Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.1.21 (CPT)
 4,580 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the relationship between insulin and reactivity to the cold pressure test four groups of mildly obese patients (12 per group: normotensive, essential hypertensive, normotensive (N-NIDD) and hypertensive non-insulin-dependent diabetics (H-NIDD)) underwent a standardised oral glucose tolerance test. During the test, BP and heart rate were monitored and venous blood samples were obtained at 0, 60 and 120 minutes to determine serum levels of glucose, insulin (microU/ml), sodium, potassium (mEq/I), renin activity (ng/ml/hour), aldosterone, noradrenaline and adrenaline. The cold pressure tests were performed before glucose ingestion (I-CPT) and again at 60 minute after ingestion (II-CPT). As expected, glucose ingestion caused a significant increase in glycaemia and serum insulin; the latter rose significantly more at 60 minutes in normotensives (85 +/- 6) and essential hypertensives (83 +/- 5) than in N-NIDD (30 +/- 4) and H-NIDD (29 +/- 3). Plasma K significantly decreased in normotensives (4.4 +/- 0.1 vs. 3.6 +/- 0.1, P < 0.05) and essential hypertensives (4.3 +/- 0.1 vs. 3.5 +/- 0.1, P < 0.05) but did not change in either N-NIDD or H-NIDD. PRA significantly increased in normotensives (0.6 +/- 0.1 vs. 1.2 +/- 0.1, P < 0.01) and essential hypertensives (0.8 +/- 0.1 vs. 1.5 +/- 0.2, P < 0.05) but did not change in N-NIDD or H-NIDD. Plasma sodium and catecholamines did not change in any group. I-CPT induced similar reactivity in all the groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of glucose load on cardiovascular and humoral responses to a cold pressure test. 775 81

Polycystic kidney diseases result from disruption of the genetically defined program that controls the size and geometry of renal tubules. Cysts which frequently arise from the collecting duct (CD) result from cell proliferation and fluid secretion. From mCCD(cl1) cells, a differentiated mouse CD cell line, we isolated a clonal subpopulation (mCCD-N21) that retains morphogenetic capacity. When grown in three-dimensional gels, mCCD-N21 cells formed highly organized tubular structures consisting of a palisade of polarized epithelial cells surrounding a cylindrical lumen. Subsequent addition of cAMP-elevating agents (forskolin or cholera toxin) or of membrane-permeable cAMP analogs (CPT-cAMP) resulted in rapid and progressive dilatation of existing tubules, leading to the formation of cystlike structures. When grown on filters, mCCD-N21 cells exhibited a high transepithelial resistance as well as aldosterone- and/or vasopressin-induced amiloride-sensitive and -insensitive current. The latter was in part inhibited by Na(+)-K(+)-2Cl(-) cotransporter (bumetanide) and chloride channel (NPPB) inhibitors. Real-time PCR analysis confirmed the expression of NKCC1, the ubiquitous Na(+)-K(+)-2Cl(-) cotransporter and cystic fibrosis transmembrane regulator (CFTR) in mCCD-N21 cells. Tubule enlargement and cyst formation were prevented by inhibitors of Na(+)-K(+)-2Cl(-) cotransporters (bumetanide or ethacrynic acid) or CFTR (NPPB or CFTR inhibitor-172). These results further support the notion that cAMP signaling plays a key role in renal cyst formation, at least in part by promoting chloride-driven fluid secretion. This new in vitro model of tubule-to-cyst conversion affords a unique opportunity for investigating the molecular mechanisms that govern the architecture of epithelial tubes, as well as for dissecting the pathophysiological processes underlying cystic kidney diseases.
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PMID:cAMP-dependent chloride secretion mediates tubule enlargement and cyst formation by cultured mammalian collecting duct cells. 1905 3