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)

The influence of captopril on pressor responses to exogenously administered vasopressor substances was investigated in normal subjects. Norepinephrine (0.05, 0.1 and 0.2 micrograms/kg . min -1; n = 5), angiotensin II (5, 10 and 20 ng/kg . min -1; n = 5) and vasopressin (2 mU/kg . min -1; n = 5) were infused each for 10 minutes; each infusion was repeated twice. Captopril (50 mg orally) significantly attenuated the pressor response to norepinephrine (0.1 [p less than 0.05], 0.2 [p less than 0.01] micrograms/kg . min -1; n = 7) and to vasopressin (p less than 0.01, n = 5), but not to angiotensin II; these responses were reproducible. Attenuation of the pressor responses to norepinephrine did not occur when a subpressor dose of angiotensin II (ng/kg . min-1) was infused in addition to captopril (n = 5). Infusion of a subpressor dose of bradykinin (0.1 ng/kg . min-1) had no influence on the pressor responses to norepinephrine (n = 5). In the five subjects treated with indomethacin (225 mg/54 hours) captopril still attenuated the pressor responses to norepinephrine. These results suggest that the attenuation by captopril of the pressor responses to norepinephrine and vasopressin might have been due to reduction of endogenous angiotensin II.
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PMID:Captopril attenuates pressor responses to norepinephrine and vasopressin through depletion of endogenous angiotensin II. 704 92

Norepinephrine and epinephrine concentrations in the caudal and rostral part of the nucleus tractus solitarii (NTS) and in locus coeruleus (LC) of Sabra hypertension prone (SBH) rats are 2-4-fold higher than in the parent Sabra (SB) strain; SB rats have higher concentrations than the Sabra hypertension resistant (SBN) rats. Dopamine concentrations were higher in SBH as compared to SB and SBN rats only in the caudal NTS. Vasopressin concentrations in the NTS of SBH were 3-fold higher than the levels found in SB or SBN rats. These data suggest that catecholamines and vasopressin in specific brainstem nuclei are involved in either the pathogenesis or central response to hypertension in SBH rats.
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PMID:Catecholamines and vasopressin in hindbrain nuclei of hypertension prone and resistant rats. 717 1

Plasma arginine-vasopressin (AVP) was measured before and after 24 h of a 26-hour renal concentration test in 47 patients treated with lithium for 6-180 months (mean 70 months). In 34 of the patients, plasma AVP was also measured before and after a 2- to 4-hour period of water loading, and in 31 of the patients, creatinine, 125iothalamate, 131I-hippuran and lithium clearances were measured. Plasma AVP values were compared to those obtained in 8 healthy controls. Baseline AVP levels were significantly higher in the lithium-treated patients than in healthy controls. During the period of water deprivation AVP values increased significantly and during oral water loading a significant decrease took place, AVP values still being significantly higher in the lithium-treated patients than in the healthy controls. During oral water loading a slight increase in lithium clearance as well as fractional lithium excretion was seen as compared to values obtained during the last 2 h of a renal concentration test. This study demonstrates that antidiuretic hormone production is neither blocked nor inhibited during lithium treatment. The hypothalamic system reacts on water deprivation as well as on water loading. This study supports the notion that the main lithium-induced renal affection is a vasopressin-resistant impairment of renal concentrating ability.
Nephron 1982
PMID:Plasma arginine-vasopressin, renal-concentrating ability and lithium excretion in a group of patients on long-term lithium treatment. 717 89

