UNIPROT:P01185 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Target Concepts:

Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This work was performed to gain more information on the role of pyruvate kinase isoenzymes in the regulation of renal carbohydrate metabolism. Immunohistochemically, pyruvate kinase type L is shown to be localized in the proximal tubule of the nephron and pyruvate kinase type M2 in the distal tubule and the collecting duct. a tight relationship between gluconeogenesis and pyruvate recycling was found. The rate of gluconeogenesis (8 mumol/g wet wt. per 30 min) was of the same order of magnitude as the rate of pyruvate recycling (10.92 mumol/g wet wt. per 30 min). Stimulation of gluconeogenesis from 20 mM lactate in kidney cortex slices of 24-h-starved rats by dibutyryl-cAMP, alanine and parathyroid hormone was connected with a decrease in pyruvate recycling; inhibition of gluconeogenesis due to a lack of Ca2+ in the incubation medium was linked with an increase in pyruvate recycling. The degradation of [6-14C]glucose to lactate, pyruvate, ketone bodies and CO2 and of [2-14C]lactate was unaffected by dibutyryl-cAMP, alanine, epinephrine, vasopressin or the omission of Ca2+ from the incubation medium. 1 mM dibutyryl-cAMP or 5 mM alanine did not alter the activities of oxaloacetate decarboxylase, 'malic' enzyme and malate dehydrogenase from rat kidney cortex. Since aerobic glycolysis in the distal tubules and the collecting ducts is not influenced by hormones, dibutyryl-cAMP and Ca2+, pyruvate kinase type M2 residing in this tissue is unlikely to be a control point of glycolysis. Since this tissue degrades only one-seventh of the glucose formed via gluconeogenesis, it does not contribute significantly to pyruvate recycling. Therefore, the decrease of pyruvate recycling in the presence of dibutyryl-cAMP and alanine in rat kidney cortex slices, leading to increased renal gluconeogenesis, has to be ascribed to the regulation of pyruvate kinase type L.
...
PMID:Localization and role of pyruvate kinase isoenzymes in the regulation of carbohydrate metabolism and pyruvate recycling in rat kidney cortex. 300 99

These experiments studied the effect of parathyroid hormone (PTH) (1-84) on water and Ca transport in isolated toad bladder sacs and toad bladder epithelial cells. Serosal addition of PTH significantly inhibited maximal water flow induced by vasopressin or exogenous cyclic AMP. This effect was seen over a wide range of concentrations, with the threshold for the effect occurring at 1 ng/ml. Pretreatment of the toad bladder sacs with prostaglandin inhibitors (indomethacin or ibuprofen, 1 X 10(-6) M) or preincubation in low-Ca medium (0.089 mM) abolished the effect of PTH on vasopressin-stimulated water flow. Pretreatment of the toad bladders with lanthanum (5 X 10(-5) M) also abolished the effect of PTH on vasopressin-stimulated water flow. Synthetic PTH (1-34) inhibited vasopressin-stimulated water flow only at a high concentration (1 microgram/ml). PTH increased 45Ca uptake by toad bladder epithelial cells but had no effect on 45Ca efflux. These results demonstrate that PTH inhibits water transport beyond the generation of cyclic AMP. That the effect of PTH was abolished in a low-Ca medium or by pretreatment with lanthanum suggests that cell Ca uptake is required for the effect of PTH on water transport. That prostaglandin inhibitors also block the effect of PTH on vasopressin-stimulated water flow suggests that prostaglandin synthesis is required for the effect. These data suggest that the effect of PTH on water flow is mediated by an increased cellular uptake of Ca that stimulates prostaglandin release. Prostaglandin release, in turn, appears to mediate the inhibitory effect of PTH on vasopressin-stimulated water transport.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Parathyroid hormone inhibits water flow in the isolated toad bladder. 300 14

