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R J Balment

Publications and source records attributed to R J Balment.

At least 55 records · Page 3Linked to original sources
PubMed1997

Arginine vasopressin increases renal sodium excretion in the anesthetized rat through V1 receptors.

We have previously suggested that the increase in renal Na+ excretion in response to physiological doses of arginine vasopressin (AVP) is not directly linked to the V2-mediated antidiuretic effect. In the present study we investigated the possible involvement of AVP V1 receptors in this natriuresis using a specific AVP V1 antagonist [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid), 2-O-methyltyrosine arginine vasopressin, d(CH2)5[Tyr(Me)2]AVP, infused at a rate of 15 ng.min-1. Male anesthetized Sprague-Dawley rats were placed on a continuous jugular infusion of 0.077 M NaCl at 150 microL.min-1. After a 3-h equilibration period, samples were collected at 20-min intervals for 4 h for the determination of urine flow, and Na+ and K+ excretion rates. In those animals in which the effects of AVP were studied, a 1-h control period was allowed following which AVP was infused at 0.02-0.08 pmol.min-1 for 1 h 20 min in separate groups of animals and then returned to the infusate alone for the last part of the experiment. In other groups the AVP V1 antagonist d(CH2)5[Tyr(Me)2]AVP (15 ng.min-1) alone or in combination with AVP (at various dose rates) was also administered for 1 h 20 min. All dose rates of AVP produced an antidiuresis which was associated significantly to increased Na+ excretion rate. However, AVP administration at the median dose rate (0.04 pmol.min-1) significantly (p < 0.01) decreased the amount of urine voided by comparison with control animals (6.34 +/- 1.05 ml vs. 11.892 +/- 0.03 mL, n = 7) although the urinary Na+ was elevated (967 +/- 18 mumol, vs. 742 +/- 81 mumol, n = 7). This AVP-induced increase in urinary Na+ loss was abolished in animals receiving combined AVP (0.04 pmol.min-1) and AVP V1 antagonist (674 +/- 47 mumol, n = 7) although the antidiuretic effect persisted. Urine flow and Na+ excretion rates remained unchanged in groups of animals administered AVP V1 antagonist alone. In all groups, the K+ excretion rates did not significantly differ. It is concluded that the V1 receptor mediates the natriuretic effect of AVP.

Anesthesia↗
PubMed1996

Synthesis and release of acetylcholine by the isolated perifused trout caudal neurosecretory system.

The neurons of the caudal neurosecretory system of teleosts contain, in addition to urotensin I and urotensin II, a high concentration of acetylcholine (T. Ichikawa, 1978, Gen. Comp. Endocrinol. 35, 226-233). The isolated urophysis (and attached terminal spinal cord region) of the rainbow trout Oncorhynchus mykiss was incubated with [3H]choline (0.2 MBq/ml) for 45 min at 22 degrees in the presence of the cholinesterase inhibitor, physostigmine. Unreacted choline was removed by perifusion with fish Ringer solution. Incorporation of radioactivity into newly synthesized [3H]acetylcholine was 4.9 +/- 2.1 x 10(5) Bq/g wet tissue wt. When incubations were carried out in the presence of hemicholinium-3, an inhibitor of high-affinity choline uptake, or when physostigmine was omitted from the incubation buffer and/or when [3H]inulin was substituted for [3H]choline, the incorporation of radioactivity was greatly reduced (< 0.5 x 10(5) Bq/g). The release of [3H]acetylcholine from the preparation increased to 338 +/- 59% of basal (P < 0.05) when the concentration of K+ in the perifusion buffer was raised to 41 mM, but neither urotensin I (10(-7) M) nor urotensin II (10(-6) M) had a significant effect on release. The data indicate that the trout caudal neurosecretory system possesses a high-affinity uptake system for choline and that newly synthesized acetylcholine is released in response to a depolarizing stimulus.

Acetylcholine↗
PubMed1996

Arginine vasopressin mediates the chloroquine induced increase in renal sodium excretion.

