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)

Synthesis of prostaglandins (PGs) was characterized in the lateral wall (LW) of guinea-pig cochlea. Basal synthesis at 37 degrees C was about 480 pg/LW (12.8 ng X mg-1 protein) for PGI2 and 85 pg/LW (2.3 ng X mg-1 protein) for PGE2, levelling out after 10 min of incubation. Incubation with arachidonic acid (10(-5) M) increased PGI2 and PGE2 synthesis by 44% and 1020%, respectively, showing that arachidonic acid availability is a synthesis-limiting factor. The stimulating effect of the Ca++ ionophore A23187 (5 X 10(-6) M) on PG synthesis was weak (about +50%) but was enhanced (about +140%) by preincubation with arachidonic acid. Angiotensin II (10(-6) M), vasopressin (5 X 10(-7) M), and furosemide (10(-8) to 10(-3) M) did not alter PG secretion. Neither aspirin nor indomethacin prevented the development of furosemide ototoxicity (endocochlear potential) in the rat. Perfusion with PGI2 influenced the furosemide effect in some instances.
 ...
PMID:Strial prostaglandins and leukotrienes. Biochemical characteristics and interrelationship with furosemide. 311 70

The effects of vasopressin, angiotensin II, and calcium ionophore A23187 were examined and compared on endogenous prostaglandin E2 (PGE2) production, in the absence of exogenous arachidonate, by glomeruli and cortical and medullary collecting tubules freshly prepared from rat kidney. Angiotensin II stimulated PGE2 production in the glomeruli but not in the collecting tubules. Vasopressin at concentrations which stimulate cAMP production in collecting tubules failed to stimulate PGE2 production in both glomeruli and collecting tubules. Significant stimulation of PGE2 production occurred in response to calcium ionophore A23187 in both glomeruli and collecting tubules. These results showed that vasopressin failed to stimulate PGE2 production from endogenous precursors in both glomeruli and collecting tubules of the rat kidney while angiotensin II stimulates PGE2 production in the glomeruli but not in collecting tubules. In addition, an ability to produce PGE2 may be greater in medullary than in the cortical portions of collecting tubules as judged by the response to calcium ionophore.
 ...
PMID:Prostaglandin E2 production by glomeruli and collecting tubules isolated from rat kidney. 312 55

The production of prostaglandins by rat renal tubular cells and by rat vascular smooth muscle cells (VSMC) in response to vasoactive hormones was examined. A superfusion technique was used to stimulate collagenase-dispersed renal cortical or medullary tubular cells and trypsinized rat aortic smooth muscle cells with vasoactive hormones and ANF. All cell types responded promptly to the stimuli in a dose-dependent manner. Renal tubular cells produced mainly PGE2, less PGF2 alpha and no 6-keto-PGF1 alpha, while VSMC produced exclusively 6-keto-PGF1 alpha. This production of PG was strictly dependent on the presence of extracellular Ca2+ and was not inhibited by antagonists of voltage-dependent Ca2+-channels. Angiotensin II (Ang II) was active on cortical tubular cells and VSMC. Sar1-Ala8-angiotensin II blocked this action. Arginine-vasopressin (AVP acted on medullary tubular cells and VSMC and its effect was inhibited by selective V1-antagonists. The V2-agonist dDAVP had no effect on PG production. A clear distinction between V1-receptor mediated PG release and V2-receptor mediated cAMP extrusion was observed in medullary tubular cells. Bradykinin was a weak agonist on medullary tubular cell. The synthetic (1-24) atrial natriuretic peptide did not prevent 6-keto-PGF1 alpha release induced by Ang II or AVP in VSMC nor the PGE2 release in cortical tubular cells induced by Ang II.
 ...
PMID:The regulation of prostaglandins by vasoactive hormones in renal tubular and vascular smooth muscle cells. 312 55

The ability of angiotensin II to down-regulate its receptor was tested on rat hepatocytes in primary culture for 4 h. Angiotensin II treatment decreased [3H]angiotensin II specific binding in a concentration- and time-dependent manner. The effect was maximum with 1 microM angiotensin II and after 2 h. There was a decrease in the maximum number of binding sites (56% of control) with no significant effect on the apparent dissociation constant. The down-regulation was blocked by the angiotensin II antagonist [Val4,Ile7]angiotensin III and was not induced by other hormones (e.g. vasopressin, norepinephrine, or glucagon) or by 4 beta-phorbol 12 beta-myristate 13 alpha-acetate or A23187 ionophore. The decrease in angiotensin II receptors resulted in correlated decreases in the potency of angiotensin II to activate phosphorylase or lower glucagon-induced cAMP accumulation. However, high concentrations of the agonist were still able to elicit maximal responses in both parameters. Down-regulation of the receptor was not dependent upon active Gi, since it was still observed after ADP-ribosylation and inactivation of Gi by pertussis toxin. The above results indicate that the down-regulation of the hepatic angiotensin II receptor induced by its agonist is homologous and does not involve Gi, Ca2+, or protein kinase C. The correlation of receptor loss with decreases in the potency of angiotensin to activate phosphorylase and inhibit glucagon-induced cAMP accumulation is consistent with the idea that a single receptor population regulates two different messengers, i.e. calcium and cAMP.
 ...
PMID:Agonist-induced down-regulation of the angiotensin II receptor in primary cultures of rat hepatocytes. 313 62

