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

After perfusing the vascular circuit of the mesenteric artery of the rat with a Ca-free solution for 20 min, extracellular Ca was depleted, and the vasoconstrictor effect of high K solutions was abolished, while the vasopressin response was reduced by 40%, serotonin by 30% and noradrenaline and adrenaline responses by about 20%. When the Ca-free perfusion was prolonged for 2 h or more, the vascular responses to the agonists were further reduced due to depletion of cellular Ca. Successive doses of each agonist injected at 1 min intervals showed a decline of the responses, that recovered when 4 min or more were allowed to pass after the last injection. This reversible desensitization or tachyphylaxis was rapidly abolished by Ca. Noradrenaline and adrenaline showed crossed tachyphylaxis, which depressed the responses to serotonin and vasopressin. Tachyphylaxis to serotonin and vasopressin did not depress the response to the other two agonists. These findings support the conclusion that not only do noradrenaline and adrenaline share a Ca pool, but that so do serotonin and vasopressin. These two agonists each require a separate Ca pool.
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PMID:Calcium pools in the contraction of arterial smooth muscle induced by several agonists. 653 May 55

To assess in vivo functional interactions of vasopressor substances, norepinephrine and vasopressin, with renal prostaglandins and kallikrein-kinin system which are responsible for the vasodepressor mechanism in the kidney, we evaluated chronic effects of norepinephrine (1.8 mg/kg/day ip) and vasopressin (7.2 U/kg/day ip) on urinary prostaglandin E excretion and urinary kallikrein excretion in conscious rats. Both norepinephrine and vasopressin induced a sustained increase in systolic blood pressure. Norepinephrine induced slight but significant increases in urinary prostaglandin E excretion and urinary kallikrein excretion which were sustained for up to 6 days. Vasopressin induced a marked increase in urinary prostaglandin E excretion which was sustained for up to 6 days, whereas it induced a sustained decrease in urinary kallikrein excretion. Circulating angiotensin II levels was not changed by norepinephrine, but was decreased by vasopressin. These results indicate that renal prostaglandin E may not correlate with renal kallikrein-kinin and renin-angiotensin system in the responses to norepinephrine and vasopressin, and that vasopressin may be a more potent stimulator of the synthesis or release of renal prostaglandin E.
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PMID:Chronic effects of norepinephrine and vasopressin on urinary prostaglandin E and kallikrein excretions in conscious rats. 656 34

The effects of local intra-arterial infusions of serotonin (5 or 25 micrograms base/min) or norepinephrine (1 or 5 micrograms base/min) on cutaneous (skin) and skeletal muscle vasculatures were investigated in canine forelimbs perfused at constant flow in dogs anesthetized with pentobarbital. Norepinephrine produced dose-related constriction of the skin and skeletal muscle vasculatures. In the cutaneous vascular circuit, norepinephrine produced large artery, small vessel, and large vein constriction. The increase in cutaneous vascular resistance was primarily due to an increase in small vessel resistance. Serotonin did not increase skeletal muscle vascular resistance but produced marked cutaneous vasoconstriction subsequent to large artery and large vein constriction. The small vessels, if anything, tended to dilate. The skin and skeletal muscle vascular responses to serotonin and norepinephrine were similar in innervated and acutely denervated forelimbs. Phentolamine pretreatment completely blocked all vascular actions of norepinephrine, and largely inhibited the cutaneous vasoconstriction produced by the infusion of the low dose of serotonin. However, the cutaneous large artery and large vein constriction produced by the infusion of the high dose of serotonin was not affected by phentolamine pretreatment. Cyproheptadine pretreatment blocked or largely inhibited the cutaneous vasoconstriction produced by serotonin only in doses which also inhibited norepinephrine and vasopressin cutaneous vasoconstriction. Pretreatment with methysergide blocked or largely inhibited the cutaneous large artery and large vein constriction produced by infusions of serotonin. Norepinephrine and vasopressin produced significant vasoconstriction in the presence of methysergide. These data suggest that the cutaneous large artery and large vein constriction produced by serotonin is not due to the activation of postjunctional alpha-adrenergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence that serotonin receptors mediate the cutaneous vasoconstriction produced by 5-hydroxytryptamine in canine forelimbs. 662 7

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

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

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

Norepinephrine (NE) infused at doses of 0.7, 2.2 and 6.7 micrograms/min/kg body weight into conscious, salt and water loaded ducks dose-dependently induced arterial hypertension, reflex bradycardia and diuresis/natriuresis at unchanged glomerular filtration and reduced renal blood flow. NE-induced changes in plasma concentrations of osmoregulatory hormones consisted of a slight increase for the antidiuretic hormone, no change for angiotensin II and a nearly 4-fold increase for atrial natriuretic factor. Sub-pressor doses of NE infused close to the origin of the renal arteries induced diuresis without a rise in urinary sodium concentration. The results suggest pressure diuresis in ducks as a response to hypertensive NE doses with a possible contribution of atrial natriuretic factor to natriuresis.
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PMID:Noradrenergic modulation of avian kidney function. 791 51


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