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

Recent interest has focused on the role of vasopressin (AVP) in blood pressure (BP) regulation. This study was performed to determine if vasopressin has a compensatory pressor role following acute diuresis in both normal rats and in rats with subtotal nephrectomy (SN) or in rats with SN-salt induced hypertension. An inhibitor (AVP-I), specific for the AVP vascular smooth muscle receptor, was administered intravenously to assess the AVP dependency of the BP. Furosemide administration significantly increased plasma AVP levels in all rats. Administration of AVP-I did not change BP in the normal rats with or without prior furosemide administration or in the SN rats without furosemide administration. In contrast, after furosemide administration, AVP-I significantly decreased mean BP in the SN rats. The administration of AVP-I to the SN-salt hypertensive rats, with or without furosemide administration, significantly decreased mean BP. In conclusion, AVP has a compensatory pressor role in SN rats after acute diuresis, with or without salt-induced hypertension, but not in the normal rat.
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PMID:Compensatory pressor role of vasopressin following acute diuresis. 318 69

Recently we demonstrated that increased chloride reabsorption in Henle's loop is a major contributor to the blunted furosemide response observed during prostaglandin synthesis inhibition. Because antidiuretic hormone (ADH) modulates chloride reabsorption in the loop and because prostaglandin synthesis inhibition potentiates ADH-mediated water reabsorption, ADH may be necessary for the attenuated furosemide response observed during prostaglandin synthesis inhibition. If such were the case, then prostaglandin synthesis inhibition should have no effect on furosemide's chloruretic response in the absence of ADH. To test this hypothesis, the effect of indomethacin on furosemide chloruresis was determined in homozygous (ADH-deficient) Brattleboro rats and in homozygous Brattleboro rats receiving ADH (2.4 mU/hr) over a short period of time. Furosemide-induced chloruresis was not different (P was not significant) between indomethacin-treated homozygous Brattleboro rats and homozygous Brattleboro rats receiving the indomethacin vehicle (fractional excretion of chloride: 6.28% +/- 1.08% vs. 6.24% +/- 0.98%). However, in ADH-infused Brattleboro rats, furosemide chloruresis was lower in indomethacin-treated rat groups than in vehicle-treated rat groups (fractional excretion of chloride: 3.09% +/- 0.62% vs. 6.61% +/- 0.88%; P less than 0.02) and lower than in indomethacin-treated ADH-deficient Brattleboro rats as well (P less than 0.05). Mean arterial pressure, inulin clearance, and renal blood flow were not different between any groups. Urinary prostaglandin excretion rates were not different between ADH-deficient Brattleboro rats and ADH-treated Brattleboro rats during furosemide administration and were markedly reduced by indomethacin in both circumstances. Thus, ADH is necessary for the blunted furosemide response observed during prostaglandin synthesis inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of antidiuretic hormone in the attenuated furosemide response observed during indomethacin administration. 333 76

Experiments were performed on luminally perfused, isolated, canine, jejunal segments in vivo to determine the effects of vasopressin on intestinal motility, myoelectrical activity and absorption. Intravenous vasopressin abolished spike activity and sometimes disrupted slow wave activity. The jejunum became atonic with intraluminal pooling of perfusate. Transit time was prolonged and intestinal absorption of water was decreased. Radionuclide imaging of the intestinal contents showed a doubling of intraluminal volume with vasopressin and confirmed the loss of intestinal motility. It is suggested that the high plasma levels of vasopressin which are known to follow laparotomy may be a factor in the development of postoperative ileus.
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PMID:Vasopressin effects on the small intestine: a possible factor in paralytic ileus? 401 14