We postulated that chloroquine increases plasma arginine vasopressin (AVP) concentrations thus altering renal Na+ clearance. Therefore, we studied a relationship between plasma AVP concentrations and urinary Na+ output in separate groups of Sprague-Dawley (SD) rats administered chloroquine (3 micrograms/min) for 1 h 20 min. We also monitored Na+ excretion rates in Brattleboro AVP-deficient Di rats challenged with hypotonic saline load and administered chloroquine for 1 h 20 min. To establish whether chloroquine-induced changes in renal Na+ excretion were mediated via AVP V1 receptors, we studied Na+ excretion rates in groups of SD rats administered chloroquine or AVP in the presence of AVP V1 receptor antagonist (1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid)-2-O-methyltyrosine arginine vasopressin (d(CH2)5(Tyr(Me)2) AVP) at 11 pmol/min for 1 h 20 min. The Na+ excretion rate rose significantly (P < 0.01) from a pretreatment level of 9.8 +/- 1.0 mumol/min to a peak of 14.1 +/- 0.9 mumol/min in SD rats (n = 7) administered chloroquine. The Na+ excretion rate remained unaltered around 8.5 mumol/min in rats simultaneously administered chloroquine and the AVP V1 receptor antagonist. This compared with control rats (8.1 +/- 0.5 mumol/min, n = 7) and animals administered AVP V1 receptor antagonist alone (8.7 +/- 0.6 mumol/min, n = 7). Chloroquine did not affect urine flow, Na+ or K+ excretion rates in Brattleboro AVP-deficient Di rats. Administration of AVP alone was associated with significant increases in renal Na+ excretion rate. Blockade of AVP V1 receptors abolished the AVP-dependent increase in urinary Na+ loss. We conclude that at least part of the chloroquine-induced increase in Na+ excretion is mediated by chloroquine stimulating an increase in plasma AVP concentration.

Aldosterone↗
PubMed1996

Adrenergic receptor activation hyperpolarizes the caudal neurosecretory cells of the flounder, Platichthys flesus.

The physiological factors that govern activity of the caudal neurosecretory system in teleost fish are poorly understood. Immunocytochemical evidence indicates that the neurosecretory Dahlgren cells are innervated by descending monoaminergic fibres. Using intracellular recording techniques in an isolated preparation of the posterior spinal cord of the flounder (Platichthys flesus) we have demonstrated that superfusion of adrenaline or noradrenaline (10(-7) - 10(-3) M) causes hyperpolarization of Dahlgren cells (up to -30 mV). This hyperpolarization is likely to reflect an inhibitory effect of noradrenergic nerves on the neurosecretory system in vivo, reducing the rate of hormone release. Fluctuations in the input resistance and membrane time constant suggest involvement of a multiplicity of cellular mechanisms, including the opening and closing of populations of ion-selective channels. Superfusion with dopamine (10(-7) - 10(-3) M) had no effect. Superfusion with the beta-adrenoreceptor agonist, isoprenaline, caused hyperpolarization but to a markedly lesser extent than the maximum effect of adrenaline or noradrenaline, suggesting that their effects are mediated, only in part, by a beta-adrenoreceptor subtype. Superfusion of the preparation with a membrane permeable, non-hydrolysable cyclic AMP analogue (8-[4-chlorophenylthio]-cAMP) resulted in a slight hyperpolarization which was accompanied by a small, but significant, increase in input resistance. These data are consistent with at least part of the beta-adrenoreceptor mediated effect involving closure of cAMP-sensitive ion channels. Superfusion with the alpha 1-adrenoreceptor agonist, phenylephrine, had no effect on any electrophysiological parameter studied. However, the alpha 2-adrenoreceptor agonist, clonidine, caused hyperpolarization which again failed to reach the maximum level produced by adrenaline or noradrenaline. Together, these data suggest that the adrenergic inhibition of Dahlgren cell activity is mediated by both alpha 2- and beta-adrenoreceptor subtypes.

Adrenergic alpha-2 Receptor Antagonists↗
PubMed1995

A peptide from the caudal neurosecretory system of the dogfish Scyliorhinus canicula that is structurally related to urotensin I.

Using reversed-phase HPLC in combination with a radioimmunoassay for ovine corticotropin-releasing hormone (CRH), a peptide with CRH-like immunoreactivity was isolated in pure form from an extract of the caudal spinal cord region of the spotted dogfish, Scyliorhinus canicula. The primary structure of the peptide was established as Pro-Ala-Glu-Thr-Pro-Asn-Ser-Leu10-Asp-Leu-Thr-Phe-His-Leu-Leu-Arg- Glu-Met-Ile- Glu20-Ile-Ala-Lys-His-Glu-Asn-Gln-Gln-Met-Gln30-Ala-Asp-Ser- Asn-Arg-Arg-Ile-Met - Asp-Thr40-Ile.NH2. This amino acid sequence shows moderate structural similarity to Catostomus urotensin I (51%) and to human CRH (56%). The data provide, therefore, chemical evidence to support the conclusions of earlier immunohistochemical studies that the diffuse caudal neurosecretory system of elasmobranchs produces a peptide that is immunochemically related to teleost urotensin I peptides. However, the primary structure of urotensin I has been poorly conserved during evolution.

