentration. These results indicate that cerebrospinal fluid is subject to modest chronic and acute changes in osmolality and sodium concentration which may contribute to the osmotic control of AVP secretion. The disturbed control of vasopressin secretion in hypertensive rats may in part be related to the abnormal cerebrospinal fluid composition in these animals.

Animals↗

PubMed1992

Plasma atrial natriuretic peptide in vasopressin deficiency: the effects of acute water deprivation in rats.

Plasma concentrations of atrial natriuretic peptide (ANP) and other renally active hormones were measured in Long-Evans (LE) rats and vasopressin-deficient Brattleboro rats with diabetes insipidus (DI) in conditions of water repletion and deprivation, and in DI rats following chronic vasopressin replacement. In water-replete rats, vasopressin deficiency was associated with elevated circulating ANP and angiotensin II (AII) concentrations, while plasma adrenal steroid concentrations were depressed by comparison with LE rats. These differences were fully reversed after 7 days of vasopressin replacement in DI rats to restore normal water turnover. Water deprivation for 4 h had little effect on plasma tonicity or hormone profile in LE rats. In contrast, however, the unreplaced fluid loss during 4-h water deprivation in the DI rat was associated with a marked increase in plasma tonicity evident within 30 min. Plasma ANP concentrations fell substantially to levels below those in LE rats, coincident with a rise in adrenal steroid levels and independent of any clear change in AII. These changes in circulating ANP concentration were directly correlated with changes in plasma Na+ concentration, osmolality and tissue water content in the DI rats, underlining the importance of body fluid status in modulating the secretion of ANP. These data clearly show that plasma ANP concentration is increased in vasopressin deficiency, but emphasize the sensitivity of circulating hormone levels in vasopressin-deficient animals to acute changes in the state of hydration, underscoring the complex and labile interaction between body fluid and hormonal factors involved in the control of ANP secretion.

Aldosterone↗

PubMed1991

Pituitary and plasma arginine vasotocin levels in teleost fish.

The role of arginine vasotocin (AVT) in teleostean osmoregulation is unclear. Its administration may produce dose-dependent effects on renal fluid loss though the physiological significance of such effects is unknown due to the paucity of data on the normal range in pituitary and plasma AVT levels. The present study addresses these questions by examining the pituitary AVT activity in the flounder and plasma AVT concentrations in the flounder, trout, and carp following alterations in environmental tonicity. Flounder pituitary AVT content, measured by bioassay, was elevated in freshwater (FW)-acclimated compared to seawater (SW)-acclimated fish and rapidly fell or rose, respectively, following transfer from FW to SW or from SW to FW to attain a new steady state. Plasma levels of AVT were higher in FW than in SW in both flounder and trout and it would, therefore, appear that the synthesis, storage, and secretion of AVT may be enhanced in FW. In the stenohaline carp plasma levels of AVT were unchanged on acclimation from FW to 40% SW. In SW flounder there was a significant positive correlation between plasma osmolality and plasma AVT concentration. Such a relationship was not apparent in FW fish, which may reflect differing roles for the hormone in these two extremes of osmotic environment.

Animals↗

PubMed1991

Sexual dimorphism in renal function and hormonal status of New Zealand genetically hypertensive rats.

Renal water and electrolyte handling and related plasma hormone levels were measured in male and female New Zealand genetically hypertensive and normotensive rats, in an attempt to establish any potentially important sex-related differences in these parameters. Male hypertensive rats had higher blood pressure than female hypertensive rats, but normotensive rats showed no such sex difference. Both groups of males had higher fluid turnover rates than respective females, and this was associated with raised plasma vasopressin in hypertensive males. Female hypertensive rats excreted more sodium, potassium and chloride in association with lower plasma aldosterone and higher corticosterone levels compared with the other groups. Plasma electrolytes did not differ between the four groups, but plasma osmolality was higher in hypertensive than normotensive rats of both sexes. A higher rate of electrolyte loss and lower fluid turnover in association with reduced plasma vasopressin may contribute to the lower blood pressure of female compared with male hypertensive rats.

