Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

alpha 2-Adrenoceptor subtype expression was investigated in cultured rat inner medullary collecting duct (IMCD) cells using radioligand binding studies, Northern blot analysis, and adenosine 3',5'-cyclic monophosphate (cAMP) assays. [3H]rauwolscine bound to a single class of alpha 2-adrenoceptors with high affinity [Kd = 1.7 +/- 0.3 nM, maximum binding (Bmax) = 45.2 +/- 10.8 fmol/mg protein]. alpha 2-Adrenoceptor ligands inhibited [3H]rauwolscine binding with a rank order of potency characteristic of interaction with the alpha 2B-adrenoceptor [inhibitory constant (Ki) values (in nM) rauwolscine (1.95) greater than ARC-239 (8.52) greater than prazosin (237) greater than oxymetazoline (30,000)]. Northern blot analysis was performed using poly(A)+ RNA isolated from 90% confluent rat IMCD cells and probes derived from alpha 2-adrenoceptor DNA sequences from the rat nonglycosylated alpha 2B-adrenoceptor and the human alpha 2A-adrenoceptor. The alpha 2B probe hybridized to a 4.2-kb band under high stringency conditions, but the alpha 2A-adrenoceptor probe did not hybridize to this band. In functional studies, the full alpha 2-adrenoceptor agonists epinephrine and UK-14,304 potently inhibited vasopressin-stimulated cAMP accumulation by 50 to 70% [half-maximal response (EC50) (in nM) epinephrine = 11.2, UK-14,304 = 6.4]. Guanabenz and clonidine were partial agonists, inhibiting cAMP accumulation by 30 to 40% and were less potent than the full agonists [EC50 (in nM) 56.0 guanabenz and 94.5 clonidine]. Epinephrine-induced inhibition of cAMP accumulation was blocked by rauwolscine, prazosin, and ARC-239 but not by the alpha 1-adrenoceptor antagonist corynanthine. We conclude that rat IMCD cells in primary culture express functional alpha 2-adrenoceptors of the alpha 2B-subtype.
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PMID:Characterization of prazosin-sensitive alpha 2 B-adrenoceptors expressed by cultured rat IMCD cells. 171 24

The effects of 3 alpha 2-adrenergic receptor agonists on renal function in vasopressin (AVP)-deficient Brattleboro (DI) rats were evaluated. The aim of this study was to determine the relative contribution of central versus peripheral alpha 2-adrenoceptors in mediating diuresis and natriuresis, as well as the role of alpha 2-adrenoceptors in antagonizing the actions of AVP. In addition to the studies of renal function, the effects of AVP deficiency on renal alpha 2-adrenoceptor affinity and number was evalauted along with determination of peripheral catecholamine stores. The centrally acting alpha 2-adrenergic agonists guanabenz and guanfacine significantly increased urine output and sodium excretion in Long-Evans (LE) rats. Guanabenz and guanfacine increased urine output in DI rats but failed to increase sodium excretion. The polar alpha 2-adrenergic agonist, ST-91, increased sodium excretion in both LE and DI rats, however, at a dose of 1.0 mg/kg urine output was significantly decreased in DI rats. The 3 alpha 2-adrenergic agonists increased potassium excretion in LE rats, but at the 1.0-mg/kg dose of guanabenz and ST-91, potassium excretion was significantly inhibited in DI rats. Renal alpha 2-adrenergic receptors and norepinephrine stores were not altered in DI rats. Adrenal NE stores were significantly elevated in DI rats relative to LE rats. The results of this study suggest that in the absence of AVP, centrally acting alpha 2-adrenergic agonists have limited natriuretic action, although peripheral activation of alpha 2-adrenoceptors is sufficient to elicit natriuresis irrespective of the presence of AVP. The chronic deficiency of AVP does not alter renal alpha 2-adrenergic receptor number, but the natriuretic and kaliuretic actions of alpha 2-adrenergic agonists are altered in DI rats.
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PMID:Central and peripheral actions of alpha 2-adrenergic agonists on renal function in Long-Evans and Brattleboro rats. 257 60

Marked differences in the characteristics of alpha-2 adrenoceptors in the kidney of various species have been reported. In addition, there are functional differences in alpha-2 adrenoceptors in various nephron segments of the same species. In this study we have characterized alpha-2 adrenoceptors in the medullary thick ascending limb (MTAL) isolated from the rabbit kidney. The equilibrium binding of [3H]rauwolscine to MTAL homogenates was measured after incubation for 45 min at 25 degrees C in the absence and presence of 10 microM phentolamine. The specific binding of [3H]rauwolscine was saturable with a Kd of 2.6 +/- 0.1 nM and maximal binding of 234 +/- 18 fmol/mg of protein. Adrenergic drugs competed with MTAL-bound [3H]rauwolscine with the following order of potency: 1) antagonists: rauwolscine = yohimbine > phentolamine >> prazosin = propranolol; and 2) agonists: oxymetazoline > clonidine > epinephrine > BHT 933 (azepexole) > alpha-methylnorepinephrine. Our results indicate that specific alpha-2 adrenoceptors are present in the rabbit MTAL. The high (> 1600) ratio of Ki of prazosin: oxymetazoline suggests that the alpha-2 adrenoceptors in the rabbit MTAL belong to an alpha-2A subtype. Guanabenz, iodoclonidine and epinephrine at high concentrations decreased forskolin- and vasopressin-stimulated cyclic AMP formation in the rabbit MTAL. These results suggest that alpha-2 adrenoceptors are negatively coupled to adenylate cyclase system in the MTAL.
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PMID:Alpha-2 adrenoceptors in medullary thick ascending limbs of the rabbit kidney. 839 54