production will decrease if there is reduced access to water or food.
III Renin‐Angiotensin‐Aldosterone‐System (RAAS) (see Figure 5.2)
The role of the RAAS is the long‐term management of blood volume and arteriolar tone.
This is achieved by increasing reabsorption of sodium and water, and increasing vascular tone.
In contrast, the baroreceptor reflex manages smaller and short‐term changes.Figure 5.2 Schematic of the renin angiotensin‐aldosterone‐system (RAAS).
The RAAS has three main components:Renin.Angiotensin II.Aldosterone.
A decrease in renal blood pressure results in these components acting to increase arterial pressure or decrease salt delivery to the distal convoluted tubule.
These mechanisms allow for prolonged increases in systemic blood pressure.
Renin
Renin is synthesized by myofibroblast‐like cells located in the renal afferent arterioles.These cells are commonly referred to as juxtaglomerular cells.
The primary physiologic triggers for renin release are:Decreases in extracellular fluid volume.Sodium depletion.Prostaglandins.Hypotension (MAP < 80 mmHg).Increases in sympathetic output.
The factors inhibiting renin release are:Angiotensin II.Atrial natriuretic peptide.Vasopressin.
Renin converts angiotensinogen (a protein synthesized by the liver) to angiotensin I.This is the rate‐limiting step of the RAAS.
Angiotensin I to Angiotensin II
Angiotensin‐converting enzyme (ACE), an enzyme found in vascular endothelium, converts Angiotensin I to Angiotensin II.
Effects of Angiotensin II
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 III and IV
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.
Aldosterone
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.
Angiotensin‐converting enzyme (ACE) inhibitors (e.g. enalapril)
Decrease the activity of ACE, resulting in decreased formation of angiotensin II.
IV Effects of anesthetics on renal function
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.
Comment: It is important to consider the co‐morbidities associated with renal disease (e.g. azotemia, acid–base imbalance, electrolyte imbalance, anemia, coagulopathy, hypertension) when determining an anesthetic protocol.
A Changes in RBF with anesthetics
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.
B Inhalational anesthetics
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.
