Increase In Water Reabsorption Research Articles

Novel intrinsic neurogenic and myogenic mechanisms underlying the formation of faecal pellets along the large intestine of guinea-pigs.

Soft faecal material is transformed into discrete, pellet-shaped faeces at the colonic flexure. Here, analysis of water content in natural faecal material revealed a decline from cecum to rectum without significant changes at the flexure. Thus, pellet formation is not explained by changes in viscosity alone. We then used video imaging of colonic wall movements with electromyography in isolated preparations containing guinea-pig proximal colon, colonic flexure and distal colon. To investigate the pellet formation process, the colonic segments were infused with artificial contents (Krebs solution and 4-6% methylcellulose) to simulate physiological faecal content flow. Remarkably, pellet formation took place in vitro, without extrinsic neural inputs. Infusion evoked slowly propagating neurogenic contractions, the proximal colon migrating motor complexes (∼0.6cpm), which initiated pellet formation at the flexure. Lesion of the flexure, but not the proximal colon, disrupted the formation of normal individual pellets. In addition, a distinct myogenic mechanism was identified, whereby slow phasic contractions (∼1.9cpm) initiated at the flexure and propagated short distances retrogradely into the proximal colon and antegradely into the distal colon. There were no detectable changes in the density or distribution of pacemaker-type interstitial cells of Cajal across the flexure. The findings provide new insights into how solid faecal content is generated, suggesting the major mechanisms underlying faecal pellet formation involve the unique interaction at the colonic flexure between antegrade proximal colon migrating motor complexes, organized by enteric neurons, and retrograde myogenic slow phasic contractions. Additional, as yet unidentified extrinsic and/or humoral influences appear to contribute to processing of faecal content in vivo. KEY POINTS: In herbivores, including guinea-pigs, clearly defined faecal pellets are formed at a distinct location along the large intestine (colonic flexure). The mechanism underlying the formation of these faecal pellets at this region has remained unknown. We reveal a progressive and gradual reduction in water content of faecal content along the bowel. Hence, the distinct transition from amorphous to pellet shaped faecal content could not be explained by a dramatic increase in water reabsorption from a specific site. We discovered patterns of anterograde neurogenic and retrograde myogenic motor activity that facilitate the formation of faecal pellets. The formation of 'pellet-like' boluses at the colonic flexure involves interaction of an antegrade migrating motor complex in the proximal colon and retrograde myogenic slow phasic contractions that emerge from the colonic flexure. The findings uncover intrinsic mechanisms responsible for the formation of discrete faecal scybala in the large intestine of a vertebrate.

Vasopressin-independent regulation of collecting duct aquaporin-2 in food deprivation

Humans and animals are frequently subjected to food deprivation or starvation. However, the adaptation of the kidney to this condition is not well understood. The purpose of these studies was to examine the effects of food deprivation on water handling by the kidney, the expression levels of collecting duct (CD) water channel aquaporin-2 (AQP2), and to determine the role of vasopressin in the adaptation of AQP2 to food deprivation. Sprague-Dawley (SD) and Brattleboro rats were placed in metabolic cages and deprived of food but had free access to water for 72 hours. Water balance and urine osmolality were measured daily. Kidney tissues were isolated and examined for the expression of AQP2 using semiquantitative immunoblotting and Northern hybridization. The circulating level of vasopressin and the mRNA expression levels of its precursor were determined by radioimmunoassay and Northern hybridization, respectively. In SD rats, the first 24 hours of food deprivation is associated with a significant polyuria and decreased urine osmolality (Uosm). This correlated with a significant down-regulation of AQP2 in the cortex and outer medulla. After 72 hours of food deprivation, Uosm increased above baseline, and urine volume dropped to a lower value. This was associated with a rebound increase in AQP2 expression in the cortex and OM and its up-regulation in the inner medulla. Interestingly, vasopressin mRNA expression and plasma levels were unchanged during food deprivation. Further, in homozygous Brattleboro rats, in which endogenous vasopressin is absent, food deprivation caused changes in urine volume, urine osmolality, and AQP2 expression, which are qualitatively similar to those observed in normal rats. Food deprivation impairs water handling by the kidney by causing dual changes in urine volume and urine osmolality. This effect is associated with parallel alterations in the expression of AQP2 and is independent of vasopressin activity. It is concluded that the increase in water reabsorption in the CD is an adaptive response of the kidney to a long period of food deprivation and is mediated via a vasopressin-independent mechanism.

