No abstract

The nonapeptides of neurohypophysis, vasotocin and mesotocin, detected in most vertebrates, are replaced by vasopressin and oxytocin in mammals. Using bioinformatics methods, we determined the spectrum of receptor subtypes for these hormones in mammals and their physiological effects in the kidneys of rats. A search for sequences similar to the vertebrate vasotocin receptor by proteomes and transcriptomas of nine mammalian species and the rat genome revealed three subtypes of vasopressin receptors (V1a, V1b, and V2) and one type of oxytocin receptors. In the kidneys of non-anesthetized rats, which received a water load of 2 ml per 100 g of body weight, three effects of vasopressin were revealed: 1) increased reabsorption of water and sodium, 2) increased excretion of potassium ions, and 3) increased excretion of sodium ions. It has been suggested that each of the effects on the kidney is associated with selective stimulation of the vasopressin receptor subtypes V2, V1b, and V1a depending on the concentration of nonapeptide. In experiments on non-anaesthetized rats with a water load, the injection of oxytocin reduces the reabsorption of solute-free water in the kidneys and increases the excretion of sodium ions. The possible physiological mechanisms behind the realization of both effects with the participation of a single type of oxytocin receptors are being analyzed. Thus, the spectrum of activated receptor subtypes varies depending on the current concentration of neurohypophyseal hormones, as a result of which the predominant effect on renal function changes, which ensures precise regulation of water-salt homeostasis.

The role of subtypes of vasopressin receptors in modulation of renal sodium reabsorption was studied in in vivo experiments on Wistar rats. Selective V1a receptor agonist reduced sodium reabsorption in the kidneys and expression of these receptors increased by practically 100 times. This effect was similar to the effect of furosemide. Selective V2 receptor agonist enhanced sodium reabsorption in the kidney and simultaneously increased reabsorption of solute-free water. Stimulation of V1b receptors did not affect sodium transport. Our findings attest to the key role of V1a receptors in the regulation of renal excretion of sodium ions.

No abstract

The effects of vertebrate neurohypophysial nonapeptides (vasopressin, vasotocin and their synthesized analogs) on urinary magnesium excretion were studied in rats. Neurohypophysial hormones and their analogs at doses stimulating V 2 -receptors (0.0001-0.001 nmol/100 g BM) exerted antidiuretic effect and reduced urinary magnesium excretion. At higher doses, activating V 2 and V 1a -receptors (0.025-0.1 nmol/100 g BW), vasotocin and its analogs (deamino-vasotocin (dAVT), deamino-Thr 4 -vasotocin, deamino-hArg 8 -vasotocin, deamino-monocarbo-vasotocin) enhanced excretion of magnesium and sodium ions. A direct relationship was revealed between the enhanced renal excretion of sodium and magnesium ions under these conditions. After the V 1аreceptor antagonist injection, dAVT caused a 10-fold lower increase in magnesium excretion. The V 2 -receptor antagonist did not affect dAVT-induced magniuresis. The data obtained suggest that V-receptors are involved in magnesium transport regulation in the rat kidney.