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PubMed2001

Parallel metabotropic pathways in the heart of the toad, Bufo marinus.

This study examined the transduction pathways activated by epinephrine in the pacemaker region of the toad heart. Recordings of membrane potential, force, and intracellular Ca(2+) concentration ([Ca(2+)](i)) were made from arrested toad sinus venosus. Sympathetic nerve stimulation activated non-alpha-, non-beta-adrenoceptors to evoke a membrane depolarization and a transient increase in [Ca(2+)](i). In contrast, the beta-adrenoceptor agonist isoprenaline (10 microM) caused membrane hyperpolarization and decreased [Ca(2+)](i). The phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (0.5 mM) mimicked the isoprenaline-evoked membrane hyperpolarization. Epinephrine (10-50 microM) caused an initial membrane depolarization and an increase in [Ca(2+)](i) followed by membrane hyperpolarization and decreased [Ca(2+)](i). The membrane depolarizations evoked by sympathetic nerve stimulation or epinephrine were abolished either by the phospholipase C inhibitor U-73122 (20 microM) or by the blocker of D-myo-inositol 1,4,5,-trisphosphate-induced Ca(2+) release, 2-aminoethoxydiphenyl borate (2-APB, 60 microM). Neither U-73122 nor 2-APB had an affect on the membrane hyperpolarization evoked by beta-adrenoceptor activation. These results suggest that in the toad sinus venosus, two distinct transduction pathways can be activated by epinephrine to cause an increase in heart rate.

Adrenergic Agonists↗
PubMed1994

Lack of edema in toad lungs after pulmonary hypertension.

Pulmonary hypertension and hyperperfusion were experimentally induced in conscious toads (Bufo marinus) to test whether excessive transcapillary filtration might result in pulmonary edema. Elimination of pulmocutaneous baroreceptor afferent input by bilateral sectioning of recurrent laryngeal nerves caused mean pulmonary arterial pressure to increase by nearly 25 mmHg and pulmonary blood flow to increase fourfold. Left lungs of control (normotensive) and hypertensive toads were isolated by snares at the hilus and excised for compartmental lung fluid analysis. Total lung water was significantly elevated in hypertensive toads (8.44 +/- 0.30 ml/g dry mass) compared with control animals (7.15 +/- 0.22 ml/g dry mass), but this increase was apparently not due to an accumulation of transcapillary filtrate (extravascular fluid volumes = 4.57 +/- 0.21 and 4.35 +/- 0.17 ml/g dry mass, respectively). Instead, significant increases in pulmonary intravascular fluid volume accounted for 83% of the increase in total lung water. Such absence of pulmonary edema under these extreme cardiovascular states suggests that mobilization of pulmonary lymph is unusually effective in these animals.

Animals↗
PubMed1978

Cholinergic agents inhibit sodium transport across the isolated toad bladder.

Acetylcholine and carbamylcholine (carbachol) inhibited sodium transport across the toad bladder. This effect was blocked by atropine. Carbachol increased the uptake of 45Ca by isolated toad bladder epithelial cells. This increased 45Ca uptake was blocked by atropine, pentobarbital, or lanthanum chloride. The inhibitory effect of cholinergic agents on sodium transport was dependent on external calcium concentration and was abolished by decreasing external calcium from 2 to 0.2 mM or by agents (pentobarbital, lanthanum chloride) which prevent the movement of calcium into cells. Carbachol increased modestly, but significantly, the levels of cyclic GMP in isolated toad bladder epithelial cells. This effect was blocked by atropine. Whether the decrease in sodium transport produced by cholinergic agents is the result of increased intracytoplasmic calcium levels, increased cyclic GMP levels, or a combination of both remains to be established.

Acetylcholine↗
PubMed1980

Osmolar influences on urinary acidification and metabolism in the Colombian toad bladder.

