The primary mineralocorticoid , aldosterone , is produced in the adrenocortical zona glomerulosa by the action of the enzyme aldosterone synthase (also known as CYP11B2 ).   Aldosterone is largely responsible for the long-term regulation of blood pressure .  Aldosterone effects on the distal convoluted tubule and collecting duct of the kidney where it causes increased reabsorption of sodium and increased excretion of both potassium (by principal cells) and hydrogen ions (by intercalated cells of the collecting duct).  Sodium retention is also a response of the distal colon, and sweat glands to aldosterone receptor stimulation. Although sustained production of aldosterone requires persistent calcium entry through low-voltage activated Ca 2+ channels , isolated zona glomerulosa cells are considered nonexcitable, with recorded membrane voltages that are too hyperpolarized to permit Ca 2+ channels entry.  However, mouse zona glomerulosa cells within adrenal slices spontaneously generate membrane potential oscillations of low periodicity; this innate electrical excitability of zona glomerulosa cells provides a platform for the production of a recurrent Ca 2+ channels signal that can be controlled by angiotensin II and extracellular potassium , the 2 major regulators of aldosterone production.  Angiotensin II originates from plasmatic angiotensin I after the conversion of angiotensinogen by renin produced by the juxtaglomerular cells of the kidney .