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

---

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

Insulin-induced hypoglycemia causes an increase in plasma vasopressin (AVP) in healthy subjects but the response in diabetics is not established. We investigated the effect of insulin-induced hypoglycemia on ten insulin-dependent diabetics with asymptomatic hypoglycemia, and compared the results with those for seven healthy subjects. The lack of adrenergic symptoms of hypoglycemia in insulin dependent diabetics being attributed to a diminished beta-adrenergic sensitivity, the effect of isoprenaline infusion was investigated as control. Insulin-induced hypoglycemia resulted in both populations in significant increase (P less than 0.01) in AVP in addition to significant increases in heart rate, plasma epinephrine (E), norepenephrine (NE) and cortisol (COR). Effective osmolality and mean arterial blood pressure did not vary. Diabetics showed smaller increase in AVP (P less than 0.01) and heart rate (P less than 0.05) than controls. Maximal E, NE and COR values did not differ between the two populations. Isoprenaline infusion resulted in increase in heart rate and plasma renin activity, but AVP and COR did not vary in the two populations. In conclusion, insulin-induced hypoglycemia released AVP in diabetics with asymptomatic hypoglycemia, but the response was weaker than in healthy subjects. A causal hypothalamic alteration of beta-adrenergic or glycopenia sensitivity is discussed.
...
PMID:Arginine vasopressin response to insulin-induced hypoglycemia in insulin-dependent diabetics with asymptomatic hypoglycemia. 219 Sep 3

This study examined the possible existence and nature of Ca2+ transport in frog skin using 45Ca fluxes and short-circuiting technique. Following the addition to full-thickness frog skin (FTFS) of 8-[p-chlorophenylthio]cAMP (8-CPT-cAMP), forskolin, or 1-methyl-3-isobutylxanthine, the secretory Ca2+ flux increased severalfold, inducing net Ca2+ secretion. The absorptive flux was unchanged. Isoproterenol (10(-6)M) reproduced the effects of cAMP on Ca2+ secretion (-3.76 +/- 0.80 nmol X cm-2 X h-1 vs. +0.04 +/- 0.05 in control) while vasopressin and parathyroid hormone did not alter Ca2+ fluxes. Because FTFS contains subepidermal glands capable of Cl- secretion in response to beta-adrenergic stimulation, split-thickness frog skin (STFS) consisting of the gland-free Na-absorbing surface epithelium was used to localize the anatomic site of Ca2+ secretion. In STFS, addition of 8-CPT-cAMP or isoproterenol failed to induce Ca2+ secretion, suggesting that this transport in FTFS is localized in skin glands. Additional studies explored the relationship between Ca2+ and Cl- transport in FTFS. Furosemide prevented the stimulation of both Ca2+ and Cl- secretion. Removal of Cl- from the bathing medium abolished Ca2+ secretion. Thus, FTFS exhibits a beta-adrenergic, cAMP-stimulated net Ca2+ secretion that is Cl- dependent. As this effect is not observed in STFS, the pathway of Ca2+ secretion in frog skin is probably localized in the subepidermal glandular epithelium in association with Cl- secretion. Frog skin glands may represent a useful model for the study of Ca2+ transport in Cl--transporting epithelia.
...
PMID:cAMP- and beta-adrenergic-stimulated chloride-dependent Ca2+ secretion in frog skin. 241 6

Agents known to elevate intracellular cyclic AMP (cAMP) in cultured mesangial cells (e.g., isoproterenol with and without isobutylmethylxanthine (MIX] inhibit vasopressin-induced contraction. Since contraction of these cells in response to vasopressin is accompanied by release of inositol trisphosphate and increased intracellular ionized calcium, we wanted to determine whether cAMP is exerting its relaxing effect by altering phosphoinositide metabolism. Isoproterenol and MIX did not diminish the release of inositol trisphosphate in response to vasopressin. However, the stimulated 32P incorporation into phospholipids seen with vasopressin treatment was diminished by prior treatment with isoproterenol-MIX. Since incorporation of 32P into phospholipids is not only dependent on phospholipid synthesis but also on the amount of label in the gamma-phosphate of ATP, we determined the specific activity of 32P in ATP. We found that suppression of 32P incorporation into phospholipids in cells treated with isoproterenol-MIX was paralleled by a decline of specific activity of 32P in ATP. Furthermore, the changes in ATP specific activity were paralleled by similar changes in phosphate uptake into the cells. Thus, diminished phosphate uptake (transport) could account for the decline of 32P content in phospholipids and ATP following treatment of mesangial cells with isoproterenol-MIX.
...
PMID:Elevation of cAMP in cultured mesangial cells diminishes vasopressin-stimulated increases of phosphate uptake and 32P-specific activity in ATP but has no effect on phosphoinositide metabolism. 243 83

