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 triglycyl-lysine-vasopressin (TGLVP) on cardiovascular responses to orthostatic stress was studied. Arterial pressures, heart rate (HR) and stroke volume (SV) were measured in eight healthy males subjected to 20 min 70 degrees head-up tilt. On different days they received either 0.01 mg/kg b.w. of TGLVP or a corresponding volume of 0.9% saline i.v. after 15 min supine rest. After the drug injection, in supine subjects, HR had decreased from 58 to 50 beats min-1, total peripheral resistance (TPR) was elevated by 29%, systolic (SAP) and diastolic pressure (DAP) had increased by 7 and 8 mmHg, respectively. During tilt, values for HR and SAP were similar with and without TGLVP whereas DAP and MAP were elevated 8 and 7 mmHg, respectively, by the drug. 4-8 min into the tilt, TGLVP caused an 8% sustained curtailment of SV. Both with and without the drug TPR increased by about 30% in response to head-up tilt. Thus, the marked peripheral arteriolar constriction after vasopressin in the supine position was not affected by head-up tilt. Tilting also abolished the drug-induced elevation in SAP, most likely explained by the reduction in SV. Although TPR was markedly increased by TGLVP during head-up tilt, reflected in the behaviour of DAP, the response of SV speaks against any beneficial effect of this drug on orthostatic tolerance in healthy subjects.
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PMID:Effects of triglycyl-lysine-vasopressin on cardiovascular responses to orthostatic stress. 362 70

The effects of passive tilt on arterial and central venous pressures (MAP and CVP), heart rate (HR), arterial concentrations of vasopressin (AVP) and aldosterone (ALDO), osmolality, and hematocrit were studied in eight healthy young men. Tilting was performed at 30 degrees/min to 20 or 40 degrees and maintained for 45 min. The 20 degrees tilt did not change MAP while CVP fell by 5.9 mmHg (P less than 0.01) and HR increased by 5 beats/min (51-56 beats/min, P less than 0.05). AVP and ALDO concentrations were unchanged. At 40 degrees, MAP increased by 5.7 mmHg (86.0-91.7 mmHg, P less than 0.01), CVP decreased by 7.4 mmHg (P less than 0.01), HR rose by 8 beats/min (55-63 beats/min, P less than 0.01), and pulse pressure fell by 6 mmHg (P less than 0.05). ALDO increased fivefold (P less than 0.05), but AVP did not change. Infusions of AVP at 0.25 or 1.0 ng X min-1 X kg body wt-1 elevated plasma AVP to 11 +/- 1 and 52 +/- 8 pg/ml. Only the larger dose caused a small increase in MAP while CVP and HR remained unchanged; however, washout of a subcutaneous depot of Xe was reduced greater than 60% even by the lower dose. It is concluded that small-angle nonhypotensive passive tilt does not affect AVP measurably despite substantial reductions of CVP and a marked increase in ALDO. Elevations of AVP elicit marked subcutaneous vasoconstriction also in the absence of changes in CVP, HR, and MAP.
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PMID:Cardiovascular and endocrine responses to head-up tilt and vasopressin infusion in humans. 376 73

The effects of intravenous (i.v.) and intracarotid (IC) angiotensin II (AII) infusion on systemic and renal hemodynamics, renal water excretion, and plasma antidiuretic hormone (ADH) levels were examined in six conscious dogs under water loaded and hydropenic conditions. In the first group of seven studies, AII in a mean dose of 12.7 ng/kg/min was administered i.v. to water loaded dogs. The infusion induced a significant increase in mean arterial pressure (MAP, 99 to 118 mm Hg, P less than 0.001), and significant reductions in both glomerular filtration rate (GFR, 67 to 57 ml/min, P less than 0.05) and para-aminohippurate clearance (CPAH, 280 to 212 ml/min, P less than 0.005) occurred. Despite this decrement in renal hemodynamics, urine remained maximally dilute (Uosm, 58 to 61 mOsm/kg H2O, NS). Furthermore, plasma ADH was suppressed maximally after water load and did not increase after i.v. AII infusion. The IC infusion of AII (mean dose 5.8 ng/kg/min) produced similar changes in hemodynamics; plasma ADH remained undetectable. When AII was administered i.v. to hydropenic animals (mean dose 8.3 ng/kg/min), MAP again increased (86 to 111 mm Hg, P less than 0.001) as GFR (81.3 to 68.6 ml/min, NS) and CPAH (291 to 223 ml/min, P less than 0.05) declined modestly. In these animals, Uosm decreased significantly (1429 to 1114 mOsm/kg H2O, P less than 0.005) and plasma ADH did not change significantly (1.66 to 1.88 pg/ml, NS). When IC AII (4 ng/kg/min) was repeated in hydropenic dogs pretreated with indomethacin, neither Usom (1787 to 1664 mOsm/kg H2O, NS) nor plasma ADH were altered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of angiotensin II on plasma antidiuretic hormone and renal water excretion. 378 90

