Little effect on RBF or GFR.

       Little effect on RBF or GFR.

       In some species, morphine increases the release of ADH resulting in an inhibition of diuresis, and this is accompanied by an increase in chloride excretion.

       Increase RBF and renal vascular resistance.

       As the dose increases, renal sympathetic nerve activity increases. This decreases RBF while increasing renal vascular resistance.

       Ketamine can inhibit dopamine transporter proteins in the kidney but the clinical significance is uncertain.

       Ketamine and its metabolites are highly dependent on renal excretion.

       Minimal effects on RBF or GFR.

       Increases in intrathoracic pressure reduce venous return. This decreases right and left ventricular preload.Cardiac output decreases as a result.The effect on cardiac output is more pronounced in hypovolemic patients.

       Baroreceptors become activated, initiating a cascade of neurohormonal mechanisms to stimulate the kidney to decrease GFR and increase tubular reabsorption.

       Other mechanisms involved are:Release of ADH.Stimulation of the RAAS.Stimulation of the sympathetic nervous system.Inhibition of tonic vagal influences.

       This results in decreased urine volume, decreased renal plasma flow, and retention of sodium and water.

       Stress associated with anesthesia and surgery can result in the release of catecholamines, aldosterone, ADH, and renin.

       This results in decreased RBF and GFR, leading to fluid retention.

       These effects resolve over time after anesthesia.

       There are several different classes of diuretics with different mechanisms of action, ultimately resulting in increased urine production.

       See Table 5.1 for a summary of the diuretic classes.

       Inhibit water and sodium reabsorption predominantly at the PCT with some effects on the descending LOH and collecting duct.

       Expand extracellular fluid and plasma volume, increasing RBF.This will lead to medullary washout and an inability to concentrate urine.

       They are filtered through the glomerulus and increase osmotic pressure in the tubule. This reduces transmembrane water flow.

       Acetazolamide is highly protein bound and is not filtered by the glomerulus.It is secreted by the proximal tubule.Secretion is GFR dependent.

       It inhibits the activity of membrane and cytoplasmic carbonic anhydrase in the PCT, preventing reabsorption of bicarbonate. This results in decreased activity of the Na+/H+ exchanger, causing more sodium to remain in the filtrate.

       Increases renal excretion of Na+, K+, HCO3−.

       Results in a proximal renal tubular acidosis.

       Can cause metabolic acidosis.Hence, its potential use as a treatment for metabolic alkalosis.

       Other clinical uses of acetazolamide include glaucoma and neurologic disorders.

       In equine practice, their main use is in horses likely to be affected by a hyperkalemic periodic paralysis (HYPP) episode.

       Acetazolamide may be administered to horses prone to develop HYPP in order to increase potassium excretion prior to an anesthetic event, for example. It is generally recommended that acetazolamide be administered for a minimum of two days prior to anesthesia.

       Furosemide is the most commonly used diuretic in horses.

       Furosemide inhibits the Na+‐K+‐Cl− cotransporter in the luminal membrane of the thick ascending limb of the LOH.It binds specifically and reversibly to the Cl− binding site of the transporter's transmembrane domain.

       Because this transporter reabsorbs about 25% of