The fine structure of the kidney and the bladder of the bullfrog (Rana catesbeiana), the bullfrog tadpole, and the mudpuppy (Necturus maculosus) were studied with special attention to the innervation of renal tubule cells and bladder epithelial cells. In the bullfrog kidney, nerve terminals and varicosities were frequently associated with the tubule cells, apparently in an increasing order from the proximal tubule to the connecting tubule. Although these terminals and varicosities did not directly contact the tubular cell membrane, an aggregation of synaptic vesicles on the side facing the tubule was considered as morphological evidence that neurotransmitter can be released here and can affect the transport activity of the tubule cells. The association of nerve varicosities with canaliculi cells in the connecting tubule was also demonstrated. In the bullfrog tadpoles, renal tubule cells were occasionally innervated. In the mudpuppy, renal tubule cells were only poorly innervated. The epithelium of the bullfrog bladder was commonly innervated. Nerve terminals with synaptic vesicles were located very near basal cells and even contacted them directly on rare occasions. In the mudpuppy, the innervation of the bladder epithelium was observed infrequently. The bullfrog tadpoles did not possess an apparent bladder. In all materials studied, renal arterioles and bladder smooth muscle cells were innervated.
The renal effects of neurohypophysial hormones in fishes and amphibians are discussed. Injections of arginine vasotocin (AVT) elicit diuresis in fishes, but antidiuresis in amphibians. However, the physiological significance of these hormonal responses remains to be demonstrated. Studies with bioassays and radio-immunoassays on circulating levels of AVT indicate that hypovolemia may be a very potent stimulus for the release of the hormone. Hyperosmotic stimuli may not be as important. In anurans, mesotocin has a glomerular diuretic effect. This neurohypophysial hormone appears to dilate, while AVT constricts, the afferent glomerular circulation in bullfrogs, Rana catesbeiana.
Abstract Extraintestinal calcium influxes were measured in the killifish, Fundulus heteroclitus , in solutions with different calcium concentrations, from distilled water level (near 0) to seawater level (approximately 12 mM). The extraintestinal influx is modified by the concentration of calcium in the medium during the adaptive period. In freshwater‐adapted fish, calcium depletion resulted in an increase in calcium uptake. Such an adaptation was not observed in calcium‐depleted fish in artificial calcium‐deficient seawater. Calcium depletion in either medium seems to increase the calcium permeability. No correlation was found between Ca‐ATPase activity in the gill tissue and calcium uptake.
The removal of Stannius corpuscles elicited hypercalcemia in male killifish, Fundulus heteroclitus, maintained in calcium rich sea water. Such a response was absent in fish adapted to calcium-poor fresh water or artificial calciumdeficient sea water. The presence of calcium in food also affected the degree of hypercalcemia. Transplants of the corpuscles or injections of a homogenate of the gland corrected the rise in serum calcium. (Endocrinology93: 705, 1973)
Synthetic bovine parathyroid hormone fragment containing the N-terminal 1 – 34 amino acids (bPTH-(1 – 34)) relaxed the guinea-pig trachea constricted with histamine in vitro. Peptides with bovine and human sequences purchased from Peninsula Laboratories and Beckman Bioproducts produced similar effects. Substitution of methionine in positions 8 and 18 by norleucine did not affect this property of bPTH-(1 – 34). However, when the methionines were oxidized by treating the peptide with hydrogen peroxide, the peptide could no longer produce relaxation in the trachea. Oxidation of the methionine-replaced analog did not affect the action of the peptide on the trachea. It seems that the methionines per se are not necessary, but once oxidized the conformation of the molecule may be sufficiently altered to affect its ability to relax the trachea. While propranolol can block the relaxing action of isoproterenol, this blocking agent produces no inhibition of the bPTH-(1 – 34) effect. This action of PTH on the trachea may be related to cAMP because isobutyryl-methylxanthine, a phosphodiesterase inhibitor, potentiates and imidazole, a phosphodiesterase stimulator, inhibits the trachea relaxing action of bPTH-(1 – 34).
Promethazine and cimetidine blocked the hypotensive actions of 2-pyridylethylamine, and H1 agonist and dimaprit, an H2 agonist, respectively, but not that of bovine parathyroid hormone fragment [bPTH-(1-34)]. Rats were treated repeatedly with the histamine releaser, compound 48/80, until the release could no longer produce a decrease in blood pressure. The hypotensive action of bPTH-(1-34) could still be seen. Rats with histamine partially depleted with one injection of compound 48/80 were injected with cimetidine and pyrilamine, and H1 antagonist, which together blocked the hypotensive action of subsequent injections of compound 48/80, but not that of bPTH-(1-34). These data suggest that the vasodilatory action of bPTH-(1-34) does not involve the release or action of histamine.
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