It is a potent vasoconstrictor, directly increasing blood pressure by constricting systemic arterioles.

       It increases sodium reabsorption, leading to fluid retention and increased extracellular fluid volume.

       Catecholamines are released from the adrenal medulla, secondarily affecting systemic blood pressure.

       It diminishes the sensitivity of the baroreceptor reflex leading to an increase in blood pressure.

       It increases thirst via its effect on the hypothalamus.

       It increases the release of ADH. This leads to the insertion of aquaporin channels in the cell membranes of the collecting duct, causing increased water reabsorption.

       Angiotensin II has a short half‐life (one to two minutes) in plasma.It is degraded by peptidases into angiotensin III and IV.

       Angiotensin III has an effect which is equipotent to angiotensin II in causing the release of aldosterone, but has less potent pressor effects.

       Angiotensin IV has decreased systemic effects compared to angiotensin II, but has multiple functions in the nervous system.

       It is released from the zona glomerulosa of the adrenal gland; it promotes sodium retention, leading to fluid retention and increased blood pressure.

       It increases the excretion of K+ and H+.

       It increases the release of ADH from the posterior pituitary.

       Decrease the activity of ACE, resulting in decreased formation of angiotensin II.

       Virtually all anesthetic drugs modulate RBF and GFR by direct and indirect effects.GFR is likely to be reduced due to decreased RBF.The ability to excrete sodium is reduced. This is thought to be a result of inhibition of Na/K‐ATPase.Urine volume is usually decreased.

       A number of factors are involved in initiating anesthetic‐induced changes in renal function, and the contribution of each factor is primarily dependent on the horse's physiologic state and the anesthetic regimen. Factors include:Decreases in cardiac output and arterial blood pressure.Increases in sympathetic outflow from renal nerves.Activation of the RAAS.Increased release of ADH.Direct renal effects of anesthetics.

       Many drugs (or metabolites) have some degree of renal metabolism and/or excretion.Renal dysfunction may, in theory, prolong the effects of anesthetic drugs, but this is rarely of clinical importance.

       May partially result from the systemic changes invoked by anesthetics.

       A redistribution of cardiac output occurs with an increase in flow to the vessel‐rich areas (e.g. brain) and a reduction of flow to the splanchnic system.

       The effects of anesthetics on autoregulation and intrarenal blood flow are specific to the drug class and depends on renal perfusion pressure.

       α1‐adrenergic receptors are numerous in the renal vasculature and modulate RBF by mediating vasoconstriction.

       Most inhalational anesthetics have dose‐dependent effects on renal function.

       In general, RBF is decreased.

       All inhalants decrease GFR.

       Urine production decreases with inhalational anesthetics, which increase secretion of ADH and favors fluid retention in the extravascular space.

       Light planes of inhalational anesthesia can preserve renal autoregulation.

        Renal vascular resistance increases with most anesthetics.

       Nephrotoxicity is mainly a problem with “older” inhalants (e.g. methoxyflurane).Non‐steroidal anti‐inflammatory drugs (NSAIDs) and some antibiotics (e.g. aminoglycosides, tetracyclines) potentiate the nephrotoxicity of inhalants.

       It undergoes extensive biotransformation (50–75%) in the kidney, producing free fluoride ion and oxalate.

       Prolonged administration may result in polyuric renal failure.

       The fluorinated anesthetics sevoflurane and enflurane have not been associated with a decrease in renal function post‐operatively.

       Sevoflurane undergoes minimal biotransformation (2–5%) in the liver. Nevertheless, hepatic metabolism results in the formation of inorganic fluoride and an organic metabolite.Serum inorganic fluoride concentrations can attain values of 20–40 μmol/l after 2 MAC hours of exposure in humans, and >50 μmol/l after prolonged exposure.Values >50 μmol/l are considered to be nephrotoxic after exposure to methoxyflurane, as determined by a decrease in the kidney's concentrating abilities, with clinical signs of toxicity occurring at values >90 μmol/l.The difference in nephrotoxicity between the two anesthetic agents may be related to methoxyflurane undergoing intrarenal metabolism, whereas sevoflurane is primarily metabolized by the liver.Additionally, methoxyflurane is highly soluble in the tissues and takes many hours to be completely cleared from the body. Therefore, the area under the curve of exposure to fluoride is much larger with methoxyflurane than it is with sevoflurane.

       Desiccated CO2 absorbents react with sevoflurane to form compound A, a vinyl ether.

       Compound A causes nephrotoxicity in rats following prolonged exposure.

       The amount of compound A formed is regulated by the concentration of cysteine conjugate β‐lyase, which transforms cysteine conjugates into toxic products.

       The pathway of compound A production has not been described in the horse.

       Little effect on RBF or GFR.

       Diuresis results as alpha2‐adrenergic agonists:Inhibit ADH release, leading to a redistribution of aquaporin channels on the distal tubule and collecting duct.Inhibit renin release.Inhibit renal sympathetic activity.Inhibit tubular sodium reabsorption.Increase atrial natriuretic peptide release.