A relationship between blood pressure and the functional character of osmoreceptor controlling vasopressin secretin under usual physiological situations in the rat was studied by employing Na-nitroprusside as depressor agent or norepinephrine as pressor agent and the sensitive and specific radioimmunoassay of arginine vasopressin (AVP). Na-nitroprusside or control saline was given s.c. 15 min after an i.p. injection of 2% (v/w) hyper, hypo or isotonic saline. Norepinephrine or control saline was given s.c. with a concurrent i.p. injection of 2% (v/w) hyper, hypo or isotonic saline. 30 min after this osmotic load, plasma AVP (pAVP) and osmolality (pOSM) were measured on trunk blood as previously described (J. Clin. Invest. 52: 3212, 1973). In rats given Na-nitroprusside, 2 mg/kg body weight, osmotic loading produced a rise in pAVP which correlated relationship (pAVP=1.9 [pOSM-276.6]; N=16; r=0.81) raised significantly (p less than 0.001) to the left of that in the control vehicle (pAVP=1.4[pOSM,-293.8]; N=8; r=0.86). In rats given norepinephrine, 0.1 mg/kg body weight, the regression line generated by osmotic loading (pAVP=1.2[pOSM-229]; N=7; r=0.88) fell significantly (p less than 0.001) to the right of that in the control vehicle (pAVP=1.4[pOSM-202]; N=6; r=0.99). In 4 rats, the same dose of Na-nitroprusside and norepinephrine resulted in a significant (p less than 0.001) decrease (40%) and increase (20%) from the basal level for the same time of osmotic loading in mean arterial blood pressure as measured directly via chronically implanted aorta catheters, respectively. These results indicate that hypotension increases pAVP by lowering the threshold or set and increasing the sensitivity of the osmoregulatory system and hypertension decreases pAVP by raising the threshold or set and reducing the sensitivity of the mechanism without abolishing the system.
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PMID:[Effects of baroregulation on osmoregulation of arginine vasopressin in rats (author's transl)]. 732 90

Segments of colon were denervated, vascularly isolated, and autoperfused at normal arterial pressure in the anesthetized dog. Norepinephrine, vasopressin, isoproterenol, and histamine were infused i.a. in graded doses. Norepinephrine and vasopressin reduced colonic blood flow and increased the arteriovenous oxygen difference; oxygen uptake by the colon fell, and the capillary filtration coefficient (Kf,c) was reduced. Isoproterenol and histamine increased colonic blood flow and reduced the arteriovenous oxygen difference; oxygen uptake by the colon did not change significantly. The Kf,c increased with isoproterenol, but changes due to histamine were more variable. Vasoconstrictor drugs tend to reduce, and vasodilators tend to increase oxygen uptake by the colon; the effects of altered blood flow are, however, alleviated by changes in colonic oxygen extraction, such that moderate drug-induced changes in blood flow (-25 to +50%) are not associated with appreciable (less than or approximately 10%) changes in oxygen uptake.
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PMID:Effects of norepinephrine, vasopressin, isoproterenol, and histamine on blood flow, oxygen uptake, and capillary filtration coefficient in the colon of the anesthetized dog. 737 72

Micropuncture and clearance studies were performed on normal untreated and polyuric lithium chloride treated rats (10-12 days). A persistent hypernatremic state quickly developed in the polyuric lithium treated rats during hydropenia resulting from an increased urinary loss of water over sodium chloride, as the fractional excretion of sodium remained at control levels. Superficial proximal tubule and loop of Henle fluid reabsorption was depressed by 8 and 17%, respectively, in lithium-treated rats during this period. By contrast, water reabsorption in the distal tubule and collecting system was significantly increased in the lithium animals, being 27% of the filtered load compared with 20% in normal rats. These results suggest that the urinary-concentrating defect induced by lithium treatment is due primarily to a depression of proximal tubule and possibly loop of Henle function, and that water reabsorption within the distal nephron may in fact be augmented: thus it is unlikely that the action of antidiuretic hormone is significantly impaired. Marked phosphaturia and hypocalciuria were also noted in the lithium-treated rats.
Nephron 1980
PMID:Effect of lithium treatment on rat renal tubule function. Evidence against impaired antidiuretic hormone action. 739 71

The purpose of this study was to investigate the vascular contractile and inositol phosphate responses in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation (PVL) in Sprague-Dawley rats. Sham-operated rats served as controls. Pressures, vasoconstrictor responses, and inositol phosphate responses were determined at 14 days after surgery. The portal venous pressure was significantly higher, while systemic arterial pressure and heart rate were lower, in PVL rats. Dose-dependent contractile responses were observed for both norepinephrine (1 x 10(-8) - 3 x 10(-6) M) and vasopressin (3 x 10(-10) - 3 x 10(-8) M) in the tail artery of both groups. The contractile response to norepinephrine was significantly decreased in PVL rats compared with controls at all doses. The contractile response to vasopressin was significantly decreased in PVL rats at higher doses. After myo-[3H]inositol incorporation in tail artery, the levels of 3H-labelled phosphatidylinositols (cpm/mg) were similar between the two groups. Norepinephrine (10(-7) - 10(-5) M) and vasopressin (10(-10) - 10(-8) M) dose dependently stimulated the 3H-labelled inositol phosphate production in the tail artery of both PVL and sham-operated rats. However, the response was significantly lower in PVL rats. The results suggested that the attenuation of vascular contractile responses in portal hypertension was reflected in the phosphoinositide messenger system.
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PMID:Decreased vascular contractile and inositol phosphate responses in portal hypertensive rats. 764 17

