Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the tubular action of endothelin in rat nephron segments. The effects of endothelin on arginine vasopressin (AVP)-, parathyroid hormone-, glucagon-, calcitonin-, and isoproterenol-dependent cAMP accumulation were studied. The following nephron segments were microdissected: glomerulus (Gl), proximal convoluted tubule (PCT), cortical and medullary thick ascending limbs of Henle's loop (cTAL and mTAL, respectively), cortical collecting duct (CCD), outer medullary collecting duct (OMCD), and inner medullary collecting duct (IMCD). Endothelin dose dependently (10(-8)-10(-10)M) inhibited AVP-dependent cAMP accumulation in CCD, OMCD, and IMCD. This effect was independent of the presence or absence of phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, Ca channel blocker nicardipine, or indomethacin, but was abolished in the presence of protein kinase C inhibitor H-7. Protein kinase C stimulator dioctanoyl glycerol mimicked the effect of endothelin. On the other hand, endothelin had no inhibitory effect on AVP-dependent cAMP accumulation in cTAL or mTAL, parathyroid hormone-dependent cAMP accumulation in Gl and PCT, or glucagon-, calcitonin-, and isoprotereol-dependent cAMP accumulation in OMCD. We conclude that endothelin specifically inhibits AVP-dependent cAMP accumulation in CCD, OMCD, and IMCD through activating protein kinase C. This effect possibly has a role in maintaining urine volume to counteract the decrease in GFR caused by endothelin itself.
 ...
PMID:Effects of endothelin on peptide-dependent cyclic adenosine monophosphate accumulation along the nephron segments of the rat. 169 79

The effects of glucagon on water and electrolyte transport in the kidney were investigated on hormone-deprived rats, i.e. thyroparathyroidectomized diabetes insipidus Brattleboro rats infused with somatostatin. Glucagon consistently inhibited the reabsorption of water and Na+, Cl-, K+ and Ca2+ along the proximal tubule accessible to micropuncture, leaving the reabsorption of inorganic phosphate (Pi) untouched. In the loop, besides its previously described stimulatory effects on Na+, Cl-, K+, Ca2+ and Mg2+ reabsorption, glucagon strongly inhibited Pi reabsorption, very probably in the proximal straight tubule. These effects resulted in a significant phosphaturia and considerable reductions of Mg2+ and Ca2+ excretions. The effects of glucagon at both the whole kidney and the nephron levels are very similar to those previously described for calcitonin. In the absence of an adenylate cyclase system sensitive to glucagon and calcitonin in the rat proximal tubule, and from the analogy of their physiological effects with those elicited by parathyroid hormone, it is suggested that glucagon and calcitonin exert their inhibitory effects on Na and Pi reabsorption in the proximal tubule through another pathway, which could be the phosphoinositide regulatory cascade.
 ...
PMID:Glucagon inhibits water and NaCl transports in the proximal convoluted tubule of the rat kidney. 177 68

Eleven hemodialyzed patients with uremia were examined for the effect of erythropoietin (EP) treatment carried out for 3 months on functions of different endocrine organs. EP treatment resulted in a decrease of the initial plasma levels of somatotropin, prolactin, follicle-stimulating and luteinizing hormones. EP treatment being over, there was a decrease in the plasma content of ACTH, cortisol and aldosterone. The treatment with EP was also associated with an insignificant rise of the plasma levels of parathyroid hormone and testosterone. EP treatment did not influence the plasma concentration of calcitonin and 25-OH-D. EP was found to exert no significant effect on the pituitary-thyroid reverse relationship. The 3-month treatment with EP eventuated in plasma renin activity inhibition as well as in an increase of the atrial level of natriuretic peptide in the plasma. EP treatment stimulated insulin secretion and reduced glucagon secretion. Finally, EP decreased the gastrin level and to a less degree the plasma level of pancreatic polypeptide.
 ...
PMID:[The effect of erythropoietin treatment on endocrine organ function in patients with terminal-stage kidney failure on hemodialysis]. 194 56

Pseudohypoparathyroidism is a complex disorder of renal resistance to parathyroid hormone the mechanism of which is unclear. It is often associated with skeletal abnormalities and there may also be other hormonal defects. This is an extensive endocrinological investigation of five of six affected members in two generations of one family. The phenotypic variability of the syndrome is explored: four members had hypothyroidism; two had abnormal gonadal function; all five had abnormal prolactin response to TRH; one had abnormal hepatic response to glucagon infusion. All had normal hypothalamic-pituitary-adrenal axes, renal responsiveness to vasopressin and growth hormone responses to a variety of stimuli. Special note is made of oral pathology, and evidence of platelet aggregation abnormalities is presented which has not previously been described in the syndrome.
 ...
PMID:Pseudohypoparathyroidism: its phenotypic variability and associated disorders in a large family. 204 19