Primary confluent monolayers were grown from proximal tubule fragments of rabbit kidneys. The fragments were obtained by gradient centrifugation and seeded on an ad hoc dish whose bottom was a permeable and transparent collagen membrane. The culture medium was a mixture of 50% Ham's F-12 and 50% Dulbecco's modified Eagle's medium supplemented with insulin, transferrin, ethanolamine, sodium selenite, and amino acids. The monolayers were studied at 6-14 days after seeding. Transmission electron microscopy revealed cuboidal cells 8.5-10.5 microns high, with a 1.5 to 2.5-microns apical brush border, abundant mitochondria, vacuoles, lysosomes, and irregular basal interdigitating processes. Cyclic AMP synthesis was stimulated by parathyroid hormone and was insensitive to vasopressin and isoproterenol. Electrophysiological studies performed with the same physiological salt solution on both sides revealed a transepithelial voltage of -2.6 +/- 0.6 mV (n = 10) and a basolateral membrane voltage of -51.0 +/- 4.5 mV (n = 13), both referred to the basal solution. The transepithelial electrical resistance was 7 +/- 2 omega X cm2. The apical membrane depolarized on addition of glucose to the apical side and hyperpolarized on removal of glucose. Changes in apical membrane voltage on addition of varying glucose concentrations (at [Na] = 135 mM, 37 degrees C) demonstrate the presence of a glucose transport system with an apparent Km of 3.54 +/- 0.54 and a Vmax of 7.2 +/- 0.4 mV. Thus this preparation exhibits morphological and electrophysiological characteristics of proximal tubule cells; these studies demonstrate the feasibility of the use of intracellular microelectrode techniques to study the transport properties of cultured epithelia.
...
PMID:Electrophysiological studies on primary cultures of proximal tubule cells. 301 59

We characterized altered adenosine 3',5'-cyclic monophosphate (cAMP) regulation in deoxycorticosterone acetate (DOCA)-Na hypertensive rats using endogenous cAMP accumulation in the intact cell system of microdissected renal tubule fragments. Increased cAMP accumulation in response to vasopressin (VP) in cortical collecting tubules (CCT) began on day 5 (67%) after exposure to DOCA-Na and increased by 320% on day 42. Increased blood pressure began after day 7 and polyuria after day 17. The increased response to VP was DOCA dependent and appears to be exaggerated by dietary NaCl. Anatomic and hormone specificity studies were done on days 21-30. These included cAMP responses to prostaglandin E2, parathyroid hormone, thyrocalcitonin, VP, and isoproterenol in the CCT. The cAMP response to VP was measured in the glomerulus, proximal convoluted tubule, thin descending limb of Henle, medullary thick ascending limb of Henle, cortical thick ascending limb of Henle, medullary collecting tubule, and CCT. The supersensitivity occurred only to VP and only in the CCT. Thus this alteration in the VP response is anatomic and hormone specific and does not appear to be an acute effect of DOCA, since it was not present on day 1 and on day 3 of DOCA exposure. DOCA-Na hypertension is VP dependent. A specific exaggerated cAMP response to this hormone in the CCT would be expected to cause increased sodium retention. Whether increased sodium retention at this site contributes to hypertension in the DOCA-Na rat is unknown.
...
PMID:Enhanced cAMP response to vasopressin in the CCT of DOCA-Na hypertensive rats. 302 5

Evidence for the presence of beta adrenoceptors on proximal tubules from the rat kidney has been obtained using enriched tubule suspensions prepared by Percoll centrifugation. Intact tubules demonstrated simultaneous enrichment of parathyroid hormone and isoproterenol sensitive cAMP production with no enrichment of antidiuretic hormone sensitive cAMP production. Both norepinephrine and epinephrine were less potent than isoproterenol and the stimulatory effect of catecholamines could be blocked with propranolol but not phentolamine. The stimulatory effect of norepinephrine on cellular phenylalanine uptake is blunted by co-addition of isoproterenol suggesting that the beta receptor may modulatory catecholamine stimulated transport.
...
PMID:Evidence for the presence of functional beta-adrenoceptor along the proximal tubule of the rat kidney. 302 77