An increase in the osmolarity of the serosal fluid bathing the isolated toad bladder inhibits sodium transport across the preparation. Opposite effects occur with a decrease in serosal Ringer osmolarity. The present experiments investigate the specificity of these osmolar effects by examining the role of extracellular fluid tonicity on the acidification capacity of the isolated Colombian toad bladder. Acidification, estimated by the reversed short-circuit current (RSCC) developing across the Colombian toad bladder in the absence of sodium transport, was stimulated by serosal hypotonicity and inhibited by serosal hypertonicity of acetazolamide. Changes in the mucosal Ringer tonicity had no effect on RSCC. A direct correlation was found between the acidification process and the rate of oxidation of [14C]pyruvate by quarter-bladders exposed to changes in extracellular fluid osmolarity in the presence of amiloride. The osmolar effects on RSCC may result from changes in cell metabolism.

Acetazolamide↗
PubMed1983

Effects of prostacyclin on short-circuit current and water flow in the toad urinary bladder.

The effects of prostaglandins of the E series on sodium and water transport have been studied extensively. PGE2 has been shown to inhibit the increase in osmotic water flow produced by vasopressin and to stimulate short-circuit current (SCC) in the toad bladder. On the other hand, the effects of prostacyclin (PGI2), an arachidonic acid product, on sodium and water transport have not been extensively evaluated. The present studies describe the effects of PGI2 on basal and vasopressin-stimulated osmotic water flow and on SCC in the urinary bladder of the toad. Studies were performed in the absence or presence of indomethacin. PGI2 in the absence of indomethacin had no effect on basal or vasopressin-stimulated osmotic water flow. When indomethacin was present, thereby eliminating intrinsic prostaglandin biosynthesis, PGI2 inhibited basal but not vasopressin-stimulated osmotic water flow. PGI2 increased SCC in the presence or absence of indomethacin. 6-keto PGF1 alpha, the stable metabolite of PGI2, had no effect on SCC. PGI2 stimulated cAMP production in isolated toad bladder epithelial cells. 2',5'-Dideoxyadenosine, an inhibitor of cAMP production, blocked the increase in SCC produced by PGI2, suggesting that the effects of this compound on SCC are mediated via cAMP.

1-Methyl-3-isobutylxanthine↗
PubMed1987

Cytosolic calcium and the action of vasopressin in toad urinary bladder.

The effects of experimental procedures believed to increase cytosolic calcium on basal and vasopressin-stimulated osmotic water flow and transepithelial sodium transport were examined in the toad urinary bladder. Exposure of isolated toad bladders to quinidine, calcium ionophores (A23187, X537A), or low-sodium or potassium-free serosal solutions resulted in a dose-dependent decrease in the hydrosmotic response to vasopressin or exogenous adenosine 3',5'-cyclic monophosphate (cAMP). The degree of inhibition of cAMP-induced water flow induced by low-sodium or potassium-free serosal bathing media varied, and in a similar manner, with the serosal calcium concentration. The effects of quinidine sulfate (2 X 10-4 M), X537A (2 X 10(-5) M), and low serosal sodium (20 mM), but not that of A23187 (10(-5) M), were readily reversible. Exposure to quinidine (4 X 10(-4) M), A23187 (10(-5) M), X537A (5 X 10(-6) M), or low serosal sodium (2 mM) also inhibited the basal short-circuit current (SCC). Vasopressin, 4-20 mU/ml, completely overcame the inhibition of the SCC induced by quinidine, A23187, or low serosal sodium, but a submaximal dose of hormone (4 mU/ml) failed to fully reverse the inhibitory effect of X537A, 5 X 10(-6) M. These results are consistent with the view that 1) a Na-Ca exchange process operates across the basolateral surface of the granular epithelial cells of the toad urinary bladder in vivo, and 2) the level of free calcium in the granular cell cytosol plays a modulatory role in the control of apical membrane water and sodium permeability by vasopressin, and in the regulation of the basal rate of transepithelial sodium transport.

Animals↗
PubMed1991

11-Dehydrocorticosterone, a glucocorticoid metabolite, inhibits aldosterone action in toad bladder.

The enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) metabolizes glucocorticoid hormones and diminishes their ability to induce sodium transport. In these studies, we determined the location of this enzyme in toad bladder and assessed the biological role for its 11-dehydro end product. Employing a polyclonal antibody directed toward 11 beta-OHSD and immunofluorescence techniques, we located the enzyme in the epithelial cell layer of the toad bladder. Although corticosterone (10(-7) M) can partially suppress aldosterone (10(-7) M)-stimulated short-circuit current (SCC), a clear excess of corticosterone (10(-6) M) did not inhibit the aldosterone-induced induced (10(-8) M) rise in SCC (n = 6). The 11-dehydro product of corticosterone, 11-dehydrocorticosterone (compound A) added to the serosal bath suppressed aldosterone (10(-8) M) peak SCC (360 min) in a dose-dependent fashion reaching 46 +/- 5% of control values at 10(-5) M (n = 6; P less than 0.001). Compound A (10(-5) M) in the mucosal bath also was capable of partially inhibiting the peak aldosterone rise in SCC to 63 +/- 7% of control values with aldosterone at 10(-8) M (n = 6; P less than 0.01) and to 64 +/- 10% of control values with aldosterone at 10(-7) M (n = 9; P less than 0.01). Compound A alone at 10(-5) M did not have any effect on SCC. Isolated toad bladders were not able to transform compound A (at 10(-8) and 10(-5) M) back to corticosterone. Thus the 11-dehydro end product of 11 beta-OHSD (compound A) may play a biologic role by regulating a component of mineralocorticoid-induced sodium transport.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2002

Indomethacin impairs LPS-induced behavioral fever in toads.

We tested the hypothesis that PGs mediate lipopolysaccharide (LPS)-induced behavioral fever in the toad Bufo paracnemis. Measurements of preferred body temperature (T(b)) were performed with a thermal gradient. Toads were injected intraperitoneally with the cyclooxygenase inhibitor indomethacin (5 mg/kg), which inhibits PG biosynthesis, or its vehicle (Tris) followed 30 min later by LPS (0.2 and 2 mg/kg) into the lymph sac. LPS at the dose of 0.2 mg/kg caused a significant increase in T(b) from 7 to 10 h after injection, and then T(b) returned toward baseline values. LPS at the dose of 2 mg/kg produced a different pattern of response, with a longer latency to the onset of fever (10th h) and a longer duration (until the end of the experiment at the 15th h). Tris significantly attenuated the fever induced by LPS at 0.2 mg/kg, but not at 2 mg/kg. Moreover, indomethacin completely blocked the fever evoked by LPS (2 mg/kg). These results indicate that the behavioral fever induced by LPS in toads requires the activation of the COX pathway, suggesting that the involvement of PG in fever has an ancient phylogenetic history and that endogenous PGs raise the thermoregulatory set point to produce fever, because behavioral thermoregulation seems to be related to changes in the thermoregulatory set point.

Animals↗
PubMed1991

M-wave of the toad electroretinogram.

1. In the retina, two distinct, light-evoked releases of K+ have been described. One takes place in the outer plexiform layer (OPL) and is termed the "distal K+ increase." The other takes place in the inner plexiform layer (IPL) and is termed the "proximal K+ increase." Although the distal K+ increase generates the electroretinogram (ERG) b-wave, the contribution of the much larger proximal K+ increase to the ERG is less well understood. In this paper we detail our investigation of the proximal K+ increase and its contribution to the ERG. We describe an ERG component, the M-wave, which had not heretofore been observed in the diffuse-flash, vitreal ERG. 2. We studied the proximal K+ increase and the ERG M-wave in the isolated retina preparation of the toad, Bufo marinus. We used K(+)-sensitive microelectrodes, as well as conventional intra- and extracellular microelectrodes, to record K+ changes, the local (or intraretinal) ERG, the vitreal ERG, and Müller cell responses. 3. As in earlier studies of the amphibian and cat M-wave, we readily observed an M-wave in the intraretinal, or local, ERG (LERG). The M-wave we studied had characteristics similar to those of M-waves that were previously described. Specifically, we found that the M-wave was generated by a Müller cell response to the proximal K+ increase and that both the proximal K+ increase and the LERG M-wave were spatially tuned. 4. We used the aspartate receptor agonist, N-methyl-DL-aspartate (NMA), to reveal that an M-wave is present in the vitreal ERG. Researchers who previously investigated the M-wave were unable to identify an M-wave in the vitreal ERG. We found that the toad ERG M-wave was a small, positive potential that was partially obscured by the much larger b-wave and slow PIII components. 5. We observed that picrotoxin (PTX) had an excitatory effect on inner retina, as evidenced by an enhanced proximal K+ increase and an enhanced M-wave. This result indicates that it is likely that GABAergic inhibition in inner retina plays an important role in retinal processing in the toad. 6. At threshold, we found that the ERG consisted mainly of an M-wave, indicating that the amphibian threshold ERG is driven by proximal retina. This result is analogous to previous observations of the threshold ERG in cat. However, in cat, the M-wave and threshold response have been described as distinct ERG components.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1999