Upregulation of collecting duct aquaporin-2 by metabolic acidosis: role of vasopressin.

Metabolic acidosis is associated with alteration in fluid and electrolyte reabsorption in a number of nephron segments. However, the effects of metabolic acidosis on urine osmolality and aquaporin-2 (AQP-2) remain poorly understood. In these studies, we examined the effects of chronic metabolic acidosis on water handling by the kidney. Rats were placed in metabolic cages and subjected to water (control) or 280 mM NH(4)Cl loading for 120 h to induce metabolic acidosis. The results indicated a significant increase in urine osmolality with no change in urine volume or urinary Na(+) excretion in acid-loaded animals. This effect was independent of alteration in fluid intake or salt/Cl(-) loading. Immunoblotting and Northern hybridization studies indicated that AQP-2 protein abundance and mRNA expression levels increased significantly along the collecting duct system of NH(4)Cl-but not NaCl-loaded animals. RIA results indicated that metabolic acidosis was associated with a fourfold increase in circulating levels of vasopressin (AVP) and a significant increase in brain AVP mRNA expression levels. In conclusion, metabolic acidosis upregulates the expression levels of AQP-2 and increases urine osmolality, suggesting an adaptive increase in water reabsorption in the collecting duct. A concomitant increase in AVP synthesis and secretion likely plays an essential role in the adaptation of AQP-2 in metabolic acidosis.

A micropuncture study of kidney function in the river lamprey Lampetra fluviatilis adapted to sea water.

Micropuncture techniques have been used to investigate kidney function in lampreys adapted to hyperosmotic media. Plasma electrolyte concentrations were maintained well below corresponding concentrations in the external environment. Urine composition was variable, but generally showed high concentrations of magnesium, sulphate and chloride ions. Lampreys in 50% sea water produced urine which was hypo or iso-osmotic to plasma, whereas those in 100% sea water produced hyperosmotic urine. Urine flow rate in 50% sea water was one tenth of that in fresh water, due to a reduction in filtration rate and an increase in water reabsorption by the kidney. As in fresh water, little if any filtered water was reabsorbed by the proximal segment. Almost 90% of filtered water was reabsorbed by the kidney of 100% sea water lampreys and most of this must have occurred in the distal and collecting segments.

Actions of vasotocin and some of its analogues on salt and water excretion by the frog.

The actions of small doses of arginine and lysine-vasotocin on urine flow (V), inulin (CIn), free water (CHH2O), sodium (CNa), and potassium (CK) clearances were studied in Rana esculenta and compared with those of larger doses of oxytocin, lysine-vasopressin, Val3-oxytocin, Ileu8-oxytocin, Phe2-Phe3-Lys8-oxytocin, deamino-oxytocin, and oxypressin. Injections of either arginine or lysine-vasotocin (mean dose .030 µg) induce a small decrease in glomerular filtration rate (GFR) and two marked tubular effects: a) an increase in water reabsorption, CHH2O being reduced even when related to CIn; b) an increase in tubular sodium reabsorption, CNa/CIn being lowered, whereas CK/CIn remains unchanged. Neither oxytocin nor lysine-vasopressin, even in doses 20–25 times higher, promotes the tubular effects typical of vasotocin. Oxytocin promotes a slight decrease in GFR and V. Lysine-vasopressin remains without any effect. All the other artificial analogues of oxytocin injected in large doses increase V, GFR, CNa/CIn and CK/CIn. It is concluded that the vasotocins specifically promote in the kidney tubules of the frog the same two actions described in the other target organs in the amphibians, namely an increase in osmotic permeability to water and a stimulation of active sodium transport.