Aldosterone↗

PubMed1991

Atrial natriuretic factor stimulates in-vivo and in-vitro secretion of cortisol in teleosts.

Atrial natriuretic factor (ANF) has been shown to increase circulating cortisol levels in cannulated, free-swimming seawater (SW)-adapted flounders. Increases were apparent within 30 min of i.v. injection of human ANF (hANF;10 micrograms/kg bw) and the increase in plasma cortisol was maintained throughout the 5h experimental period. No such increase was observed in vehicle-injected controls. This apparent steroidogenic effect of ANF was supported by an ANF-induced increase in in-vitro secretion of cortisol by interrenal tissue from SW-adapted trout. By contrast hANF had no significant effect on tissue derived from freshwater adapted trout. An ANF-induced increase in plasma cortisol by a direct effect on interrenal steroidogenesis in SW teleosts would be an appropriate response for survival in hypertonic media.

Animals↗

PubMed1991

Influence of oxytocin on sodium excretion in the anaesthetized Brattleboro rat.

The contribution of oxytocin to the maintenance of renal Na+ excretion in the Brattleboro rat has been examined in animals infused with hypotonic saline. Brattleboro rats exhibited hypernatraemia and hyperosmolality associated with greatly increased plasma concentrations of oxytocin by comparison with Long-Evans control rats. Neurohypophysectomy to remove the secretion of the remaining posterior pituitary peptide, oxytocin, led to greatly diminished rates of Na+ excretion in the Brattleboro rat. Oxytocin replacement to achieve plasma levels equivalent to those in intact Brattleboro rats produced a substantial and sustained natriuresis in the neurohypophysectomized animal. Oxytocin secretion evoked in response to saline infusion would thus appear to be effective in promoting renal Na+ excretion in the absence of vasopressin in the Brattleboro rat.

Anesthesia, General↗

PubMed1991

Renal effects of aldosterone in the sodium bicarbonate infused rat.

The present study investigated the renal function in male Sprague-Dawley rats receiving continuous NaHCO3 (0.077 M) infusion. The renal effects of aldosterone administration in this preparation were also examined. Continuous NaHCO3 infusion significantly (p less than 0.01) depressed plasma aldosterone concentration to 2.36 +/- 1.22 nmol (n = 8) when compared to saline infused rats (4.36 +/- 0.72 nmol, n = 7). The low plasma aldosterone levels in HCO3- infused rats was associated with renal loss of large amounts of K+ and hypokalaemia. Aldosterone administration (42 pmol/min) for 2 h significantly (p less than 0.01) reduced the Na+ excretion rate in bicarbonate infused rats from a mean peak of 9.82 +/- 1.16 to 5.16 +/- 1.20 mumol/min (n = 8). Aldosterone administration did not alter renal excretion in saline-infused rats. It is concluded that NaHCO3 loading depressed endogenous aldosterone secretion, and that this lowered endogenous plasma aldosterone level allows the mineralocortoid effect of exogenous aldosterone to be observed.

Acid-Base Equilibrium↗

PubMed1990

Post-translational processing of prepro-urotensin II.

The primary structure of a teleost prepro-urotensin II may be deduced from the nucleotide sequence of cloned DNA complementary to carp prepro-urotensin II mRNA but the pathway of post-translational processing of the precursor is unknown. In this study, we have isolated four peptides from an extract of flounder urophysis that are derived from prepro-urotensin II by proteolytic cleavage. The amino acid sequences of the peptides demonstrate that flounder prepro-urotensin II is cleaved at two monobasic processing sites (single arginine residues) to generate peptides with limited homology to carp prepro-urotensin II-(22-41)-, -(42-87)- and -(88-110)-peptides. Cleavage at a tribasic residue processing site generates a urotensin II with the primary structure: Ala-Gly-Thr-Thr-Glu-Cys-Phe-Trp-Lys-Tyr-Cys-Val. Urotensin II-(4-12)-peptide represented a minor component in the extract.