Atrial natriuretic factor (ANF) (1 microM) markedly increased cyclic guanosine monophosphate (cGMP) content in microdissected glomeruli (35-fold) and in microdissected inner medullary collecting ducts (IMCD) (20-fold). ANF caused little or no increase in cGMP content in other nephron segments. The threshold concentration for increased cGMP accumulation by ANF was 0.1-1 nM in IMCD, which is in the range reported for rat plasma. Sodium nitroprusside (1 mM), which selectively stimulates soluble guanylate cyclase, increased cGMP content in glomeruli but not in IMCD. ANF did not alter cAMP accumulation in the absence or presence of vasopressin (AVP) or parathyroid hormone (PTH) in outer and inner medullary tubule suspensions, or in microdissected proximal convoluted tubules (PCT), medullary thick ascending limbs (MAL) or IMCD. These data are compatible with the hypothesis that cGMP is a second messenger for a physiologic action of ANF in the inner medullary collecting duct. ANF apparently activates membrane-bound guanylate cyclase in this segment.
...
PMID:Effects of atrial natriuretic factor on cyclic guanosine monophosphate and cyclic adenosine monophosphate accumulation in microdissected nephron segments from rats. 302 27

Six male volunteers were infused with arginine (0.5 g/kg body weight) over 30 min, after an overnight fast and water deprivation. There was a significant decrease in renal phosphate clearance (P less than 0.025) and urinary cyclic adenosine monophosphate (cAMP) output (P less than 0.025) during the 60- to 90-min period after the beginning of the infusion; both returned to the preinfusion basal levels within 150 min. The plasma levels of parathyroid hormone (PTH) were not affected by the infusion and remained unchanged during the subsequent 150 min. Plasma levels of arginine vasopressin (AVP) were also not significantly affected although plasma osmolality increased by 6-9 mmol/kg in all subjects. The infusion resulted in a diuresis, and a fall in urine osmolality but a decrease in free-water clearance; creatinine clearance was not affected. Six other subjects were given a bolus of 230 i.u. PTH intravenously, and 20 days later this was repeated during an infusion of arginine (0.5 g/kg body weight). There was a significant decrease in urinary phosphate (P less than 0.025) and cAMP excretion (P less than 0.05) when PTH was given with arginine. It is suggested that arginine blocks the action of PTH on the proximal renal tubule but not that of vasopressin on the distal nephron and collecting ducts.
...
PMID:Arginine infusion blocks the action of parathyroid hormone but not arginine vasopressin on the renal tubule in man. 302 30

We showed previously that increasing Ca2+ concentration in the incubation medium suppressed cAMP production in response to vasopressin (AVP), glucagon or forskolin in the medullary thick ascending limb of Henle (MTAL) but not in medullary collecting tubules of mouse kidney. In the present study, we examined, using nephron segments dissected from mouse kidney, whether the inhibitory effect of high Ca2+ is specific to MTAL. Increasing Ca2+ in the incubation medium from 1 to 5 mM inhibited cAMP production in response to parathyroid hormone (PTH), calcitonin, AVP or glucagon in cortical thick ascending limbs of Henle (CTAL), but dit not inhibit cAMP production stimulated by PTH or calcitonin in proximal convoluted tubules and that by AVP in cortical collecting tubules. In CTAL, high ambient Ca2+ also inhibited cAMP production stimulated by forskolin. Thus, our present data show that high Ca2+ inhibits cAMP production specifically in thick ascending limbs of Henle but not in the other nephron segments. High ambients Ca2+ may inhibit adenylate cyclase at postreceptor site(s) one of which may be the catalytic unit of the enzyme in TAL.
...
PMID:High Ca2+ inhibits peptide hormone-dependent cAMP production specifically in thick ascending limbs of Henle. 302 19

