Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The endocrine control of electrolyte balance during development is reviewed. It is suggested that the high urinary sodium excretion observed in premature infants may be secondary to the immaturity of the adrenal gland to adequately increase the secretion of aldosterone (Sulyok et al, 1979b), and to the inability of the distal tubule to respond appropriately to a rise in circulating aldosterone levels (Sulyok et al, 1979a). On the other hand, the elevated plasma aldosterone levels observed in term newborn infants may play an important role in the blunted response of the newborn kidney to saline loading (Sulyok et al, 1979a; Spitzer, 1982). The ability of ANP to induce a natriuresis and to contribute to fluid and electrolyte homeostasis during development has been investigated. It has been found that the immature kidney is less responsive to ANP than later in life (Chevalier et al, 1988; Robillard et al, 1988). On the other hand, it has been suggested that a rise in plasma ANP during the first five days of life may contribute to the physiological weight loss associated with the extracellular volume contraction occurring shortly after birth (Tulassay et al, 1987). The role of glucocorticoids, prostaglandins and the kallikrein-kinin system in regulating electrolyte balance during development is also reviewed.
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PMID:Endocrine control of electrolyte balance during development. 269 49

The mature, fully differentiated connecting tubule (CNT) cell plays an important role in the regulation of serum potassium levels and synthesizes the enzyme tissue kallikrein, a main component of a renal vasoactive system, the kallikrein-kinin system. To characterize the growth of CNT cells (tissue kallikrein-producing cells), we studied the rat kidney at three different time points of postnatal development: at day 5, day 15, and day 30. The CNT cells were identified on tissue sections by a standardized immunohistochemical procedure. The tissue kallikrein content was determined by radioimmunoassay and the activity of the enzyme in kidney homogenates was measured using a selective synthetic substrate. The number of immunolabeled CNT and CNT cells per cortex area gradually increased from day 5 to day 30. A similar rise in the content and activity of tissue kallikrein was observed when the enzyme levels were determined by radioimmunoassay or by the enzymatic method. In addition, the morphometric analysis showed that the distal end of CNT had larger cells that displayed a more intense tissue kallikrein staining than those present in the proximal end, suggesting that the postnatal development of CNT is induced from its juxtamedullary portion. Our results show that tissue kallikrein expression is very low in the newborn rat, increasing gradually with age to reach adult levels at day 30. This finding, together with the morphometric data, suggests immaturity of CNT cells in newborn rats, a fact that could contribute to explaining the high serum potassium levels reported at this stage. In addition, the contrasting behavior of kallikrein and renin in the postnatal development (kallikrein increasing and renin decreasing) could explain the gradual decrease in renal vascular resistance and increase in renal blood flow observed after birth.
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PMID:Postnatal maturation of tissue kallikrein-producing cells (connecting tubule cells) in the rat kidney: a morphometric and immunohistochemical study. 854 32