The effects of captopril (intravenous loading dose of 20 mg, 1 h later followed by 10 mg infused during the next h) on arterial blood pressure and plasma renin activity were followed in 4 goats during the last months of pregnancy, during lactation and during anestrus. Experiments were made both when the animals were sodium-repleted and sodium-deficient. Furosemide and dietary restriction were used to deprive the animals of sodium. In sodium-replete animals, captopril caused a more pronounced fall in mean arterial blood pressure and a larger increase in plasma renin activity (PRA) when the animals were pregnant than when they were lactating or in anestrus. During sodium-deficient conditions the response was similar as during sodium repletion in pregnant goats. In anestral goats, PRA rose in response to captopril, but the blood pressure fall was similar as when the goats were sodium-replete. In lactating sodium-deficient goats, captopril caused a marked fall in mean arterial blood pressure concomitant with a 2-3 times higher rise in PRA than during corresponding sodium-repletion experiments. The respiratory rate was elevated in pregnant animals and increased further during captopril. The plasma vasopressin concentration did not change during captopril-induced hypotension. If the blood pressure fell greater than or equal to 10 mmHg the animals became very quiet and occasionally they fell asleep. All goats delivered healthy kids. The fact that the blood pressure fall was marked and consistent in all animals during pregnancy, but less and more variable during anestrus indicates that the activity of the renin-angiotensin system is of greater importance for blood pressure maintenance during pregnancy than during anestrus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of captopril on arterial blood pressure, plasma renin activity and vasopressin concentration in sodium-repleted and sodium-deficient goats. A serial study during pregnancy, lactation and anestrus. 637 25

The intravenous injection of an extract of atrial myocardium into anesthetized rats during a hypotonic diuresis resulted in an increase in the renal excretion of water, sodium, potassium, calcium, magnesium, and phosphate. There was an increase in urine concentration which was probably a result of the secretion of vasopressin since it did not occur in Brattleboro (di/di) rats. A transient increase in glomerular filtration rate and renal plasma flow occurred during the first five minutes with a more sustained rise in filtration fraction. Injection of atrial extract also caused a partial inhibition of solute-free water formation in Brattleboro rats subjected to water diuresis and a partial inhibition of solute-free water reabsorption in rats subjected to maximal antidiuresis by infusing vasopressin. In neither case was the degree of inhibition as profound as that observed after injecting furosemide in a dose which caused a comparable natriuretic response. A large dose of furosemide blocked the natriuretic response to atrial extracts whereas, when a comparable level of sodium and water output was produced by massive infusions of saline, the natriuretic response to atrial extract was increased. It is suggested that atrial natriuretic factor might inhibit sodium transport in nephron segments beyond the medullary thick ascending limb. Furosemide might also act at the same tubular site or inhibit tubular secretion of the atrial natriuretic factor.
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PMID:Effects of atrial natriuretic factor on renal handling of water and electrolytes in rats. 668 66

Animal and human studies demonstrate the dependence of renal prostaglandin (PG) production on dietary sodium chloride intake. The effect of 5 days' low salt diet (10 mmol Na/day plus 0.5 mg/kg Furanthril daily), and 5 days' high salt diet (250 mmol Na/day) on PGE2 and PGF2 alpha plasma levels and their excretion, on plasma renin activity (PRA) aldosterone (A) and vasopressin (VP) was evaluated on 30 normal subjects. Sodium restriction significantly increased plasma PGE2 and PGF2 alpha and their excretion in the urine. High salt intake reduced renal PG production to normal levels. Under low salt conditions PRA and A increased significantly and fell to normal values on high salt regimen. A negative correlation between renal PG production and VP plasma levels and excretion was demonstrated during the changes of dietary sodium intake.
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PMID:Humoral factors involved in the regulation of sodium-fluid balance in normal man. I. Effect of dietary sodium chloride intake on renal prostaglandins, vasopressin and renin-angiotensin-aldosterone system. 674 63

Seven out of nine patients with chronic inappropriate secretion of antidiuretic hormone were successfully treated with 40 mg frusemide daily. One patient needed 80 mg, and the remaining patient achieved only a small increase in diuresis after 40 mg frusemide; this was probably related to his low creatinine clearance. In order to maintain a salt intake high enough to compensate for the loss of urine electrolytes 3 to 6 g sodium chloride was added as tablets to the sodium-free diet in six patients. Hypokalaemia occurred in five patients but was easily corrected with either supplements of potassium chloride or a potassium-sparing diuretic. These findings add further weight to evidence that Frusemide is a good alternative for the treatment of patients with inappropriate secretion of antidiuretic hormone who cannot tolerate water restriction.
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PMID:Inappropriate secretion of antidiuretic hormone treated with frusemide. 680 39

