The relationship between arterial pressure and the rate of Na+ excretion is regulated by a number of mechanisms-some well known, some newly discovered, and probably some yet to be discovered. These mechanisms affect either the amount of Na+ filtered at the glomerulus or its rate of reabsorption from the proximal or distal tubule. Other than physical factors (plasma protein concentration, glomerular capillary and tubular pressures) and glomerular ultrafiltration properties (K(f)), important regulators of both filtration and reabsorption include the renin-angiotensin system, aldosterone, and renal nerves, although much remains to be learned about renal sympathetic innervation, especially neural control of renal tubular function. It has recently become evident that other factors may also be important, in particular, nitric oxide, endothelin, and medullipin. The latter is a vasodepressor hormone released from the renal medulla by increased arterial pressure, and its role in pressure-related Na+ excretion is only now being studied. Despite the central importance of this mechanism in the regulation of arterial pressure, there has been little study of many other potentially important mechanisms, especially those capable of affecting active Na+ transport across the tubule, including the imidazoline-preferring receptors. New techniques to study the relationship between arterial pressure and Na+ excretion are becoming available, and these will allow a better assessment of the potential of pharmacologic agents capable of modifying this relationship.
|Journal||Journal of Cardiovascular Pharmacology|
|Issue number||SUPPL. 2|
|Publication status||Published - 1995|
- Angiotensin II
- Blood pressure
- Nitric oxide
- Renal nerves