Amino Acid Sequence↗
PubMed1995

Plasma sialic acid in animal models of diabetes mellitus: evidence for modulation of sialic acid concentrations by insulin deficiency.

An elevated circulating sialic acid concentration is a risk factor for cardiovascular disease. Serum sialic acid levels are elevated in NIDDM but not in uncomplicated IDDM. To study why sialic acid is increased in some types of diabetes, we assayed plasma sialic acid in various animal models of diabetes: obese (ob/ob) mice, before and after streptozotocin treatment, neonatal streptozotocin-treated (nSTZ) rats, and diabetic BB rats during and after insulin treatment. In obese mice, which exhibit moderate hyperglycemia and marked hyperinsulinemia, plasma sialic acid was decreased by 45% (fed) and 42% (fasted), compared to lean controls. Fasting reduced plasma glucose and insulin but increased sialic acid in the obese and lean mice. There was a negative correlation (r = -0.84, P < 0.001) between log plasma insulin and sialic acid in the lean and obese mice. The plasma sialic acid:globulin ratio was reduced by 35% in obese mice vs. lean controls, indicating that there may be altered sialylation of glycoproteins in obese mice. Streptozotocin treatment of obese and lean mice reduced plasma insulin but increased sialic acid. In nSTZ rats, hyperglycemia was associated with mild hypoinsulinemia, but not significantly different from control animals, and sialic acid was not altered. In diabetic BB rats, plasma glucose rose from a mean of 4.9 to 23.5 mM 48 hr after insulin withdrawal but sialic acid did not change. We conclude that an elevated plasma sialic acid level is associated with marked insulin deficiency, rather than hyperglycemia per se. The magnitude and speed of this change in sialic acid varies between species.

Animals↗
PubMed1995

Renal, endocrine and vascular effects of atrial natriuretic peptide in a novel vasopressin-deficient genetically hypertensive strain of rat.

In the absence of the potentially confounding influence of vasopressin in hypertension, the effects of atrial natriuretic peptide (ANP) on arterial blood pressure and renal handling of water and sodium were assessed from comparison of responses to intravenous ANP infusion in anaesthetized vasopressin-deficient New Zealand genetically hypertensive (DI/H) rats and their normotensive substrain (DI/N). After 320 min of hypotonic saline infusion, plasma ANP concentration was significantly higher in DI/H compared with DI/N rats. ANP administration increased circulating ANP concentration in both groups. Plasma angiotensin II concentration was higher in DI/H than in DI/N rats; infusion of ANP raised circulating angiotensin II in both groups though this achieved statistical significance only in DI/N rats. Plasma aldosterone concentrations were initially similar in normotensive and hypertensive animals and, in both, were reduced markedly by I.V. ANP infusion. Administration of ANP produced sustained hypotension in both groups. However, the hypotensive effect of ANP was more pronounced in DI/H compared with DI/N rats. Heart rate was initially similar in the two groups, and infusion of ANP produced no detectable change. By comparison with animals maintained on hormone-free infusate, urine flow increased markedly over the 80 min period of ANP infusion in both groups, by 142% in DI/H rats and 127% in DI/N rats. ANP administration produced a natriuresis in both groups but the increase in Na+ excretion was much greater in DI/H (342%) than in DI/N (139%) rats. It appears from the current study that vasopressin-deficient hypertensive rats are more sensitive to ANP with regard to effects on blood pressure and renal excretion than their vasopressin-deficient normotensive substrain. These differences may, in part, reflect adjustments to long-term elevation in blood pressure and in plasma ANP concentration in hypertension and, in part, rely on the associated disturbances in related endocrine systems.

Aldosterone↗
PubMed1995

Effect of acute manipulation of blood volume and osmolality on plasma [AVT] in seawater flounder.

