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)

Experiments were performed in anesthetized rats to examine the effect of an intravenous infusion of norepinephrine or vasopressin on the tubuloglomerular feedback (TGF) response of stop flow pressure (PSF). During infusion of norepinephrine at an average rate of 107.5 ng/kg min, mean femoral arterial pressure (MAP) increased from 102.1 +/- 3.55 to 113.7 +/- 3.44 mm Hg and PSF-max increased from 7.45 +/- 1.13 to 9.95 +/- 1.19 mm Hg. When MAP was returned to control by a suprarenal aortic clamp PSF-max was 5.64 +/- 1.09 mm Hg (NS vs. control). Similarly, at an infusion rate of 226.5 ng/kg min PSF-max was not significantly different from control (6.79 +/- 1.61 mm Hg). V1/2, the half-maximum flow rate, was not altered by norepinephrine whether MAP increased or was kept constant. Infusion of vasopressin at the pressor dose of 13.0 mU/kg min increased MAP by about 25 mm Hg and raised PSF-max from 6.56 +/- 0.84 to 14.45 +/- 1.54 mm Hg. However, when MAP was returned to normal PSF-max was 5.41 +/- 0.75 mm Hg (NS). Our data show that in contrast to angiotensin II, norepinephrine and vasopressin do not augment TGF responses when a rise in MAP is prevented. Angiotensin II appears to play a specific role in altering the sensitivity of the TGF mechanism.
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PMID:Effect of angiotensin and other pressor agents on tubuloglomerular feedback responses. 225 82

We studied trophic effects of angiotensin II, vasopressin and oxytocin on explanted ventral spinal cord cultures derived from 13 to 14-old day rat embryos. There was a significant neurite promoting effect in angiotensin II and vasopressin-treated cultures. Angiotensin II had the most potent effect at any concentrations. It became clear that minimum effective concentration was 10(-8)M in both angiotensin II and vasopressin. However, oxytocin had no neurotrophic effect at any concentrations. Our results demonstrated that angiotensin II and vasopressin have a neurotrophic effect on ventral spinal cord in cultures, and may contribute to therapeutic strategy of amyotrophic lateral sclerosis.
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PMID:[Trophic effect of angiotensin II, vasopressin and oxytocin on the ventral spinal cord of rat embryo]. 227 65

Cisplatin-containing chemotherapy regimens are known to produce intense nausea and vomiting. Angiotensin II (AII) and vasopressin (AVP) have been shown to have emetic properties. The role of these two peptides on cisplatin-induced vomiting was investigated in beagle dogs. Cisplatin (2 mg/kg, IV over 5 min) produced consistent emesis in all dogs after a mean latency time of 144 +/- 4 min. Serum Angiotensin Converting Enzyme (ACE) and plasma AII levels did not significantly change 3 hr after cisplatin administration (at the time of nausea and emesis) in control animals. AVP levels rose from 0.3 pg/ml to 7.5 pg/ml 3 hrs after cisplatin. Complete inhibition of ACE with enalapril (given at 3 mg/kg p.o., 3 hrs prior to cisplatin) reduced AII levels by 70%, but failed to significantly modify the increase in AVP levels (7.2 +/- 2.2 pg/ml), the latency time to emesis (149 +/- 2 min) and the number of emetic episodes induced by cisplatin. These results suggest that AII does not mediate cisplatin-induced emesis, nor does it mediate the increase in AVP observed at the time of emesis. We propose that AVP may be a good marker for nausea and emesis, and that increases in AVP may be neurally-mediated. The large increase in circulating AVP may represent a desirable water conservation response in anticipation of fluid losses induced by vomiting.
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PMID:Role of angiotensin II and vasopressin in cisplatin-induced emesis. 231 91

The renin-angiotensin system has a range of physiological actions concerned with the control of the circulation. Angiotensin II has both an immediate and a delayed pressor effect; it stimulates the secretion of aldosterone and antidiuretic hormone, promotes thirst, stimulates the sympathetic nervous system at various sites while inhibiting vagal tone, and has a range of direct effects on the kidney. Several aspects of this range of actions can become deranged in a number of forms of hypertension as well as in congestive cardiac failure. Hence much effort has been directed in recent years to the development of agents designed to interfere with the renin-angiotensin system and to apply these clinically in the treatment of hypertension and congestive cardiac failure. Orally active converting enzyme inhibitors are of proven benefit not only in renovascular hypertension, but also, when combined with loop diuretics, in the treatment of intractable hypertension as well as, both alone and in combination with thiazide diuretics, in the treatment of essential hypertension. In congestive cardiac failure controlled trials have shown that converting enzyme inhibitors can improve exercise tolerance while diminishing lassitude, correct potassium deficiency, and limit ventricular arrhythmias. Energetic efforts are being made to develop orally active inhibitors of the enzyme renin itself, since these should be more specific in action than the presently available and very successful converting enzyme inhibitors.
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PMID:Circulatory basis for the use of angiotensin converting enzyme inhibitors in hypertension and cardiac failure. 242 88