Plasma antidiuretic hormone (ADH) was measured before and after furosemide administration in hypertensive patients (essential benign hypertensions with low plasma renin activity) and in normal subjects. Furosemide-induced reduction of plasma volume was about 10% after 2 hours. In normal subjects, plasma ADH rose progressively till the end of the study (1.5 pg/ml per hour corresponding to about 3 pg/ml per liter of plasma water lost) whereas it remained unchanged in hypertensive patients. There was an early increase of plasma renin activity (PRA) in normal subjects followed by a progressive fall. PRA response was blunted in hypertensive patients. These results show that volume-dependent ADH secretion is inhibited in patients with essential benign hypertension.
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PMID:Effects of furosemide-induced plasma volume reduction on plasma antidiuretic hormone in normal and hypertensive subjects. 701 73

Furosemide caused a significant reduction in mesenteric blood flow and conductance as early as 10 min after administration. When fluid losses were not replaced, conductance continued to decline. In volume-repleted animals, conductance fell initially but failed to decrease further. Thus, furosemide decreases mesenteric conductance in two ways: a small early decrease which is not related to volume loss and a later more marked decrease which is related to volume loss. The initial decrease in conductance seen in furosemide-treated animals appears to be mediated via the renin-angiotensin system. In volume-repleted as well as volume-depleted animals, the plasma concentrations of renin and angiotensin II, but not antidiuretic hormone, were increased 10 min after furosemide administration. Also, inhibitors of the renin-angiotensin system abolished the response. The later decrease in mesenteric conductance induced by furosemide is more complex. When fluid losses were not replaced, plasma levels of angiotensin II and renin, as well as antidiuretic hormone, were increased 40 min after furosemide administration. Neither an infusion of Sar1-Ile8-angiotensin II nor hypophysectomy, alone, prevented the furosemide-induced decrease in conductance. The decrease in conductance was reversed when Sar1-Ile8-angiotensin II was infused into hypophysectomized dogs. Thus, the later more marked decrease in conductance induced by furosemide is related to three factors: volume loss, plasma concentration of angiotensin II and plasma concentration of antidiuretic hormone. Mesenteric conductance is decreased by furosemide if plasma concentrations of one or both vasoactive factor are elevated in the presence of a decrease in extracellular volume.
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PMID:The role of volume depletion, antidiuretic hormone and angiotensin II in the furosemide-induced decrease in mesenteric conductance in the dog. 702 66

1. The effects of intravenous chlorthiazid and frusemide on urinary osmolality were compared in 19 hyponatraemic oedematous patients. 2. Frusemide (1 mg/kg) caused production of a dilute urine (urine/plasma osmolality ratio, Uosm./Posm., 1.64-0.84, P less than 0.01) whereas chlorthiazid (10 mg/Kg) did not (Uosm./Posm, 1.54-1.34, not significant. 3. The Osmolar clearance (Cosm.) was higher after frusemide than after chlorthiazid (11.45 vs 4.99 ml/min, P less than 0.01). When the doses of frusemide (0.25-0.5 mg/Kg) and chlorthiazid (20 mg/Kg) were chosen to give a similar Cosm. (7.25 vs 7.48 ml/min, not significant), the Uosm./Posm. was still lower after frusemide (2.20-1.00, P less than 0.001) than after chlorthiazid (1.75-1.26, P less than 0.01). 4. Exogenous vasopressin did not increase the low Uosm./Posm. after frusemide (1.00-1.00, not significant) but increased the ratio after chlorthiazid (1.34-1.68, p less than 0.01). 5. These results indicate that frusemide, but not chlorthiazid, lead to the excretion of a dilute urine in hyponatraemic oedematous patients. This dilution is not due to a greater solution excretion but is associated with a resistance to the action of vasopressin.
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PMID:Comparative effect of diuretics on renal water excretion in hyponatraemic oedematous disorders. 705 22


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