We have previously reported that cultured monolayers of folliculo-stellate cells (FC) of adenohypophysial pars tuberalis (PT) and pars distalis (PD) origin express morphological and electrical properties typical of ion and fluid transporting epithelia. The objective of the present study was to examine whether cells expressing similar transport properties exist also in the pars intermedia (PI), an area of the adenohypophysis very poorly vascularized, where a cell type expressing such functions would be expected to play an especially significant role in the local regulation of the interstitial fluid content and circulation. Enzymatically and mechanically dispersed bovine pars intermedia fragments yield monolayers of polygonal, contact inhibited cells which rapidly develop domes. Such cells exhibit morphological features and growth properties very similar or identical to those expressed by cells previously identified af FC cells in PD and PT cultures. Similarly to their counterparts in the PD and PT, the PI FC display a potential difference and a resistance when mounted in Ussing chambers. Isoproterenol, prostaglandin E2, bradykinin and lysine vasopressin are able to stimulate active ion transport across FC monolayers. These data indicate that the PI contains ion transporting FC and suggest important local regulatory functions for these cells.
...
PMID:Regulation of ion transport in hypophysial pars intermedia follicular cell monolayers. 246 71

Isoprenaline, a beta adrenergic agonist, strongly increases both transepithelial fluxes across the urinary bladder of Bufo bufo; this effect is dose dependent, 10(-6)M being necessary for the maximal action. This effect is less selective than that of vasopressin: the ratio J urea/J thiourea is 3.8 under isoprenaline and 30.4 under vasopressin treatment. Both hormones differently affect the permeability of a mainly liposoluble molecule, i.e. antipyrine: vasopressin increases antipyrine permeability, while isoprenaline decreases it. Moreover diethylpyrocarbonate treatment of the luminal membrane strongly inhibits vasopressin effect on urea permeability leaving unmodified that of isoprenaline. However, the actions of both hormones are not additive. These results allows to assume that the tissue has a feedback mechanism which inhibits other hormonal action while the bladder is stimulated by a particular hormone.
...
PMID:Permeability properties of the Bufo bufo bladder as affected by isoprenaline and vasopressin. 248 13

Tritiated phosphatidyl choline (1-palmitoyl,2-[3H]palmitoyl or 1-stearoyl,2-[3H]arachidonyl) is taken up unchanged by the isolated perfused rabbit heart. Isoproterenol, vasopressin or A23187 enhanced the output of tritium in these hearts, whereas bradykinin, angiotensin II or acetylcholine had no effect. These data demonstrate that [3H]phosphatidyl choline is incorporated directly into a phospholipid pool that is accessible to some, but not all, hormonally stimulated lipases. In hearts labeled with 1-stearoyl,2-[3H]arachidonyl phosphatidyl choline, the radioactivity released by isoproterenol consisted of free fatty acid and lysophosphatidyl choline, indicating that isoproterenol stimulates both phospholipase(s) A1 and A2. Vasopressin and A23187 increased the release of free fatty acid, but not lysophosphatidyl choline, suggesting that these agents stimulate only phospholipase A2.
...
PMID:Uptake and hormonally induced hydrolysis of [3H]phosphatidyl choline in the isolated rabbit heart. 249 94

In rat adipocytes, the breakdown of phosphoinositides labelled by a 3 h incubation with [3H]inositol resulted in the accumulation of labelled inositol mono-, bis- and trisphosphates in the presence of oxytocin, vasotocin or vasopressin. Oxytocin at a concentration of 1 nM markedly increased phosphoinositide breakdown. Incubation of adipocytes both during the 3 h labelling and the 10 min breakdown period in a low adenosine medium (presence of adenosine deaminase) or high adenosine medium (presence of 0.1 microM N6-(phenylisopropyl)adenosine) (PIA) did not affect basal or ligand-stimulated phosphoinositide breakdown. The addition of 1 microM PIA only during the measurement of phosphoinositide breakdown variably stimulated basal breakdown but significantly potentiated that due to oxytocin. Isoproterenol similarly had little effect on basal but inhibited oxytocin stimulation of phosphoinositide breakdown. Insulin did not affect basal or ligand-stimulated phosphoinositide breakdown in the low or high adenosine medium. However, in adipocytes incubated in the absence of added adenosine deaminase or PIA, insulin stimulated basal accumulation of inositol phosphates by about 20% and inhibited that due to oxytocin by about 20%. There was no significant effect of insulin on the stimulation by vasopressin or vasotocin of phosphoinositide breakdown. These results indicate that, in adipocytes, phosphoinositide breakdown stimulated by oxytocin is enhanced by adenosine, inhibited by isoproterenol and, under some conditions is inhibited by insulin.
...
PMID:Regulation of oxytocin-induced phosphoinositide breakdown in adipocytes by adenosine, isoproterenol and insulin. 255 83