The rat adipocyte contains two separate mechanisms for prostaglandin (PG) production. Norepinephrine stimulates prostacyclin (PGI2) and PGE2 production and triglyceride lipolysis in isolated rat adipocytes. In contrast, the vasoactive peptides angiotensin II, vasopressin, and bradykinin stimulate PGI2 production, but not PGE2 production or triglyceride lipolysis, in these cells. In this study, we characterized the two separate mechanisms of PG production with respect to the time course, the role of cAMP, the identity of the adrenergic receptor, and the effects of insulin and glucocorticoids. Angiotensin II stimulated PGI2 production rapidly (at 5 min) and independently of cAMP. beta-Adrenergic stimulation with isoproterenol produced a rapid 11-fold increase in the cAMP concentration and stimulated PGI2 production more slowly (at 120 min). The phosphodiesterase inhibitor 1-methyl-3-isobutylxanthine (0.2 and 0.5 mM) and the adenylate cyclase activator forskolin (10 microM) also stimulated cAMP production rapidly and PGI2 production more slowly. 1-Methyl-3-isobutylxanthine (5.0 mM) further stimulated cAMP levels, but prevented the increase in PGI2 production and blunted the increase in glycerol release seen at lower concentrations. beta-Adrenergic blockade with propranolol or timolol completely inhibited the norepinephrine- or isoproterenol-stimulated production of PGI2 and triglyceride lipolysis, respectively. Insulin selectively inhibited isoproterenol-stimulated PGI2 production and triglyceride lipolysis at physiological concentrations, but had no effect on angiotensin II-stimulated PGI2 production. In contrast, dexamethasone inhibited PGI2 production induced by both isoproterenol and angiotensin II. We conclude that: angiotensin II stimulates PGI2 production rapidly and independently of cAMP, but isoproterenol stimulates PGI2 production more slowly, an effect that is cAMP dependent; insulin inhibits the cAMP-dependent beta-adrenergic stimulation of PGI2 production (and triglyceride lipolysis), but not the cAMP-independent angiotensin II-induced stimulation of PGI2 production (this suggests that the former effect is mediated by a decrease in cAMP levels in the adipocyte); and dexamethasone inhibits both mechanisms of PGI2 production. Both mechanisms of PGI2 production by rat adipocytes are exquisitely sensitive to hormonal regulation.
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PMID:Prostacyclin production by isolated rat adipocytes: evidence for cyclic adenosine 3',5'-monophosphate-dependent and independent mechanisms and for a selective effect of insulin. 242 31

Modulation of intracellular Ca2+ concentration [( Ca2+]i) is a signal for the contraction of vascular smooth muscle cells responding to vasoreactive substances. We prepared confluently cultured smooth muscle cells from rat aorta, loaded them with Ca2+ sensitive fluorescent dye, fura-2, and measured the [Ca2+]i transient by microscopic spectrofluorometry. The [Ca2+]i was distributed heterogeneously in cytosol. Angiotensin II (10 nM) transiently doubled the [Ca2+]i. It was also increased by arginine-vasopressin (10 nM), even after stimulation by angiotensin II was saturated. In contrast, acetylcholine (10 microM) or rat atrionatriuretic peptide (10 nM) did not change the [Ca2+]i in the same detecting field of the same cell, contradicting previous reports.
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PMID:Response of intracellular Ca2+ transients in cultured vascular smooth muscle cells to angiotensin II, vasopressin, acetylcholine and atrionatriuretic peptide. 252 12