Several hormones stimulate the adenylate cyclase system of the thick ascending limb (TAL). There are, however, some species differences concerning the cyclase sensitivity and the hormonal response in this nephron segment. In the mouse, antidiuretic hormone (ADH), parathyroid hormone, glucagon, calcitonin, and isoproterenol stimulate Na+, Cl-, Mg2+, and Ca2+ transports in the cortical TAL, whereas ADH, glucagon, and isoproterenol stimulate NaCl transport only in the medullary TAL. Many of these effects are different from those previously described for the corresponding segments of the rabbit nephron. The close similarity of the cyclase responsiveness to hormones of the mouse and rat TALs makes it possible to interpret the micropuncture data obtained in vivo in the rat superficial (S) and juxtamedullary (JM) nephrons, in the light of the in vitro data obtained in the mouse. Long-term treatment of Brattleboro rats with ADH also elicits differential effects along the TAL. Their consequences on the function of the S and JM nephrons are also examined. There are several indications supporting the view that the newly described hormonal effects in the mouse and rat are of physiological relevance.
 ...
PMID:Consequences of differential effects of ADH and other peptide hormones on thick ascending limb of mammalian kidney. 205 31

1. A direct action of vasoactive intestinal peptide (VIP) upon human kidney was sought by measurement of renal adenylate cyclase in tissue homogenates and plasma membranes isolated from tissue samples excised for therapeutic reasons. 2. VIP (1 microM) produced a mean stimulation of adenylate cyclase activity of 3.5-fold compared to basal values in cortical plasma membranes; comparative stimulations of 2.8-fold and 27.3-fold were obtained with 1 microM-glucagon and 1 microM-h(1-34) parathyroid hormone respectively. 3. Half-maximal stimulation of human renal cortical plasma membrane adenylate cyclase was observed with a mean value of 35 nM-VIP. 4. The stimulation of renal adenylate cyclase by VIP appeared to be specific because stimulation by glucagon was additive to that obtained with VIP, and the VIP receptor antagonist (4 Cl-D-Phe6, Leu17)-VIP inhibited the VIP-dependent stimulation of adenylate cyclase activity.
 ...
PMID:Vasoactive intestinal peptide stimulation of human renal adenylate cyclase in vitro. 216 66

The effect of antidiuretic hormone (arginine vasopressin, AVP, 10(-10) mol.l-1), parathyroid hormone (PTH, 10(-8) mol.l-1) and glucagon (10(-8) mol.l-1) on the transepithelial potential difference (PDte) and the transepithelial resistance (Rte) were tested in in vitro perfused cortical (cTAL) and medullary (mTAL) thick ascending limbs of Henle's loop of the mouse nephron. When compared with mTAL segments (PDte: 8.5 +/- 0.4 mV, n = 16), cTAL segments displayed a high PDte of 15.7 +/- 0.9 mV (n = 11) at the beginning of perfusion experiments which reached a value of 9.4 +/- 0.6 mV (n = 11) after 38 +/- 4 min perfusion. Simultaneously Rte increased significantly from 24 +/- 3 to 28 +/- 1 omega cm2 (n = 11). When PTH, AVP or glucagon were added to the bath solution, PDte increased with PTH from 10.3 +/- 0.8 to 15.2 +/- 0.8 mV (n = 13), with AVP from 10.2 +/- 0.5 to 15.0 +/- 0.7 mV (n = 24) and with glucagon from 11.3 +/- 1.9 to 15.3 +/- 2.1 mV (n = 8). At the same time Rte decreased from 30 +/- 3 to 23 +/- 2 omega cm2, from 28 +/- 1 to 23 +/- 1 omega cm2 and from 23 +/- 2 to 18 +/- 2 omega cm2, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effects of antidiuretic hormone, parathyroid hormone and glucagon on transepithelial voltage and resistance of the cortical and medullary thick ascending limb of Henle's loop of the mouse nephron. 233 47