Chronically cannulated seawater (SW)-adapted flounder (Platichthys flesus) were used unanesthetized and unrestrained in an experimental series that acutely manipulated blood volume and plasma osmolality to determine their influence on plasma arginine vasotocin (AVT) concentrations. Immunoreactive AVT was measured using a radioimmunoassay validated for flounder and other teleosts. After hemorrhage-induced hypovolemia or hypervolemia produced by saline infusion, no major changes in plasma AVT concentrations were detected. Raising plasma osmolality by intraperitoneal injection of 1 M NaCl compared with control 150 mM NaCl-injected fish (329.4 +/- 3.4 vs. 320.4 +/- 3.0 mosmol/kgH2O, P < 0.05) produced an increase in plasma AVT concentration (6.7 +/- 1.2 vs. 4.2 +/- 0.2 fmol/ml, P < 0.05). In a separate study, plasma composition in a large number of uncannulated SW-adapted flounder was determined. This demonstrated a positive linear relationship between the natural variation in plasma AVT concentrations and plasma osmolality and Na+ and Cl- concentrations observed between fish. These data indicate that AVT secretion in SW-adapted flounder is closely related and perhaps directly sensitive to changes in plasma tonicity.

Animals↗
PubMed1995

Renal fluid and electrolyte handling in streptozotocin-diabetic rats.

Male Sprague-Dawley rats (300-400 g) were made diabetic by an i.p. injection of streptozotocin (STZ, 60 mg/kg in citrate buffer, n = 8) to examine renal function in well-established diabetes mellitus. Vehicle-injected animals (n = 8) acted as controls. The mean weekly total amounts of food taken by control and STZ-diabetic rats did not differ, but diabetic rats exhibited diarrhea and drank more water. STZ-diabetic rats progressively lost weight from the first to the third week but gained weight in the fourth week. At 5 weeks the weight stabilized, plasma glucose concentration was elevated, and this was associated with increased kidney weight. The weekly urine volume from STZ-diabetic rats was elevated throughout the 5-week period of study and this was associated with significantly lower urinary outputs of Na+ and higher outputs of K+ than those of control animals. After 5 weeks of STZ diabetes, plasma corticosterone and aldosterone concentrations in unanesthetized rats did not differ significantly from values seen in controls. To examine renal function in more detail, groups of Inactin-anesthetized 5-week STZ-diabetic rats (n = 7) and control rats (n = 7) were placed on continuous jugular infusion of 0.077 M NaCl at 150 microL/min for 8.5 h. Following a 3.5-h equilibration period, urine flow and Na+, K+, and Cl- outputs were determined for the subsequent 5-h period, with mean arterial pressure and glomerular filtration rate (GFR). STZ-diabetic rats voided significantly less of the infused fluid and the urinary excretions of Na+ and K+ were lower than those of controls. Mean arterial blood pressure and GFR values in STZ-diabetic rats did not differ statistically from those seen in controls. Following hypotonic saline infusion for 8.5 h the levels of aldosterone were elevated significantly (p < 0.01) in STZ-diabetic rats by comparison with control animals (5.36 +/- 1.58 nmol/L, n = 7 vs. 2.36 +/- 0.12 nmol/L, n = 7). It is concluded that a challenge of hypotonic saline load to rats with 5 weeks of STZ diabetes mellitus elevates plasma aldosterone to reduce the ability to excrete Na+.

Aldosterone↗
PubMed1994

Peptide hormones influence in vitro interrenal secretion of cortisol in the trout, Oncorhynchus mykiss.

Adrenocorticotrophic hormone (ACTH), angiotensin II (AII), and the urophysial peptides, urotensins I and II (UI and UII), stimulate cortisol secretion by interrenal preparations of seawater (SW) and freshwater (FW) adapted trout. Steroid secretion was not disturbed in sham-treated control groups. The increased cortisol secretion following perifusion of tissue with 10(-7) M ACTH in combination with 10(-7) M AII, 10(-7) M UI, or 10(-7) M UII was greater than after separate administration of ACTH, AII, UI, or UII. These responses were no greater than the summation of the separate effects of ACTH, AII, or UII in SW and FW derived tissue or of ACTH and UI in FW derived tissue. However, the increased cortisol secretion (600-700%) after UI and ACTH in combination in SW adapted fish was significantly higher than the summated responses (100-200%) to UI and ACTH when administered separately. These results suggest that in SW fish interrenal UI enhances the steroidogenic action of ACTH, a potentially important response in SW teleost fish.