Angiotensin II (ANG II) and vasopressin (AVP) are two powerful vasoconstrictors, and atrial natriuretic peptide (ANP) is a potent vasorelaxant. The changes in the density or affinity of binding sites for these agents that may alter target organ responsiveness in hypertension are reviewed. ANG II binding in mesenteric arteries was unaltered in one-kidney, one-clip (1-K, 1-C) and in 2-K, 1-C hypertensive rats, while in deoxycorticosterone acetate (DOCA)-salt hypertensive rats ANG II binding to blood vessels was significantly increased. A role of mineralocorticoids to increase the number of vascular ANG II sites in some hypertensive models is suggested. In spontaneously hypertensive rats (SHR) ANG II receptors were increased in young rats in the prehypertensive stage with respect to Wistar-Kyoto (WKY) control rats, but normal in older rats. AVP binding in the vasculature of hypertensive rats was uniformly decreased in inverse correlation to plasma AVP levels, but vascular responsiveness to AVP was exaggerated. Inositol trisphosphate production by blood vessels of SHR in response to AVP showed that increased AVP receptor-coupled phospholipase C activity may mediate in part the exaggerated pressor response in spite of reduced or normal density of receptors for vasoconstrictor peptides. Vascular ANP sites in 2-K, 1-C, 1-K,1-C, and DOCA-salt hypertensive rats varied inversely with plasma concentrations of ANP. Normal densities of ANP receptors in saralasin-sensitive 2-K, 1-C hypertensive rats correlated with ANP sensitivity, while saralasin-insensitive 2-K, 1-C hypertensive rats, which did not respond to ANP, had significantly decreased density of ANP vascular receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vascular receptors for angiotensin, vasopressin, and atrial natriuretic peptide in experimental hypertension. 255 50

The substances stimulating the release of immunoreactive corticotropin-releasing factor from cultured human placental cells were investigated. Monolayer primary cultures of trophoblast cells from pregnant women at term were used. The immunoreactive corticotropin-releasing factor released in the culture medium eluted from high-performance liquid chromatography with the same retention time as human corticotropin-releasing factor. Norepinephrine and acetylcholine increased immunoreactive corticotropin-releasing factor release into the culture medium in a dose-related manner. Epinephrine was partially active, whereas dopamine and serotonin did not induce significant changes of immunoreactive corticotropin-releasing factor release from placental cultures. Angiotensin II, interleukin-1, oxytocin, and arginine-vasopressin also increased placental immunoreactive corticotropin-releasing factor release in a dose-related manner, whereas other peptides (vasoactive intestinal peptide, substance P, somatostatin, atrial natriuretic factor, interleukin-2) were ineffective. These results showed that several neurotransmitters and peptides stimulate the release of immunoreactive corticotropin-releasing factor from placental cells, suggesting their possible involvement in the physiologic regulation of placental immunoreactive corticotropin-releasing factor release during pregnancy and parturition.
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PMID:Neurotransmitters and peptides modulate the release of immunoreactive corticotropin-releasing factor from cultured human placental cells. 256 97

The effects of intracerebroventricular (icv) injections of 10 ng angiotensin II (ANG II) on mean arteriolar diameter and spontaneous arteriolar vasomotion were studied in subcutaneous tissue of conscious, restrained hamsters, using the skin fold window chamber preparation. Angiotensin II caused a significant decrease in mean arteriolar diameter which was associated with a significant elevation in the amplitude of vasomotion. The frequency of vasomotion did not change significantly. The central ANG II-induced effects on arteriolar vasomotion were not significantly altered by continuous intravenous (iv) infusion of hexamethonium (1 mg.kg-1.min-1). In contrast, iv bolus injection of the vascular vasopressin receptor antagonist d(CH2)5Tyr(Me)AVP (10 micrograms.kg-1) 5 min prior to icv injection of ANG II significantly attenuated the effects of the neuropeptide on mean arteriolar diameter and the amplitude of vasomotion. These data indicate that central ANG II stimulation enhances arteriolar vasomotion in peripheral subcutaneous tissue of conscious hamsters and that this effect may be mediated by release of vasopressin.
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PMID:Central angiotensin II stimulates arteriolar vasomotion in conscious hamsters. 257 95

We studied trophic effects of angiotensin II, vasopressin and oxytocin on explanted ventral spinal cord cultures from 13-14-old day rat embryos. There was a significant neurite promoting effect in angiotensin II and vasopressin-treated cultures. Angiotensin II had the most potent effect at any concentrations. It became clear that minimum effective concentration was 10(-8) M in angiotensin II and vasopressin respectively. Effect of these two neuropeptides was concentration-dependent. However, oxytocin had no neurotrophic effect at any concentrations. Our results demonstrated that angiotensin II and vasopressin have a neurotrophic effect on ventral spinal cord in cultures, and may contribute to therapeutic strategy of amyotrophic lateral sclerosis.
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PMID:Neurotrophic effect of angiotensin II, vasopressin and oxytocin on the ventral spinal cord of rat embryo. 258 29


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