The effect of heparin on the renal adenylate cyclase (AC)/cyclic adenosine monophosphate (cAMP) system was studied in vitro in renal cortical membrane preparations and in vivo on hormone-stimulated nephrogenous cAMP excretion. The heparin dose dependently inhibited basal and hormone-stimulated rat renal cortical AC activity. The heparin concentration causing 50% inhibition was 45 micrograms/ml for the basal activity and 33 and 85 micrograms/ml for the parathyroid hormone (PTH) and glucagon-stimulated activities, respectively. PTH- and glucagon-stimulated AC activity was inhibited by the non-antithrombotic heparinoid, N-acetylated N-disulfated heparin, but not by a structural analogue of heparin, dextran sulfate. Forskolin- and Mn2(+)-stimulated AC activity was also inhibited by heparin, while NaF stimulated activity was resistant to it. Increasing Mg2+ concentration did not affect the inhibition of basal and PTH-stimulated AC activity by heparin. The urinary excretion of nephrogenous cAMP was determined in parathyroidectomized rats treated with glucagon (group 1), glucagon and heparin (group 2), heparin alone (group 3) and control (group 4). Glucagon induced a significant increase in nephrogenous cAMP excretion. The urinary excretion of nephrogenous cAMP, however, was significantly lower in group 2 (receiving glucagon and heparin) than in group 1 (receiving glucagon alone). There were no significant changes in nephrogenous cAMP in groups 3 and 4. These results suggest that heparin is a potent inhibitor of renal AC in vivo and in vitro. Taken together, our data point out the catalytic unit of the AC system as the site of heparin interaction.
 ...
PMID:Effect of heparin on cortical adenylate cyclase activity and on urinary excretion of 3',5'-adenosine monophosphate in rat. 248 35

After burn trauma, a very marked endocrine response occurs. Almost all the known hormones take part in it. Their response influences very much the postburn metabolic changes and participates in the integration of the body's response with the nervous and immune systems. In this review, mainly the changes in various hormone levels are described, as well as the possible role of the acute phase response after burn trauma, and the communications between the endocrine and immune systems, the cells of the latter are able to respond to various hormonal stimuli and to secrete various hormones themselves. Some of the hormones are very sensitive indicators of the burn stress, e.g., the T3 levels (very low), testosterone in males (very low), dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) (very low), ADH, catecholamines, renin and angiotensin II, cortisol (high), 17-beta-estradiol in males (usually elevated). Other hormones are usually elevated, but not always (ACTH, aldosterone, prolactin, glucagon, immunoreactive insulin, beta-endorphin, rT3, 11-beta-hydroxyandrostenedione), but there are hormones that are unually low (T4, FSH, androstenedione, progesterone--the latter especially in females). Calcitonin, parathyroid hormone, growth hormone are sometimes elevated, as well as LH (measured with RIA methods). TSH is usually normal, the biologically measured LH was reported to be low. The levels of the sensitive indicators of burn stress may be used to evaluate the effect of treatment: if the burn patient is properly treated, the indicators may become earlier normal.
 ...
PMID:Endocrine changes after burn trauma--a review. 251 73

We have examined the regulation by prostaglandin E2 (PGE2) of hormone-induced adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in cells isolated by immunodissection from both the medullary and cortical thick ascending limb of Henle's loop of rabbit kidney. At concentrations greater than 10(-8) M, PGE2, but not sulprostone (16-phenoxy-17,18,19,20-tetranor-PGE2 methylsulfonilamide), caused cAMP accumulation in both cortical and medullary thick limb cells. However, at concentrations of less than or equal to 10(-8) M, both PGE2 and sulprostone inhibited arginine vasopressin (AVP)-, calcitonin-, and glucagon-induced cAMP accumulation in medullary thick ascending limb (mTAL) cells. In cortical thick limb (cTAL) cells, sulprostone also inhibited AVP-, calcitonin-, and parathyroid hormone (PTH)-induced cAMP accumulation. The inhibitory effects of PGE2 and of sulprostone were blocked by pretreatment of mTAL and cTAL cells with pertussis toxin. Membranes prepared from mTAL cells exhibited a [3H]PGE2 binding activity that was stimulated on addition of the stable guanosine 5'-triphosphate (GTP) analogue, 5'-guanosine gamma-thiotriphosphate (GTP gamma S); moreover, sulprostone inhibited [3H]PGE2 binding. Our results suggest that PGE2 can function via a prostaglandin E receptor linked to a guanine nucleotide regulatory protein, Gi, to attenuate hormone-induced cAMP formation in both mTAL and cTAL cells of rabbit kidney.
 ...
PMID:Regulation of cAMP metabolism by PGE2 in cortical and medullary thick ascending limb of Henle's loop. 253 67


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