Toad

About: Toad is a research topic. Over the lifetime, 1624 publications have been published within this topic receiving 28732 citations.

Comparative effects of tetracyclines on water flow across toad urinary bladders.

Abstract: Demeclocycline causes nephrogenic diabetes insipidus in man and inhibits antidiuretic hormone (ADH)-induced water flow (W) in toad urinary bladders. To clarify the possible mechanism for this action, the effects of five serosally applied tetracycline derivatives on ADH- and cyclic adenosine 39, 59-monophosphate (cAMP)-induced W were studied in paired toad urinary hemibladders ( Bufo marinus). Inhibition of cAMP-induced W was not clearly dose-related and did not correlate with any known physicochemical property of the tetracyclines. However, the relative inhibition of ADH-induced W by these drugs was dose-dependent, and followed the sequence: demeclocycline > doxycychine > minocycline > tetracycline > oxytetracycline. This sequence correlates exactly with the relative degree of serum protein binding of these drugs, but not with divalent cation chelation or lipid solubility, suggesting that ADH inhibition requires binding to cell membrane proteins important in ADH-induced water transport.

Nitric oxide regulation of the central aortae of the toad Bufo marinus occurs independently of the endothelium.

Abstract: Nitric oxide (NO) signalling pathways were examined in the lateral aortae and dorsal aorta of the cane toad Bufo marinus . NADPH diaphorase histochemistry and nitric oxide synthase (NOS) immunohistochemistry found no evidence for endothelial NOS in the endothelium of toad aortae, but it could be readily demonstrated in rat aorta that was used as a control. Immunohistochemistry using a specific neural NOS antibody showed the presence of neural NOS immunoreactivity in the perivascular nerves of the aortae. The anatomical data was supported by in vitro organ bath physiology, which demonstrated that the vasodilation mediated by applied acetylcholine (10-5 mol l-1) was not dependent on the presence of the vascular endothelium; however, it was significantly reduced in the presence of a neural NOS inhibitor, vinyl-L-NIO (10-4 mol l-1). In addition, atropine (10-6 mol l-1) (a muscarinic receptor inhibitor), L-NNA (10-4 mol l-1) (a NOS inhibitor) and ODQ (10-5 mol l-1) (an inhibitor of soluble guanylyl cyclase) abolished the vasodilatory effect of applied acetylcholine. In conclusion, we propose that an endothelial NO system is absent in toad aortae and that NO generated by neural NOS in perivascular nerves mediates vasodilation.

Role of prostaglandin E (PGE) in the modulation of the action of vasopressin on water flow in the urinary bladder of the toad and mammalian kidney.

Abstract: PGE1 and PGE2 are known to interfere with the water permeability effect of vasopressin in toad bladder and kidney. It has been proposed that endogenous prostaglandin E (PGE), synthesized within cells of vasopressin-sensitive tissues, serves to modulate the permeability changes elicited by the neurohypophyseal hormone. Direct evidence in support of this hypothesis is as follows: vasopressin increases the biosynthesis of PGE2 in renal interstitial cells and in isolated toad bladder. In the latter, inhibition of vasopressin-induced synthesis of PGE by a variety of inhibitors results in a greater water permeability response to vasopressin. It appears that vasopressin has two effects in toad bladder and kidney: (i) it activates adenylate cyclase thereby increasing the concentration of adenosine 3′,5′ monophosphate (cyclic AMP), the nucleotide responsible for the resultant increase in water permeability; and (ii) it activates a phospholipase that serves to release arachidonic acid, the precursor of PGE2 from intracellular pools. The PGE derived from the arachidonic acid diminishes adenylate-cyclase activity, in consequence of which the response of the enzyme to vasopressin is modulated.