Both lungs and kidneys function to control this balance. A little too much chemistry for me ... :-/

http://www.merck.com/mrkshared/CVMHighLight?file=/mrkshared/mmanual/section2/chapter12/12g.jsp%3Fregion%3Dmerckcom&word=pH&word=balance&domain=www.merck.com#hl_anchor

Acid-Base Metabolism 

The blood hydrogen ion (H+) concentration is maintained within narrow limits. The arterial plasma H+ concentration ranges from 37 to 43 nmol/L (37 × 10-6 to 43 × 10-6 mEq/L). The maintenance of H+ at such low levels is essential for normal cellular function because of the high reactivity between H+ and other compounds, especially proteins. The pH (negative logarithm of H+ concentration) is a much less cumbersome measure of physiologic H+ concentrations and is widely used in clinical medicine. The normal arterial blood pH ranges from 7.37 to 7.43.

Both pulmonary and renal function maintain blood pH within this range. Respiratory changes in minute ventilation occur quickly in response to acid-base disturbances and rapidly alter blood pH by changing carbonic acid concentration through changes in blood PCO2. The kidneys vary the renal excretion of acid or base equivalents and ultimately alter plasma HCO3- concentration to alter blood pH. Renal adaptations to changes in acid-base balance occur over several days while respiratory-driven changes generally occur in minutes to hours. Both pulmonary and renal function act to compensate for disturbances in acid-base balance to maintain blood pH within normal ranges.

Wide fluctuations in H+ concentration are also prevented by the presence of several pH buffers. These buffers are weak acids that exist in equilibrium with the corresponding base at physiologic pH. Buffers respond to changes in [H+] by shifting the relative concentrations of the buffer and the corresponding base to dampen the change in pH. Phosphates; ammonia; proteins, including hemoglobin; and bone all provide pH buffering capacity, but the major pH buffer in the blood, and that which is most relevant to clinical acid-base disturbances, is the bicarbonate/carbonic acid system.

The enzyme carbonic anhydrase quickly converts carbonic acid in the blood to CO2 and water. The partial pressure of CO2 gas (PCO2) is readily measured in blood samples and is directly proportional to blood CO2 content; therefore, PCO2 is used to represent the concentration of acid in the system. The concentration of base in the system can be directly determined by measuring HCO3- concentration. Plasma bicarbonate and CO2 concentrations and pH are chemically related to one another by the Henderson-Hasselbalch equation:

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where 6.1 is the pKa (negative logarithm of the acid dissociation constant) for carbonic acid and 0.03 relates PCO2 to the amount of CO2 dissolved in plasma. Although cumbersome and somewhat difficult to use at the bedside, the Henderson-Hasselbalch equation represents a very important relationship. It predicts that the ratio of HCO3- to dissolved CO2, rather than their actual concentrations, determines blood pH. This buffer system is of physiologic importance because both the pulmonary and renal mechanisms for regulating pH work by adjusting this ratio. The PCO2 can be modified rapidly by changes in respiratory minute ventilation, while plasma [HCO3-] can be altered by regulating its excretion by the kidneys.

Clinical disturbances of acid-base metabolism classically are defined in terms of the HCO3-/CO2 buffer system. Rises or falls in HCO3- are termed metabolic alkalosis or acidosis, respectively. Rises or falls in PCO2 are termed respiratory acidosis or alkalosis, respectively. Simple acid-base disturbances include both the primary alteration and an expected compensation. For example, in metabolic acidosis there is a primary fall in plasma HCO3- concentration and a secondary fall in the PCO2 due to respiratory compensation. Table 12-8 shows primary changes in the four simple acid-base disturbances and the expected compensation.

Mixed acid-base disturbances are more complex disorders in which two or more primary alterations coexist. Compensatory mechanisms also exist in mixed acid-base disturbances. Mixed disturbances are generally recognized when less or more than the predicted compensation for a given primary acid-base disturbance is present. Nomograms allow simultaneous plotting of pH, HCO3-, and PCO2, and greatly simplify the recognition of mixed disorders. Treatment must address each primary disturbance. Measurement of arterial pH, PCO2, and HCO3- along with recognition of the underlying disease process is usually sufficient to correctly solve most clinical acid-base disturbances.

Acid-base disturbances can greatly affect O2 transport and tissue oxygenation. Acute changes in H+ concentration rapidly affect the oxyhemoglobin dissociation curve (Bohr effect); acidemia shifts the curve to the right (decreased affinity of Hb for O2; facilitated release of O2 to tissues), and alkalemia shifts the curve to the left (increased affinity of Hb for O2; diminished O2 release to tissues). However, when acidosis or alkalosis is chronic, these acute effects on Hb-O2 binding are modified by more slowly developing changes in erythrocyte concentrations of 2,3-diphosphoglycerate (2,3-DPG). Thus, chronic elevations in H+ ion inhibit 2,3-DPG formation (resulting in increased affinity of Hb for O2), and chronic depression of H+ ion increases 2,3-DPG (resulting in diminished affinity of Hb for O2). Such acute changes in O2 transport and tissue oxygenation may play a role in producing the CNS manifestations of acute alkalemia, but their clinical importance in acidosis is uncertain.

The kidneys play a major role in the regulation of ECF HCO3- concentration. Virtually all of the plasma HCO3- is filtered by the glomerulus. Large amounts of H+ ion are secreted into the renal proximal tubular lumen in exchange for Na. For each H+ ion secreted, one HCO3- ion is reclaimed to the ECF. Thus, net reabsorption of filtered HCO3- occurs. Since the pH of the fluid leaving the proximal tubule is about 6.5, most of the filtered HCO3- is reabsorbed in the proximal tubule. In the distal tubule, H+ ion secretion is partially dependent on aldosterone-mediated Na reabsorption. HCO3- reabsorption can continue in the distal nephron up a steep gradient as urine pH can be lowered in this segment of the nephron to as low as 4.5 to 5.0. Throughout the nephron, secreted H+ ion is buffered by urinary buffers such as PO4 (titratable acid) and ammonia. In this manner, filtered HCO3- operationally is reabsorbed, and new HCO3- can be generated to replace that lost in body buffer reactions. Since filtered Na is reabsorbed either in association with Cl or by cationic exchange with H+ ion or to a lesser extent K, the total Na reabsorbed approximates the sum of the Cl reabsorbed and H+ ion secreted. Thus, an inverse relationship exists between Cl reabsorption and H+ ion secretion, which is highly dependent on the existing level of Na reabsorption.

Renal HCO3- reabsorption is also influenced by body K stores. A general reciprocal relationship exists between intracellular K content and H+ ion secretion. Thus, K depletion is associated with increased H+ ion secretion and attendant HCO3- generation, leading to an HCO3- increase in ECF and metabolic alkalosis. Finally, renal HCO3- reabsorption is influenced by the PCO2 and the state of chloride balance. Increased PCO2 leads to increased HCO3- reabsorption. Cl depletion leads to increased Na reabsorption and HCO3- generation by the proximal tubule. Although Cl depletion may be produced experimentally without ECF volume depletion, Cl depletion generally is synonymous with ECF volume depletion in clinical settings.