Effects of sodium metavanadate infusion on renal hemodynamics and tubular functions in anesthetized dogs

Abstract

This research has the objective to study the in vivo effects of intravenous sodium metavanadate infusion in a dose of 0.2 µmole/kg/min on cardiovascular, renal hemodynamics and renal tubular functions (group I) and elucidate the mechanisms responsible for this alterations which mediated by indirect the other affection or direct result of the actions of ATPase system of cell in anesthetized dogs pretreated with selective alpha-1 adrenergic receptor blocker, prazosin (group II) or selective beta-1 adrenergic receptor blocker, atenolol (group III) or angiotensin converting enzyme inhibitor, enalapril maleate (group IV) or parasympamimetic, acetylcholine (group V) or calcium entry through voltage-dependent channel blocker, verapamil (group VI). Intravenous infusion of sodium metavanadate produced a rise in mean arterial blood pressure. Mean arterial blood pressure in group III and IV increased as a manner of group I but they were less than group I (P<0.05), while in group II and VI decreased as a opposite of group I (P<0.01). Heart rate decreased in the same pattern in all six groups. In group III and V were more than group I (P<0.05), while in group VI was less than group I (P<0.05). Glomerular filtration rate, effective renal plasma and blood flow decreased as well as the renal vascular resistance increased in group I. Only group VI renal vascular resistance increased less than group I (P<0.05). Fractional urinary excretion of potassium decreased in group I. In group II and III decreased less than group I (P<0.01), while group IV-VI increased higher than group I (P<0.01). Fractional urinary excretion of chloride decreased in group I. In group III decreased less than group I (P<0.01) , in group II and VI increased higher than group I (P<0.01). Fractional urinary excretion of bicarbonate increased in group I. Group IV and V increased less than group I (P < 0.05), but group II decreased (P < 0.01). No significant change in plasma anion gap was observed, but urine anion gap increased in group I. Blood pH decreased in all groups. Urinary pH increased in group I, but group II, IV,V, and VI it decreased (P< 0.01). Fractional net acid excretion decreased in group I. In group III and VI decreased less than group I (P< 0.05), group II and IV increased higher than group I (P< 0.01). Fractional excretion of water decreased in group I, while group III – VI increased (P< 0.05). Moreover, vanadate caused a decrease in renal threshold and transtubule maximum rate of glucose reabsorption, bicarbonate reabsorption and PAH secretion and excretion. Stopping the socium metavanadate infusion, In any of the measurement made restored to normal. These results may suggest that sodium metavanadate produced a striking but reversible in cardiovascular effects and both renal vascular and renal tubular effects especially in proximal and distal tubule entire of nephron. Central autonomic neurogenic effects via postsynaptic alpha-1 and bata-1 adrenoreceptor and rennin-angiotensin are involved in modulating of changes in cardiovascular effects of sodium metavanadate. Direct action of sodium metavanadate on both vascular and renal tubular cells ATPase system via increasing intracellular calcium concentration is a major involved in modulation of cardiovascular, renal hemodynamics and renal tubular function changes in dogs after given sodium metavanadate. The improvement of these defect response that were elicited by vanadate occur in animals pretreated with verapamil.