Adrenocorticotropic Hormone↗
PubMed1994

A radioimmunoassay for the determination of arginine vasotocin (AVT): plasma and pituitary concentrations in fresh- and seawater fish.

A specific radioimmunoassay was developed and characterized for the measurement of arginine vasotocin (AVT) in teleost fish. Specificity of the antibody for AVT was demonstrated by parallelism of a series of AVT standards with serially diluted pituitary and plasma extracts. Crossreactivity of the antibody with the other teleost neurohypophysial peptide, isotocin, was less than 1% and the sensitivity of the assay was 0.24 fmol/assay tube. AVT was extracted from plasma by reverse-phase liquid chromatography [efficiency of 87.6 +/- 9.3% (n = 5)] and demonstrated as an effective procedure for plasma volumes ranging from 0.4 to 1.2 ml. Plasma AVT concentrations measured in a range of euryhaline and stenohaline teleost fish were between 10(-12) and 2 x 10(-11) M (1-20 pg/ml). There were no consistent differences between plasma AVT levels in euryhaline fish (flounder, trout, and eel) adapted to fresh water (FW) and sea water (SW). In flounder, pituitary AVT levels in FW- and SW-adapted fish were also similar.

Adaptation, Physiological↗
PubMed1994

Interaction of aldosterone and oxytocin to influence renal sodium excretion in rats.

The possibility of an interaction between oxytocin and aldosterone to influence renal Na+ excretion was investigated in Inactin-anaesthetized male Sprague-Dawley rats. Endogenous plasma concentrations of aldosterone were suppressed by either adrenalectomy or bicarbonate infusion. The effects of 2 h intravenous administration of oxytocin (0.04 pmol/min) and/or aldosterone (42 pmol/min) on renal Na+ handling were studied in 0.077 M NaCl-infused adrenalectomized (Adx) rats and groups of intact animals that were infused with 0.077 M NaHCO3. Aldosterone alone significantly (P < 0.01) reduced Na+ excretion from pretreatment peak value of 5.0 +/- 1.0 to 1.5 +/- 0.4 mumol/min in Adx animals (n = 8) and 9.2 +/- 1.2 to 5.2 +/- 1.2 mumol/min in NaHCO3-infused rats (n = 8) by 2 h after the start of administration. However, combined administration of aldosterone and oxytocin was associated with a significantly (P < 0.01) increased Na+ excretion rate from a peak pretreatment value of 6.8 +/- 0.7 mumol/min to a peak value of 11.5 +/- 1.1 mumol/min by 1 h 40 min after the start of treatment in Adx rats (n = 7). In bicarbonate-infused rats (n = 8) Na+ excretion rose within 20 min of the start of treatment from a pretreatment peak of 9.0 +/- 0.8 mumol/min to a peak value of 13.5 +/- 0.8 mumol/min in response to combined hormone administration. In conclusion, we have shown that concomitant administration of aldosterone and oxytocin increased the rate of excretion of Na+ in two different preparations, which supports the idea of an interaction between the steroid and oxytocin to promote Na+ loss.

Adrenalectomy↗
PubMed1994

Lack of effect of atrial natriuretic peptide and urodilatin on vasopressin-stimulated cyclic AMP production in microdissected rat inner medullary collecting ducts.

It is unclear whether the diuretic effects of atrial natriuretic peptide (ANP) result, in part, from an inhibition of the renal actions of vasopressin. Moreover, accruing evidence suggests that the kidneys themselves may produce an ANP-like peptide, urodilatin, which shares many of the renal actions of ANP. The mechanism underlying the diuretic action of urodilatin has not yet been examined. Accordingly, we have investigated the potential modulatory actions of both ANP and urodilatin on vasopressin-stimulated cyclic AMP (cAMP) production in microdissected inner medullary collecting duct (IMCD) segments of rat kidney. ANP and urodilatin alone (at 10(-8) or 10(-6) M) had no demonstrable effect on cAMP accumulation in IMCD segments. Moreover, neither ANP nor urodilatin (each at 10(-6) M) significantly altered either the profile or the absolute magnitude of the cAMP response stimulated by vasopressin. These findings indicate that neither ANP nor urodilatin interacts with the vasopressin-sensitive adenylate cyclase site in the rat IMCD to contribute to its diuretic actions.

Adenylyl Cyclases↗
PubMed1994

The effects of oral chloroquine administration on kidney function.

