Renal vasoconstriction

Cooper, C.L. and Malik, K.U. (1985). Prostaglandin synthesis and renal vasoconstriction elicited by adrenergic stimuli are linked to activation of alpha-1 adrenergic receptors in the isolated rat kidney. J. Pharmacol. Exp. Ther. 233, 24-31. 

Hypoperfusion of skeletal muscles leads to fatigue, weakness, and exercise intolerance. Decreased perfusion of the central nervous system (CNS) is related to confusion, hallucinations, insomnia, and lethargy. Peripheral vasoconstriction due to SNS activity causes pallor, cool extremities, and cyanosis of the digits. Tachycardia is also common in these patients and may reflect increased SNS activity. Patients will often exhibit polyuria and nocturia. Polyuria is a result of increased release of natriuretic peptides caused by volume overload. Nocturia occurs due to increased renal perfusion as a consequence of reduced SNS renal vasoconstrictive effects at night. In chronic severe HF, unintentional weight loss can occur which leads to a syndrome of cardiac cachexia. This results from several factors, including loss of appetite, malabsorption due to gastrointestinal edema, elevated metabolic rate, and elevated levels of proinflammatory cytokines. 

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are members of a family of so-called natriuretic peptides, synthesized predominantly in the cardiac atrium, ventricle, and vascular endothelial cells, respectively (G13, Y2). ANP is a 28-amino-acid polypeptide hormone released into the circulation in response to atrial stretch (L3). ANP acts (Fig. 8) on the kidney to increase sodium excretion and glomerular filtration rate (GFR), to antagonize renal vasoconstriction, and to inhibit renin secretion (Ml). In the cardiovascular system, ANP antagonizes vasoconstriction and shifts fluid from the intravascular to the interstitial compartment (G14). In the adrenal cortex, ANP is a powerful inhibitor of aldosterone synthesis (E6, N3). At the hypothalamic level, ANP inhibits vasopressin secretion (S3). It has been shown that some of the effects of ANP are mediated via a newly discovered hormone, called adreno-medullin, controlling fluid and electrolyte homeostasis (S8). The diuretic and blood pressure-lowering effect of ANP may be partially due to adrenomedullin (V5). 

Bl. Badr, K. F., Sepsis-associated renal vasoconstriction Potential targets for future therapy. Am. J. Kidney Dis. 20,207-213 (1992). 

Ang II acts on the kidney to cause renal vasoconstriction, increase proximal tubular sodium reabsorption, and inhibit the secretion of renin. 

When renal vasoconstriction is relatively greater than the concomitant rise in blood pressure and increase in cardiac output—i.e., when total renal blood flow is lowered—the... 

Neurogenic renal vasoconstriction, with consequent activation of the renin-angio-tonin mechanism, is not a major factor in most cases of neurogenic hypertension evidence for this is seen in the limited fall in blood pressure which follows renal denervation (41, 54) and the failure of prior nephrectomy to alter the pressor response to moderator nerve section (95). However, neurogenic renal vasoconstriction may be adequate to produce a sustained hypertension after other body structures have been sympathetically denervated (42, 44)) and it is possible that neurogenic renal vasoconstriction may play a significant role in the development of essential hypertension. 

On the basis of the above discussion it would appear that the role of adrenergic blockade in the treatment of hypertension, with the exception of isolated cases clearly due to sympatho-adrenal factors, is negligible. However, the possibility remains that neurogenic factors may be involved in the early stages of human essential hypertension. Certain psychic components are known to be involved in the development of hypertension and it is possible that emotionally activated neurogenic factors may cause repeated episodes of renal vasoconstriction and ischemia, which finally lead to the development of local organic... 

Ruan, X., and Arendshorst, W. J. 1996. Calcium entry and mobilization signaling pathways in ANG II-induced renal vasoconstriction in vivo. Am J Physiol 270 F398-F405. 

The other type is non-myoglobinuric acute renal failure, in which intense exercise over a short period of time, such as sprinting, causes minimal rhabdomyolysis without myoglobinuria, i.e., acute renal failure syndrome with severe loin pain and patchy renal vasoconstriction [2]. A recent study showed that anaerobic exercise caused this syndrome, and proposed that Acute renal failure with severe Loin pain and Patchy renal ischemia after anaerobic Exercise (ALPE) (exercise-induced acute renal failure) was a new type of acute renal failure syndrome [4]. 

This case report was published in Nephron in 1981 as evidence for patchy renal vasoconstriction in humans [1],... 

Does ALPE develop via the release of a renal vasoconstricting substance by type II muscle fibers ... 

The following issues, including the etiology, remain to be clarified (a) the pathogenesis of ALPE, (b) the prevention of relapse, and future exercise guidance, (c) why delayed CT shows patchy contrast enhancement even in the recovery phase, (d) whether or not patchy renal vasoconstriction persists for 1-2 weeks, (e) why a contrast medium is present in the kidney for 72 h maximum, (f) the association between ALPE and disorders of type II muscle fibers, (g) the reasons for the less marked increases in serum myoglobin and creatine phosphokinase (CPK), and (h) why ALPE frequently develops in patients with renal hypouricemia. 

Ishikawa I, Saito Y, Shinoda A, Onouchi Z (1981) Evidence for patchy renal vasoconstriction in man observation by CT scan. Nephron 27 31-34... 

Ishikawa I, Onouchi Z, Yuri T, Saito Y, Shinoda A, Yamamoto I (1982) Acute renal failure with severe loin pain and patchy renal vasoconstriction. In Eliahou HE (ed) Acute renal failure. John Libbey, London, pp 224-229... 

Hotta O, Taguma Y, Suzuki K, Futagi G, Kurosawa T, Takahashi H, Ishizaki M, Son T, Nakamichi G (1987) Four cases of acute renal failure mainly due to renal vasoconstriction (Japanese abstract). Nippon Jinzo Gakkai Shi (Jpn J Nephrol) 29 1489... 

Kim SH, Han MC, Han JS, Kim S, Lee JS (1991) Exercise-induced acute renal failure and patchy renal vasoconstriction CT and MR findings. J Comput Assist Tomogr... 

Hisanaga S, Ueno N, Inagaki H, Tokura T, Uezono S, Yokota N, Fujimoto S, Eto T (1999) Exercise-induced acute renal failure associated with renal vasoconstriction (in Japanese with English abstract). Nippon Jinzo Gakkai Shi (Jpn J Nephrol) 41 406-412... 

Lee JY, Cho JT, Park YJ, Shin MH, Koo CH, Park TY, Kim JS, Han SS, Kang JH (1996) A case of acute renal failure with severe loin pain and patchy renal vasoconstriction after exercise (in Korean with English abstract). Korean J Med 50 840-845... 

Watanabe T (2002) Patchy renal vasoconstriction after exercise in a child without renal hypouricemia. Pediatr Nephrol 17 284-286... 

Koyama M, Ishii M, Watanabe K (2003) A case of exercise-induced acute renal failure and patchy renal vasoconstriction (Japanese abstract). J Jpn Radiol Soc 63 S413... 

The authors suggested that intense cocaine-induced renal vasoconstriction had been the likely underlying mechanism. 

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