Apomorphine alters prey-catching patterns in the common toad: behavioral experiments and (14)C-2-deoxyglucose brain mapping studies.

Previous studies on the dopaminergic modulation of visuomotor functions in amphibians showed that the dopamine agonist apomorphine (APO) alters prey-catching strategies. After systemic administration of APO in common toads Bufo bufo, prey-oriented turning and locomotion was attenuated whereas snapping toward prey was facilitated in a dose dependent manner. With systemic APO administration, toads which had previously been hunting, that is pursuing prey, behaved in a waiting position, that is sitting motionless and waiting for prey. This suggests that APO facilitates the ingestive component and inhibits the orientational and locomotory components of prey capture. To help unravel the cerebral sites of action of APO, the present study employs the (14)C-2-deoxyglucose method to compare the rate of local glucose utilization in 41 brain structures. The retinal projection fields - e.g. superficial optic tectum, pretectal nuclei, and anterior dorsal thalamic nucleus - showed an elevation in glucose utilization due to APO-induced increases in retinal output. The medial tectal layers and the ventral striatum, both involved in visuomotor functions related to prey-oriented turning and locomotion, displayed APO-induced decreases in glucose utilization. APO-induced increases in glucose utilization were observed in the medial reticular formation and the hypoglossal nucleus which participate in the motor pattern generation of snapping. APO-induced increases in glucose utilization were also detected in the nucleus accumbens and the ventral tegmentum (mesolimbic system) as well as in the ventromedial pallium ('primordium hippocampi') and the septum, both of which belonging to the limbic system. These structures contribute to motivational level control and may be responsible for the APO-induced elevation of the snapping rate. Various other structures revealed APO-induced increases in glucose utilization. These structures include the olfactory bulb, lateral pallium, suprachiasmatic nucleus, nucleus of the periventricular organ, and the nucleus of the solitary tract. The lateral amygdala displayed APO-induced decreases in glucose utilization. The APO-induced alterations in local cerebral glucose utilization are evaluated with reference to the distribution of dopaminergic structures, and this is compared with similar data obtained in the rat by other authors. A neural network explaining the APO-induced behavioral syndrome in the common toad is discussed.

Animals↗
PubMed1984

Gonadotropin-releasing hormone increases plasma catecholamines and blood pressure in toads.

Synthetic gonadotropin-releasing hormone (GnRH) was injected intravenously into conscious, adult toads (Bufo marinus) to elucidate the nervous and cardiovascular actions of the hormone. GnRH (0.001-1.0 nmol X kg-1) produced dose-dependent increases in mean arterial blood pressure and pulse pressure, beginning within 3 min after injection. These pressor responses to GnRH were specific to the hormone since they could be inhibited reversibly by [D-pGlu1, D-Phe2, D-Trp3,6]-GnRH. Arterial plasma concentrations of unconjugated catecholamines increased simultaneously with the rise in blood pressure following GnRH injection: the half-maximal pressor dose of GnRH (0.1 nmol X kg-1) caused a 3-fold increase in plasma noradrenaline and a 20-fold increase in plasma adrenaline concentrations. Pretreatment of toads with an alpha-adrenergic antagonist, prazosin, and a beta-adrenergic antagonist, propranolol, abolished the pressor responses to GnRH. We conclude that GnRH mobilizes catecholamines, which act through alpha- and beta-adrenergic mechanisms to raise blood pressure. Thus, endogenous GnRH or GnRH-like peptides may coordinate the pituitary, nervous and cardiovascular mechanisms which prepare toads for seasonal reproductive activity.