The response of lymph vessels, arterioles and venules in the exteriorized rat mesentery to endothelin-1, vasopressin and norepinephrine was examined with the aid of high-resolution television microscopy. On a molar basis, endothelin-1 was more potent than vasopressin to contract the three types of vessels. Norepinephrine, which could constrict blood microvessels, did not act on lymph vessels. Acetylcholine, sodium-nitroprusside and isoproterenol were ineffective to block the constrictive responses of lymph vessels to endothelin-1 and vasopressin. At the same concentrations, however, acetylcholine and sodium-nitroprusside antagonized the responses of arterioles and venules to endothelin-1 and norepinephrine, whereas the responses of blood microvessels to vasopressin remained unaffected. Isoproterenol, at doses capable of blocking the response of the arterioles and venules to norepinephrine, did not interfere with the constriction induced by endothelin-1 and vasopressin on these vessels. It is suggested that endothelin-1 might play a role in the regulation of lymphatic contractility apart from its vasoconstrictor activity on blood vessels.
...
PMID:Endothelin-1 induces potent constriction of lymphatic vessels in situ. 269 20

Observations in vivo suggest that catecholamines modulate reabsorptive functions of proximal tubules by acting on beta-adrenoceptors. However, beta-catecholamine binding sites or beta-adrenoceptor-sensitive adenylate cyclase (AdC) has not been found in segments of proximal tubules of rat, rabbit, or mouse kidney. In the present study, we investigated the responsiveness of AdC to catecholamines, [8-Arg]vasopressin (AVP), and to parathyroid hormone (PTH) in proximal convoluted tubules (PCT), proximal straight tubules (PST), and in late distal convoluted tubules (LDCT) microdissected from canine kidney. Isoproterenol (ISO) caused a marked and dose-dependent stimulation of AdC in PST (maximum: delta + 850%; half maximum stimulation at 10(-7) M ISO), but ISO had no effect on AdC in PCT. The AdC in both PCT and PST was markedly stimulated by PTH; AVP stimulated the AdC in LDCT but not in PST or in PCT. The stimulatory effect of 10(-5) M ISO in PST (delta + 725%) was significantly greater than in LDCT (delta + 307%); norepinephrine and epinephrine had stimulatory effects in PST similar to ISO. The stimulation of AdC in PST by ISO was blocked by propranolol and by beta 2-blocker ICI-118551. On the other hand, alpha-blocker phentolamine and beta 1-blocker metoprolol did not abolish the stimulation of AdC in PST by ISO. The accumulation of cAMP in intact PCT and PST incubated in vitro was stimulated by PTH both in PST and in PCT, but ISO elevated cAMP (delta + 683%) only in PST. Our results show that proximal tubules of canine nephron, PST but not PCT, contain beta-adrenoceptors of beta 2 subtype coupled to AdC. These observations provide direct evidence that the effects of catecholamines, either released from renal nerve endings or arriving from blood supply, can act directly on beta 2-adrenoceptors located in proximal tubules, and also suggest that at least some of the catecholamine effects in proximal tubules are mediated via cAMP generation.
...
PMID:Evidence for beta adrenoceptors in proximal tubules. Isoproterenol-sensitive adenylate cyclase in pars recta of canine nephron. 299 60

Thirst mechanisms in Brattleboro rats are activated because of a deficiency in circulating vasopressin. Plasma osmolality, renin, and angiotensin II (ANG II) are increased. We measured the responsiveness of Brattleboro rats and appropriate control strains to cellular and extracellular thirst stimuli taking the spontaneous base-line water intake into account. Brattleboro rats drank more in response to intraperitoneal hypertonic NaCl than controls, but when their fluid losses were prevented by nephrectomy they did not overdrink. Despite low urinary concentration, Brattleboro rats excreted the sodium load at least as rapidly as the controls. Brattleboro rats drank after intracranial injection of renin, renin substrate, and ANG I and II. The dose-response curves were similar to controls, although the Nottingham Long-Evans control strain drank significantly less in response to some doses of the peptides. Intracranial captopril inhibited renin- and ANG I-induced but not ANG II-induced drinking. Isoproterenol reduced spontaneous drinking of Brattleboro rats but increased drinking in controls. However, when urinary losses were prevented by ureteric ligation, isoproterenol caused markedly greater water intake in Brattleboro rats than in controls. Subcutaneous captopril in moderate, thirst-enhancing doses also caused a larger increase in water intake in Brattleboro rats than in controls. Therefore the renin-angiotensin system of Brattleboro rats is more responsive to renin-dependent thirst challenges than that of normal controls.
...
PMID:Thirst in Brattleboro rats. 304 45


<< Previous 1 2 3 4 5 Next >>

---