The efferent arterioles of the juxtamedullary nephrons enter the outer

The efferent order pitavastatin of the juxtamedullary nephrons enter the outer stripe of the outer medulla and divide into a series of vascular loops called vasa recta. The vasa recta descend into the inner stripe of the outer medulla and form vascular bundles. The descending vasa recta (DVR) in the centre of the bundles continue into the inner medulla whereas the DVR on the outer margins of the bundles give rise to a capillary plexus between the vascular bundles in the outer medulla. The DVR found in either the outer or inner medulla divide and eventually merge to form ascending vasa recta (AVR) that carry metabolic substances that enter the medulla in the DVR blood back to the cortex. To avoid the possibility of medullary hypoxia resulting from this process the kidney has adapted to exert a subtle control over regional perfusion of the outer and inner medulla (Mattson, 2003; Navar et al., 2008; Johns and Ahmeda, 2014).

Renal medullary blood flow
Although the kidney strives to maintain its perfusion within tight boundaries, considerable blood flow fluctuations do occur under normal conditions. However should these fluctuations be prolonged, target organ damage can occur (Persson, 2002). The renal medulla is renowned for its low rate of blood perfusion (Cowley, 1997) and a minimal reserve of oxygen (less than 40%) (Heyman et al., 1997), therefore the maintenance of adequate perfusion of this zone is critically important for its survival, for the functional integrity of the kidney and for the appropriate renal regulation of body fluid balance and arterial pressure (Badzynska et al., 2003). The regulation of blood flow in the renal medulla has been a subject of interest for many years. Previous reports by Persson (2002) indicate that the renal medulla has control over its own blood flow. It has also been suggested that the renal medulla has an impaired autoregulatory capacity, or may even exhibit a complete passive blood flow response to renal perfusion pressure changes however more recent findings have challenged this hypothesis (Persson, 2002). The vascular architecture of the kidney appears to be arranged in a way that protects the renal medulla from ischaemic insults (Evans et al., 2004). The details of this process are far from clear and much experimental evidence suggests there may be a complex interaction between paracrine agents and autocoids in modulating vasomotor tone at various locations along the micro-vascular circuit (Pallone et al., 2012).
Given the importance of medullary perfusion in influencing water and salt balance, it was necessary to determine which location(s) along the micro-vascular circuit provides control of medullary blood perfusion (MBP) (Pallone et al., 2012). Pallone (1994) first demonstrated that when DVR are isolated from outer medullary vascular bundles in the rat kidney they are capable of constricting at various foci after exposure to contractile agonists such as Angiotensin II. Based on anatomic considerations it is probable that DVR are an important site of regulation. It has since been reported that this regulation is mediated by contraction of the vasa recta pericytes (Pallone, 1994; Park et al., 1997; Pallone et al., 2012). The vasa recta capillaries therefore appear to be capable of exerting regional control of blood perfusion to the renal medulla. Similar studies using vascular casting methodology suggest that juxtamedullary glomerular arterioles are not the chief regulators of MBP, which is consistent with the idea that outer medullary descending vasa recta play a key role in MBP control (Evans et al., 2004).

Kidney and blood pressure control
Guyton et al. (1972) reported that raised arterial pressure was accompanied by increased urine flow and sodium excretion by way of the pressure-diuresis mechanism (Guyton et al., 1972). By increasing urine flow the effective circulating volume is reduced and thereby normalises arterial BP. This process enables the kidneys to control long-term arterial pressure by monitoring blood volume. In genetic rat models of hypertension and using micropuncture techniques, Arendshorst and Beierwaltes (1979) reported that higher BP than in the normotensive model were necessary to excrete a given amount of sodium (Arendshorst and Beierwaltes, 1979). Therefore, hypertension can occur as a result of a malfunction of the pressure-natriuresis system in the kidney, for example impaired excretory ability of the kidney. This hypothesis is supported by the fact that with anti-hypertensive treatment, for example angiotensin converting enzyme (ACE) blockers, there is an alteration in the pressure-natriuresis balance and the return sodium and water excretion back to control levels (Cowley et al., 1995).