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Renal hemodynamics: an overview.

Article Excerpt
Editor's Note: This article is a continuation of a renal physiology series in the Nephrology Nursing Journal. The articles, which offer continuing education credits and are updates of manuscripts that previously appeared in the journal, are written by experts in nephrology and contain the most up-to-date information and research available. An overview on glomular filtration (sec Volume 30, Number 3, pp. 285-290) appears in the June 2003 issue of Nephrology Nursing Journal.

Renal blood flow (RBF), which defines renal plasma flow (RPF), is controlled by a number of physical and humoral factors. These factors are both intrinsic and extrinsic to the kidney, home of the intrinsic factors include an autoregulatory mechanism, intrarenal rennin-angiotensin mechanism, eicosanoids, and kinins. Critical extrinsic factors include the Sympathetic Nervous System (SNS), angiotensin II, antidiuretic hormone, dopamine, and histamine. Endothelin, nitric oxide (NO), and atrial natriuretic peptide (ANP) also play important roles in altering renal hemodynamics. These multiple factors work in concert to sustain glomerular filtration despite wide variations in systemic pressures.

Intrinsic Factors

Autoregulation. The autoregulatory mechanism (ARM), an intrarenal system, maintains a consistent RBF despite mean arterial pressure (MAP) fluctuations from about 80-180 mmHg, but becomes dysfunctional when the MAP is outside this range. The ARM maintains renal perfusion at a constant level during exercise, postural changes, sleep, and physiological crises, even though these conditions lead to systemic pressure changes.

There are two mechanisms believed to be involved in this autoregulatory phenomena: the myogenic and the tubuloglomerular feedback (TGF) mechanisms. The myogenic mechanism is based on the function of baroreceptors (stretch receptors) in the afferent arterioles. When the MAP increases, these receptors respond to the increased vascular wall tension or stretch and cause afferent arteriolar constriction. This constriction prevents transmission of the elevated arterial pressure to the glomerulus, thus maintaining a normal [P.sub.GC] and GFR. There appears to be no effect on the efferent arteriole.

Conversely, if the MAP falls, afferent arteriolar dilation occurs to allow for increased blood flow and maintenance of a normal [P.sub.GC] and GFR. This mechanism may also be stimulated by increases and decreases in the delivery of oxygen and other nutrients to the tissues. This mechanism provides a rapid response to changes that can alter GFR and is thought to be most important during episodes where the blood pressure rises rapidly.

The TGF mechanism relates to the function of the macula densa and jux-taglomerular cells. In conditions that increase RBF and, thus, GFR, there is an increased delivery of sodium chloride (NaCl) to the macula densa cells in the distal nephron. When these cells detect this increased NaCl load, they mediate vasoconstriction of the afferent arteriole via an unknown messenger substance, resulting in a decrease in the glomerular blood flow, a decrease in [P.sub.GC] and a return of the GFR toward normal. Conversely, when there is a decrease in glomerular blood flow, there is a decrease in NaCl delivered to the macula densa cells. This leads to afferent arteriolar dilatation, increased glomerular blood flow, increased [P.sub.GC], and return of GFR toward normal. Adenosine has been identified as the possible mediator for TGF. This mechanism works more slowly than the myogenic mechanism, but is critical to GFR maintenance in conditions that cause changes in intra-arteriolar pressure.

Neither of these mechanisms alone or together fully explains the ARM, and in all likelihood numerous other factors contribute to this phenomena. There are several essential facts to be noted about the ARM. The ARM cannot completely override changes in the MAP, but it can limit the degree of change transmitted to the glomerulus and the degree to which GFR changes. The ARM will fail to function when there is...