The effects of 3 consecutive days of oral chloroquine (1 mg/100 g body weight) on kidney function and blood pressure were studied in male Sprague-Dawley rats that were challenged with hypotonic saline infusion 24 h after the last chloroquine administration. The rats were anesthetized with Inactin [5 ethyl-5-(1'-methylpropyl)-2-thiobarbiturate, Byk Gulden] and continuously infused with 0.077 M NaCl for 8 h; urine flow and electrolyte excretion rates were monitored during the last 5 h. Blood pressure and glomerular filtration rates were also measured. Kidney function was compromised in chloroquine-treated rats, which retained significantly more of the infused Na+ and Cl- by comparison to control-vehicle-treated rats. Throughout the experimental period, chloroquine-treated rats exhibited low blood pressure (80 mm Hg vs. 127 mm Hg) which was associated with low glomerular filtration rate. The plasma aldosterone concentrations were significantly (p < 0.01) elevated in rats pretreated with chloroquine at the end of the 8-h infusion of hypotonic saline, but corticosterone levels were significantly (p < 0.01) lower in the treated rats. It is concluded that chloroquine administration impairs kidney function, resulting in inappropriate Na+ and Cl- retention. This effect is likely to be mediated via chloroquine-induced increases in plasma aldosterone concentration and lowering of GFR.

Administration, Oral↗
PubMed1993

Primary structures and biological activities of substance-P-related peptides from the brain of the dogfish, Scyliorhinus canicula.

Two peptides with substance-P-like immunoreactivity were isolated in pure form from an extract of the brain of the elasmobranch fish, Scyliorhinus canicula (european common dogfish). One peptide was identical to scyliorhinin I, previously identified in dogfish intestine, and the second was the undecapeptide Lys-Pro-Arg-Pro-Gly-Gln-Phe-Phe-Gly-Leu-Met-CONH2 which is structurally similar to mammalian substance P. Scyliorhinin II or a peptide analogous to mammalian neurokinin A were not detected in the extract. Synthetic dogfish substance P ([Lys1, Arg3, Gly5]substance P) was approximately threefold more potent than mammalian substance P (Kd = 0.21 +/- 0.11 nM versus Kd = 0.74 +/- 0.17 nM; mean +/- SD; n = 6) in inhibiting the binding of 125I-labelled substance P to neurokinin (NK1) receptors in rat submandibular gland membranes. The vasodilator action of tachykinins in mammals is mediated primarily through interaction with NK1 receptors. Bolus intravenous injections of [Lys1, Arg3, Gly5]substance P (100 pmol) and scyliorhinin I (100 pmol) produced appreciable (> 4 kPa) decreases in arterial blood pressure in the rat whereas intravenous injections of up to 5 nmol of the peptides into conscious, unrestrained dogfish produced no change in arterial blood pressure, pulse amplitude or heart rate. Injections of greater amounts of the peptides (10-50 nmol) produced a slight increase (400-667 Pa) in blood pressure. The data indicate that mammalian-type NK1 tachykinin receptors are not involved in cardiovascular regulation in elasmobranch fish.

Amino Acid Sequence↗
PubMed1993

Peptide hormone-stimulated second messenger production in the teleostean nephron.

Renal actions of arginine vasotocin (AVT) and atrial natriuretic peptide (ANP) in teleosts are poorly defined. Administration of these hormones changes renal function, largely explained by systemic vascular effects. The present experiments examine the potential direct action of these hormones on the teleost nephron. This has been assessed from the hormones' abilities to stimulate their second messenger systems within isolated nephroi of the rainbow trout Onchorhynchus mykiss. Following initial experiments to define the experimental conditions, AVT was found to induce a dose-dependent increase in cAMP content of a suspension of nephroi incubated for 10 min at 10 degrees; 10(-5) M AVT provoking an increase of 846% (SW) and 829% (FW) above basal cAMP accumulation of 88 and 125 pmol/mg protein, respectively. This V2-type receptor response to AVT (or AVP) has previously been considered to be present only in the tetrapod kidney. ANP evoked a dose-dependent stimulation of cGMP accumulation from 1.3 (SW) or 1.9 (FW) pmol/mg protein basal levels to 5806 and 4405% of these levels, respectively, at the highest concentration used of 3.3 x 10(-7) M. Further experiments using isolated glomeruli from the eel Anguilla anguilla localized at least a part of the response to ANP to a glomerular site.

Anguilla↗