Kidney pressure

O. V. Sosnovtseva, E. Mosekilde, and N.-H. Holstein-Rathlou Modeling Kidney Pressure and Flow Regulation. Chapter 12 in this book. 

Modeling Kidney Pressure and Flow Regulation Table 12.1 Parameters used in the nephron model. 

Spira.1- Wound Modules. Spiral-wound modules were used originally for artificial kidneys, but were fuUy developed for reverse osmosis systems. This work, carried out by UOP under sponsorship of the Office of Saline Water (later the Office of Water Research and Technology) resulted in a number of spiral-wound designs (63—65). The design shown in Figure 21 is the simplest and most common, and consists of a membrane envelope wound around a perforated central coUection tube. The wound module is placed inside a tubular pressure vessel, and feed gas is circulated axiaUy down the module across the membrane envelope. A portion of the feed permeates into the membrane envelope, where it spirals toward the center and exits through the coUection tube. 

Gum-Saline. Gum is a galactoso—gluconic acid having molecular weight of approximately 1500. First used (16) in kidney perfusion experiments, gum—saline enjoyed great popularity as a plasma expander starting from the end of World War I. The aggregation state of gum depends on concentration, pH, salts, and temperature, and its coUoid oncotic pressure and viscosity are quite variable. Conditions were identified (17) under which the viscosity would be the same as that of whole blood. 

Calcium channel blockers cause more pronounced lowering of blood pressure in hypertensive patients than in normotensive individuals. Generally, all calcium channel blockers cause an immediate increase in PRA during acute treatment in patients having hypertension but PRA is normalized during chronic treatment despite the sustained decrease in blood pressure. These agents also do not generally produce sodium and water retention, unlike the conventional vasodilators. This is because they produce diuretic effects by direct actions on the kidney. 

Methyldopa. Methyldopa reduces arterial blood pressure by decreasing adrenergic outflow and decreasing total peripheral resistance and heart rate having no change in cardiac output. Blood flow to the kidneys is not changed and that to the heart is increased. It causes regression of myocardial hypertrophy. 

Logically, ADH receptor antagonists, and ADH synthesis and release inhibitors can be effective aquaretics. ADH, 8-arginine vasopressin [113-79-17, is synthesized in the hypothalamus of the brain, and is transported through the supraopticohypophyseal tract to the posterior pituitary where it is stored. Upon sensing an increase of plasma osmolaUty by brain osmoreceptors or a decrease of blood volume or blood pressure detected by the baroreceptors and volume receptors, ADH is released into the blood circulation it activates vasopressin receptors in blood vessels to raise blood pressure, and vasopressin V2 receptors of the nephrons of the kidney to retain water and electrolytes to expand the blood volume. 

The chromaffin cells of the adrenal medulla may be considered to be modified sympathetic neurons that are able to synthesize E from NE by /V-methylation. In this case the amine is Hberated into the circulation, where it exerts effects similar to those of NE in addition, E exhibits effects different from those of NE, such as relaxation of lung muscle (hence its use in asthma). Small amounts of E are also found in the central nervous system, particularly in the brain stem where it may be involved in blood pressure regulation. DA, the precursor of NE, has biological activity in peripheral tissues such as the kidney, and serves as a neurotransmitter in several important pathways in the brain (1,2). 

---