Animals↗
PubMed1982

Effect of colchicine on the electrophysiological properties of the toad sciatic-gastrocnemius preparations in vivo.

The effects of a single subepineural injection of colchicine on the toad sciatic-gastrocnemius preparation were studied in vivo. The resting membrane potential of the gastrocnemius muscle fibres declined by 15% at day 5. This was followed 2 days later by dispersion and reduction in the amplitude of the compound muscle action potential, decrease in the slope of the accommodation index curve (AI), and a decreased electromyographic interference pattern. These changes were progressive and led to blockage of electrical activity and appearance of pseudodenervation after 2 weeks. Pseudodenervation was confirmed on finding similar alterations in the AI profile in neurotomized toads. In contrast, the hind limbs of toads paralysed by d-tubocurarine had normal muscle AI. The decrease in the AI on the colchicine-treated side was dependent on the length of the severed nerve left attached to the muscle, indicating a centrifugal effect of the drug.

Action Potentials↗
PubMed1984

Influence of pineal gland on spermatogenesis of toad (Bufo melanostictus).

The relationship between the pineal gland and testes of the toad was investigated in breeding and hibernating seasons. Pinealectomy increased spermatogenesis in hibernating toads but it failed to exert any effect during the breeding season. The pineals were found to be active during hibernation and atrophied in the breeding season. It is speculated that the cyclic pineal activity might be responsible for the seasonal variation of spermatogenesis in the toad.

Animals↗
PubMed1988

Induction of neoplasms in the Egyptian toad Bufo regularis by gibberellin A3.

Force feeding the Egyptian toads (Bufo regularis) with gibberellin A3 (10 ppm) twice a week for 5 months induced neoplasms in 8 out of 50 (16%) experimental animals. Primary tumours developed in the liver (hepatocellular carcinomas). Two secondary tumours in the kidneys and another 2 in the ovaries of toads developed due to metastases from the hepatocellular carcinomas. The results show that gibberellic acid (gibberellin A3) has a carcinogenic effect in the Egyptian toads.

Animals↗
PubMed1992

Induction of neoplasms in Egyptian toads Bufo regularis by oil of chenopodium.

Feeding the Egyptian toad Bufo regularis with oil of the chenopodium plant induced hepatocellular carcinomas in 23% of the animals, and metastases of the primary liver tumors appeared in the kidneys of 6 toads. The earliest evidence of tumors appeared after 3 months of treatment. The average latent period of tumor induction was 3.6 +/- 0.4 months. It is speculated that oil of chenopodium may be one of the constituents of Chenopodium ambrosoides which is responsible for tumor induction in the toads B. regularis.

Animals↗
PubMed1970

The effect of dialysates and ultrafiltrates of plasma of saline-loaded dogs on toad bladder sodium transport.

In order to obtain direct evidence for the existence of a natriuretic hormone, dialysates and ultrafiltrates of plasma of dogs expanded with saline were tested for effects on sodium transport by the toad urinary bladder. Dialysate was obtained by dialysis of blood in vivo in a clinical dialyzer and by dialysis in vitro of small volumes of blood using a miniature model of the clinical dialyzer. Ultrafiltrates were prepared using selective molecular filters which permit passage of substances on the basis of molecular weight and three dimensional configuration. Dialysates and ultrafiltrates of hydropenic dogs caused a change in toad bladder potential difference of + 1% and in short circuit current of - 5%. In contrast, dialysates and ultrafiltrates from expanded dogs caused a change in potential difference of - 23% and in short circuit current of - 32%, a highly significant difference. Onset of reduction of short circuit current occurred within 3-5 min, reaching a maximum in 10-20 min. The effect was rapidly reversible, was specific for the serosal surface of the bladder, and could not be explained on the basis of nonspecific alterations in ionic composition or by dilutional effects. Ultrafiltrates of jugular vein plasma caused significantly more reduction of short circuit current than ultrafiltrates of femoral vein plasma. The data indicate the presence in plasma of saline-loaded dogs of a dialyzable inhibitor of toad bladder sodium transport. Ultrafiltrate studies using membranes of appropriate selectivity suggest the factor has a molecular weight of less than 3000.