Previous studies have suggested that the inhibition of renin secretion by acute administration of vasopressin in conscious dogs results from a reflex reduction in renal nerve activity. In the present investigation, this hypothesis was tested by studying the effect of total baroreceptor denervation or selective low pressure baroreceptor denervation on the suppression of PRA by vasopressin in conscious, chronically prepared dogs. In eight sham-operated dogs, a 45-min infusion of vasopressin (2.0 ng/kg.min, iv) decreased PRA from 10.5 +/- 1.9 to 5.9 +/- 1.0 ng/ml.3 h (P less than 0.01). Mean arterial pressure did not change (110 +/- 10 to 107 +/- 7 mm Hg), but heart rate decreased from 84 +/- 9 to 69 +/- 8 beats/min (P less than 0.05). In contrast, vasopressin infusion failed to significantly decrease PRA in seven sinoaortic/cardiac denervated dogs (9.5 +/- 1.7 to 7.4 +/- 2.0 ng/ml.3 h), although decreases did occur in three of the dogs. Mean arterial pressure increased from 104 +/- 5 to 125 +/- 6 mm Hg (P less than 0.01), but heart rate did not change (112 +/- 4 to 107 +/- 5 beats/min). When renal perfusion pressure was maintained at the preinfusion level in three sinoaortic/cardiac denervated dogs, vasopressin infusion failed to decrease PRA (2.3 +/- 0.6 to 2.4 +/- 0.6 ng/ml.3 h). In six cardiac denervated dogs, vasopressin infusion decreased PRA from 5.3 to 0.9 to 3.1 +/- 0.7 ng/ml.3 h (P less than 0.01). Results obtained with two lower doses of vasopressin (0.5 and 1.0 ng/kg.min) were generally similar to the responses observed during infusion at 2.0 ng/kg.min. Angiotensin II (5.0 ng/kg.min) suppressed PRA in all groups of dogs. These experiments demonstrate that the inhibition of renin secretion by acute administration of vasopressin in conscious dogs is prevented by total baroreceptor denervation, but not by denervation of the low pressure baroreceptors alone. These results suggest that the suppression of renin release by vasopressin is a reflex response resulting from activation of the high pressure baroreceptors.
 ...
PMID:Effect of baroreceptor denervation on the inhibition of renin release by vasopressin. 328 94

To determine the cardiac and peripheral circulatory responses to changes in afterload with angiotension and vasopressin, we increased mean aortic pressure 25% and 50% above control in splenectomized and ganglion-blocked dogs. We compared these responses to similar mechanical increases in aortic pressure produced by partial balloon occlusion of the descending aorta. With 25% or 50% increases in aortic pressure, angiotensin, vasopressin, and balloon inflation produced no changes in heart rate, right atrial, and mean pulmonary artery pressures. At 25% increase in aortic pressure, cardiac output was maintained with angiotensin and balloon occlusion but decreased with vasopressin. At 50% increase in aortic pressure, cardiac output was maintained with only balloon occlusion and decreased with both angiotensin and vasopressin. Whenever cardiac output fell, central blood volume did not increase as after-load increased. These changes in preload can be explained by alterations in the venous circulation. Vasopressin did not alter venous compliance or unstressed vascular volume but increased resistance to venous return. Angiotensin also increased resistance to venous return but decreased venous compliance and did not change unstressed vascular volume. Balloon occlusion had no effects on these parameters. We conclude that: (a) angiotensin caused significant venoconstriction resulting in maintenance of cardiac output at 25% but not 50% increase in aortic pressure; (b) vasopressin increased the resistance to venous return without venoconstriction; this resulted in a fall in cardiac output even with a 25% increase in aortic pressure; and (c) the effects of the agents on the venous circulation were independent of the mechanical effects of a pressure increase in the arterial circulation.
 ...
PMID:Cardiac and peripheral circulatory responses to angiotension and vasopressin in dogs. 340 12