The Tasmanian bettong (Bettongia gaimardi) is a small marsupial rat kangaroo without detectable brown adipose tissue (BAT). The hindlimb was perfused with constant flow at 25 degrees C after cannulation under anesthesia of the femoral artery and vein to one hindlimb. Norepinephrine (NE, 25 nM-2.5 microM) and vasopressin (VP, 10 nM-0.1 microM) each increased perfusion pressure, oxygen consumption (VO2), and lactate and glycerol efflux of the perfused hindlimb. NE-mediated increases in VO2 and the efflux of lactate and glycerol were unaffected by propranolol (10 microM) but were completely blocked by the further addition of phentolamine (10 microM). In contrast, serotonin (5-HT; 0.1-2.5 microM) inhibited VO2 and inhibited lactate efflux. The changes induced by NE, VP, and 5-HT were all rapidly reversed by nitroprusside. These results suggest that resting thermogenesis in bettong hindlimb can be differentially controlled by the vasculature, which may also contribute to the induced VO2. This vascular control of skeletal muscle VO2 appears widespread in homeotherm evolution.
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PMID:Vasoconstrictors alter oxygen, lactate, and glycerol metabolism in the perfused hindlimb of a rat kangaroo. 777 82

The syndrome of inappropriate secretion of antidiuretic hormone is a common consequence of neurologic and pulmonary infections as well as drug intake and many other clinical situations. Its association with herpes varicella-zoster virus infections is scarcely reported in the literature. It generally appears in immunosuppressed patients suffering from serious underlying diseases. There are also a few cases of syndrome of inappropriate secretion of antidiuretic hormone related to vidarabine use. We report the case of a man infected by human immunodeficiency virus who developed a disseminated herpes varicella-zoster virus infection and symptoms due to hyponatremia caused by antidiuretic hormone excess. The patient was cured with saline hypertonic infusion, water restriction, and intravenous administration of acyclovir. To the best of our knowledge, this is the first case of this association in a human immunodeficiency virus infected patient. We propose the use of acyclovir instead of vidarabine in the management of these situations.
Nephron 1994
PMID:Syndrome of inappropriate antidiuretic hormone secretion and herpes zoster infection: 1. Report of this association in a patient suffering from AIDS. 783 Aug 68

The effects of hormone stimulation on atrial natriuretic factor (ANF) release in atria were studied in experimental renal failure rats. In vitro experiments were done in two groups of male Wistar rats. Group 1 rats were sham operated, and group 2 rats were subjected to 5/6 nephrectomy. Overall glomerular filtration rate was significantly reduced (1.98 +/- 0.10 vs. 0.75 +/- 0.05 ml/min, p < 0.001) in nephrectomized rats. These rats were also mildly uremic [blood urea nitrogen (BUN): 18 +/- 0.6 vs. 60 +/- 3.9 mg/dl p < 0.001]. The right atria of partially nephrectomized and sham-operated rats were isolated and perfused in a modified Langendorff apparatus to measure ANF release rate. Experiments were done in two phases. In the initial phase, spontaneous release of ANF was measured. In the second phase, angiotensin II (10(-6) M), vasopressin (10(-6) M) or endothelin (ET 1; 10(-6) M) were added into the perfusate. Spontaneous ANF release by the atria of renal failure rats was significantly elevated compared to intact rats. A significant positive correlation was found between ANF release rate and BUN (r = 0.65, p < 0.01). This suggests that the increase in ANF release by the atria of chronic renal failure (CRF) rats is related to the severity of renal impairment. Angiotensin II, vasopressin and endothelin induced exaggerated increases in ANF release by the atria of CRF rats. These results show that a shift in stimulus response curve is present and can contribute to the observed increase in plasma ANF levels in CRF rats.
Nephron 1995
PMID:In vitro hormone-stimulated atrial natriuretic factor release is increased in experimental renal failure. 789 99


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