Amino Acid Sequence↗

PubMed1990

The renin-angiotensin system and the regulation of plasma cortisol in the flounder, Platichthys flesus.

The changes in arterial blood pressure and plasma cortisol concentration in response to exogenous angiotensin II (AII) and to manipulation of the endogenous renin-angiotensin system (RAS) have been examined in the flounder, Platichthys flesus. Intravenous [Asp1Val5]AII was pressor in a dose-dependent manner over the range of 0.25-250 micrograms/kg. Sequential blood sampling revealed steroidogenic stimulation, measured as change in plasma cortisol concentration, by doses of AII greater than 2.5 micrograms/kg. Enhanced circulating cortisol levels were measured some time after recovery of normal systemic blood pressure, suggesting that the change in plasma steroid concentration was not entirely dependent on the change in systemic blood pressure. Administration of the vasodilator papaverine produced immediate hypotension followed by gradual recovery in blood pressure, which was accompanied by a sustained increment in circulating cortisol. Both blood pressure recovery and the increased plasma steroid concentration were inhibited by prior treatment with the angiotensin converting enzyme inhibitor captopril. These results are consistent with a physiologically important role for the RAS in the control of plasma cortisol levels which complements its demonstrated pressor and dipsogenic actions in the flounder: the RAS may thus afford an integrating influence on the mechanisms of body fluid homeostasis in this euryhaline species.

Angiotensin II↗

PubMed1990

Kappa-opioid-receptor agonists modulate the renal excretion of water and electrolytes in anaesthetized rats.

1. Subcutaneous injection of the kappa-opioid agonists U50,488 (10 mg kg-1) and tifluadom (3.5 mg kg-1) into Inactin-anaesthetized, saline-infused rats was associated with a diuresis, antinatriuresis and antikaliuresis which lasted for up to 2 h. A high (5 mg kg-1), but not low (0.1 mg kg-1), dose of naloxone blocked the renal effects of U50,488. 2. U50,488 administration in anaesthetized, vasopressin-deficient Brattleboro DI rats was associated with an attenuated diuresis, though the antinatriuretic response remained intact. 3. The diuretic action of U50,488 was associated with an increase in glomerular filtration rate while fractional fluid reabsorption remained steady. In contrast, fractional sodium and potassium reabsorption were increased. 4. These data suggest that kappa-opioid agonists alter renal handling of both water and electrolytes. This appears to be mediated by two separate mechanisms: increased fluid loss largely reflects altered glomerular events while the fall in electrolyte excretion results from altered tubular handling.

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

PubMed1990

The renal and vascular effects of central angiotensin II and atrial natriuretic factor in the anaesthetized rat.

1. The interaction between atrial natriuretic factor (ANF) and angiotensin II (Ang II) within the brain to influence renal function and blood pressure was studied in Inactin-anaesthetized male Sprague-Dawley rats. 2. Central infusion of ANF produced a diuresis which was associated with a significant decrease in plasma arginine vasopressin (AVP) level. There was no change in sodium excretion rate over the 80 min of intracerebroventricular ANF infusion and ANF produced no detectable change in mean arterial blood pressure. 3. Central Ang II administration produced a significant decrease in urine flow, which was associated with elevated plasma AVP, an increase in sodium excretion and a rise in mean arterial blood pressure. 4. Combined ANF and Ang II infusion produced an antidiuresis, which was associated with increased plasma AVP concentration. Both the natriuretic and vasopressor actions of central Ang II were abolished when ANF was co-administered. 5. It is concluded that ANF and Ang II interact centrally; ANF antagonizes the pressor and natriuretic effects but not the antidiuretic effects of central Ang II. These data suggest the possibility of distinct and separate sites within the brain through which Ang II influences vasopressin release and renal sodium handling and elevates blood pressure.

Angiotensin II↗