alpha 2-Adrenoceptors were first described pharmacologically ten years ago. Within three years their capacity to inhibit adenylate cyclase had been demonstrated in many tissues. They were demonstrated biochemically in the kidneys in 1981 even before any renal physiological effects of their activation were known. They predominate numerically over alpha 1-adrenoceptors in renal membranes and their density is increased in genetic forms of rat hypertension. alpha 1-Adrenoceptors normally mediate the vasoconstriction and sodium- and water-retaining effects of sympathetic neuronally released norepinephrine. Norepinephrine or epinephrine must be infused to activate alpha 2-adrenoceptors, suggesting that renal alpha 2-adrenoceptors are extrajunctional, whereas alpha 1-adrenoceptors are postjunctional. When alpha 1-adrenoceptors are chronically blocked, renal alpha 2-adrenoceptor density increases and they assume a location at postjunctional sites, the otherwise exclusive domain of alpha 1-adrenoceptors. Results from microdissection studies have established that alpha 2-adrenoceptors are present on most segments of the nephron and that their activation can suppress adenosine 3,'5'-cyclic monophosphate (cAMP) accumulation induced by most renal hormones. However, failure of alpha 2-adrenoceptor activation to suppress cAMP accumulation in some tubular segments induced by certain hormones suggests compartmentalization of adenylate cyclase regulation that is hormone-function specific. In view of the potent inhibitory effects of alpha 2-adrenoceptor stimulation on hormone activated cAMP accumulation in several discrete areas of the nephron, we suggest that alpha 2-adrenoceptors fulfill important regulatory role(s) in renal function. To date, alpha 2-adrenoceptor activation has been shown to reverse vasopressin-induced sodium and water retention, and arachidonic acid- and furosemide-induced cAMP, sodium, and water excretion in the isolated perfused kidney. Thus the effects are qualitatively and quantitatively dependent in these studies on the hormone being infused and are therefore hormone-function specific. Physiological effects of alpha 2-adrenoceptor activation of thyrocalcitonin and on parathyroid hormone-induced effects have not been studied. alpha 2-Adrenoceptor activation can inhibit renin release in some model systems and can activate a sodium-hydrogen antiporter system in proximal tubules. The physiological roles of these actions are unknown.
...
PMID:Renal alpha 2-adrenoceptors and the adenylate cyclase-cAMP system: biochemical and physiological interactions. 302 68

Primary monolayers grown from F1 band of a Percoll gradient centrifugation ("distal" monolayers) were studied, after confluency, 6-14 days after seeding. Transmission and scanning electron microscopy revealed that two cell types, resembling principal cells of the rabbit cortical collecting tubule (CCT) and intercalated cells of either CCT or connecting tubule, constitute approximately 96% of the monolayer. About two-thirds of the intercalated cells fluoresced when treated with fluorescent peanut lectin. Indirect specific immunocytofluorescent staining revealed fluorescence in 96% of the cells, confirming that the monolayers were derived from CCT or connecting tubule cells. Exposure of monolayers to vasopressin or isoproterenol increases adenosine 3',5'-cyclic monophosphate (cAMP) content in the cells and bathing medium, whereas parathyroid hormone was ineffective. Electrophysiological studies revealed a transepithelial voltage (VT) of -11 +/- 2 mV, and basolateral membrane voltage (Vb) of -77 +/- 5 mV (n = 20). The transepithelial electrical resistance (RT) was 1,870 +/- 250 omega X cm2 (n = 13). In three out of six monolayers, amiloride (10(-5) M) applied to the apical side produced an increase in apical membrane voltage (Va) from -71 +/- 1 to -89 +/- 9 mV) and a decrease in VT (from -10 +/- 1 to -2 +/- 1 mV). The RT did not change during amiloride exposure. Exposure of the apical membrane to 140 mM K+-depolarized Va from -67 +/- 7 to -39 +/- 11 mV (P less than 0.002) and hyperpolarized VT from -7 +/- 2 to -15 +/- 3 mV (P less than 0.005). Exposure to high K+ from the basolateral side depolarized Vb from -76 +/- 11 to -43 +/- 10 mV (P less than 0.001) and depolarized VT from -9 +/- to 8 +/- 5 mV (P less than 0.001). This preparation is suitable to study basic aspects of epithelial transport by electrophysiological methods and other techniques. The findings are consistent with several of the known properties of cortical collecting tubules from rabbits studied by the isolated perfused tubule technique.
...
PMID:Electrophysiological studies of primary cultures of rabbit distal tubule cells. 303 77

<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>