To determine whether angiotensin II (A II) can modify baroreflex centrally and contribute to the central resetting of baroreflex in spontaneously hypertensive rats (SHRs), the aortic depressor nerve (ADN) was electrically stimulated following intracerebroventricular (ICV) administration of A II and/or A II analog in urethane-anesthetized normotensive Wistar rats (WKYs) and SHRs. Electric stimulation of the ADN elicited frequency-dependent depressor, bradycardic, and sympatho-inhibitory responses. Angiotensin II, administered ICV, dose-dependently attenuated these responses induced by ADN stimulation in normotensive rats. We found, however, these attenuations could be abolished by ICV pretreatment with A II analog. Vasopressin (ICV) did not change any responses to ADN stimulation. The vasopressor and sympatho-inhibitory responses to ADN stimulation were significantly less in SHRs when compared with those in WKYs: In SHRs, A II analog completely cancelled the A II-attenuated responses to ADN stimulation. These findings suggest that A II can centrally attenuate baroreflex, which might be independent from vasopressin, and in the brain A II can contribute to the central resetting of baroreflex in SHRs.
 ...
PMID:Central attenuation of baroreflex by angiotensin II in normotensive and spontaneously hypertensive rats. 341 91

Previous investigators have shown that hypotension will cause an increase in plasma levels of both vasopressin and angiotensin II. Significant increases in peripheral resistance after thermal trauma suggested that a similar increase in plasma vasopressin and angiotensin II levels might occur under this condition. This possibility has been studied in the pentobarbital anesthetized dog. Peripheral resistance was calculated from measured cardiac output and mean arterial blood pressure. Vasopressin and angiotensin II levels were measured by radio-immunoassay. The results of this study showed that vasopressin plasma levels increase 4 to 6 fold 15 minutes after thermal trauma and remained elevated (3 to 4 fold) for at least 6 hours. Angiotensin II increased in a linear manner from 15 minutes to 6 hours post trauma. At 6 hours post trauma angiotensin II plasma levels were 4 times pretrauma levels. For the first 4 hours post trauma there was a positive correlation between the sum of vasopressin and angiotensin II plasma levels and the increase in peripheral resistance. These results suggest that the trauma induced increase in peripheral resistance is due to increases in plasma vasopressin and angiotensin II.
 ...
PMID:Trauma induced increases in plasma vasopressin and angiotensin II. 366 19

We have used the "second generation" Ca indicator, fura-2, to measure cytosolic free Ca concentrations in superfused cultures of adherent primary renal mesangial cells. The basal cytosolic free Ca concentration in these cells was found to be 93 +/- 5 nM (n = 35). The Ca ionophore ionomycin (0.1 microM) increased cytosolic Ca levels to a peak value of fourfold above basal, followed by a decline to a steadily maintained concentration of twofold above basal. Two vasoactive peptide hormones, arginine vasopressin and angiotensin II, at maximally effective concentrations, transiently increased cytosolic free Ca levels to peak values of three- and sixfold, respectively, above basal levels. The angiotensin II-evoked increase declined to near basal values before rising again to a value of 1.5- to 2-fold above basal. Cells treated with vasopressin did not have a significant secondary increase of Ca above a small, time-dependent, spontaneous increase. Mesangial cells demonstrated tachyphylaxis to both peptides. However, cross-tachyphylaxis was not observed. Treatment of cells with angiotensin II in ethyleneglycol-bis-(beta-aminoethylether)-N,N'-tetraacetic acid-supplemented Ca-deficient medium, or with the Ca channel blockers nifedipine or verapamil, did not eliminate the transient phase of cytosolic Ca metabolism. In contrast, the Ca channel blockers completely inhibited the second sustained Ca response to angiotensin II. These results indicate that angiotensin II and vasopressin mobilize intracellular Ca in cultured adherent mesangial cells. Angiotensin II, but not vasopressin, also appears to increase cytosolic Ca by influx of extracellular Ca through specific channels.
 ...
PMID:Effects of vasoactive peptides on cytosolic calcium in cultured mesangial cells. 378 56

We compared the effects of three vasoactive peptides (angiotensin II, vasopressin, and bradykinin) and norepinephrine on the production of prostaglandin I2 [prostacyclin (PGI2)] and PGE2 by isolated rat adipocytes. Angiotensin II, vasopressin, and bradykinin stimulated PGI2 production but had minimal or no effect on PGE2 production or triglyceride lipolysis in isolated rat adipocytes, while norepinephrine stimulated PGI2 production, PGE2 production, and triglyceride lipolysis. The arachidonic acid that serves as substrate for PGI2 production in adipocytes in response to the vasoactive peptides appears to be derived from the cellular phospholipids rather than the triglycerides in these triglyceride-laden cells. The adipocyte contains two separate mechanisms for PG production: 1) a catecholamine-stimulated mechanism for the production of PGI2 and PGE2 that is activated concomitantly with triglyceride lipolysis, and 2) a mechanism activated by vasoactive peptides for the stimulation of PGI2 production independent of triglyceride lipolysis and PGE2 production. These mechanisms may have distinct functions.
 ...
PMID:Stimulation of prostacyclin production in isolated rat adipocytes by angiotensin II, vasopressin, and bradykinin: evidence for two separate mechanisms of prostaglandin synthesis. 388 13


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