Animals↗
PubMed1977

Effects of ionophore A23187 on base-line and vasopressin-stimulated sodium transport in the toad bladder.

The cation specific ionophore A23187 (Io) is a useful tool for studying the role of intracellular Ca++ (Ca++)i in physiologic processes. The present studies explore the role of (Ca++)i on Na transport in the toad bladder. Scraped bladder cells exposed to 1 muM Io for 60 min took up 100% more 45Ca than control cells. Io, 1 muM, added to the serosal side of bladders incubated in standard Ringers containing 2.5 mM Ca++ inhibited short circuit current (SCC) values by a mean of 30% at 60 min and 50% at 90 min. Io did not inhibit SCC significantly in bladders incubated in Ringers containing 0.2 mM Ca++. These data indicate that the effects of Io on SCC depend on the levels of external Ca++ and suggest that entry of Ca++ into cells mediates the inhibition of base-line SCC. PReincubation of the bladders with either lanthanum chloride or pentobarbital prevented the increased 45Ca uptake produced by ionophore as well as theinhibition of SCC caused by the antibiotic. Vasopressin, antidiuretic hormone (ADH). 10 MU/ml, increased peak SCC by 247% in bladders preincubated for 1 h in Ringers with 2.5 mM Ca++ and 1 muM Io and by 318% in control bladders (P less than 0.01). Bladders exposed to 1 muM Io in Ringers with 0.2 mM Ca++ had an increase in SCC after ADH comparable to that observed in controls. Since the effects of ADH on SCC are mediated by cyclic AMP, we tested the effects of Io on cAMP production by scraped toad bladder cells. ADH increased cAMP from 8 to 30 pmol/mg protein in controls but it did not increase cAMP over base-line values in the presence of Io when the Ringers contained 2.5 mM Ca++. Io did not inhibit cAMP production in response to ADH when the Ca++ in the Ringers was 0.2 mM. The results indicate that Io inhibits baseline and ADH stimulated SCC by increasing (Ca++)i or Ca++ bound to the cell membrane. It is suggested that: ()( (Ca++)i or membrane-bound Ca++ plays a key role in base-line and ADH stimulated Na transport in the toad bladder; (2) inhibition of ADH stimulated SCC may be due inpart to decreased cAMP generation in response to ADH when (Ca++)i or membrane-bound Ca++ levels are increased.

Animals↗
PubMed1977

Inhibition of vasopressin-stimulated prostaglandin E biosynthesis by chlorpropamide in the toad urinary bladder. Mechanism of enhancement of vasopressin-stimulated water flow.

Chlorpropamide is known to enhance the water permeability response of the toad urinary bladder to vasopressin and to theophylline. In other studies, we have shown that prostaglandin E synthesis by the toad bladder inhibits the water permeability response to arginine vasopressin and to theophylline. In this study, the effect of chlorpropamide on vasopressin-, theophylline-, and cyclic AMP-stimulated water flow and on prostaglandin E biosynthesis was investigated in the toad urinary bladder in vitro. Chlorpropamide inhibited prostaglandin E biosynthesis during vasopressin-, theophylline- and cyclic AMP-stimulated water flow. Tolbutamide and glyburide, two other sulfonylurea compounds, also enhanced vasopressin-stimulated water flow and inhibited vasopressin-stimulated prostaglandin E biosynthesis. We conclude that the mechanism of enhancement on vasopressin-stimulated water flow by the sulfonylureas is the inhibition of prostaglandin E biosynthesis.

Animals↗