Oestrous rats were anaesthetized with pentobarbital, one of the femoral arteries and veins and one of the ovarian veins were cannulated, and a thin polyethylene cannula was fixed in the ovarian bursa. Five-min blood fractions were collected from the ovary for 50 min. Following the control fractions 15 mU of oxytocin, 15 mU of vasopressin or 50 microliter of 0.9% NaCl solution was given into the ovarian bursa over 10 min. Blood pressure and ovarian blood flow were continuously recorded. Progesterone (P) and oestradiol-17 beta (E2) were determined from the blood samples by RIA. Oxytocin did not alter the blood pressure, whereas the ovarian blood flow showed a short increasing tendency. Later, however, it started to decrease in parallel with the decrease in blood pressure owing to blood loss. The secretion of P and E2 remained unchanged. No changes in blood pressure were observed after vasopressin administration, although the ovarian blood flow quickly decreased in parallel with the secretion of P and E2. It is suggested that oxytocin has no direct effect on ovarian blood flow and hormone secretion in the rat. Vasopressin, however, is an effective vasoconstrictor in the rat ovary and may in this way reduce hormone synthesis.
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PMID:Effects of oxytocin and vasopressin on the ovarian blood flow, progesterone and oestradiol-17 beta secretion in oestrous rats. 406 Sep 75

The role of sympathetic and other pressor systems in the development of fulminant hypertension induced by baroreceptor deafferentation is still unclear. We studied the effects of acute hypertension produced by bilateral dorsomedullary knife cuts lateral to the nucleus tractus solitarii (DMK-cut) on plasma norepinephrine (NE), epinephrine (E), and vasopressin (VP) in conscious, tail-artery-cannulated rats. In saline-pretreated (SAL) rats, DMK-cut caused a significant (p less than 0.001) rise in mean blood pressure (MAP, +68 +/- 3 mm Hg), heart rate (HR, +97 +/- 19 bpm), NE (+2.5 +/- 0.3 ng/ml), E (+2.7 +/- 0.4 ng/ml), and VP (+115 +/- 34 pg/ml) compared to sham-operated rats. Neither sympathetic blockade with chlorisondamine (CHLO, 10 mg/kg, s.c.) nor elimination of the pressor effects of VP by use of Brattleboro rats or the VP pressor antagonist resulted in a maximal MAP response significantly different from that in the SAL + DMK-cut group. However, CHLO-pretreatment of Brattleboro rats completely abolished the increase in MAP and HR. It is suggested that the bilateral DMK-cut causes acute hypertension, probably due to the abolition of baroreceptor reflexes by central interruption of neural connections of the nucleus tractus solitarii. It appears that both the increased sympathoadrenomedullary activity and VP release normally contribute to this hypertension; however, either one is sufficient to sustain the elevated blood pressure.
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PMID:Role of catecholamines and vasopressin in cardiovascular responses to bilateral dorsolateral transection of the medulla oblongata in the rat. 665 53

Bovine ovaries were obtained from the abattoir and corpora lutea were classified as: (1) early luteal phase (approximately Days 1-4); (2) mid-luteal phase (Days 5-10); (3) late luteal phase (Days 11-17); (4) regressing (Days 18-20) and (5) pregnant (Days 90-230). In addition, preovulatory follicles and whole ovaries without luteal tissue were collected. Concentrations of oxytocin, vasopressin, bovine neurophysin I and progesterone were measured in each corpus luteum by radioimmunoassay. Progesterone and neurophysin I levels increased from Stage 1 to Stage 2, plateaued during Stage 3 and declined by Stage 4. Oxytocin and vasopressin concentrations increased from Stage 1 to Stage 2 but declined during Stage 3 and were low (oxytocin) or undetectable (vasopressin) in follicles, whole ovaries and pregnancy corpora lutea. Therefore the concentrations of both peptide hormones were maximal during the first half of the cycle and declined before those of progesterone. The high concentration of oxytocin within the corpus luteum coupled with the presence of bovine neurophysin I suggests that oxytocin is synthesized locally.
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PMID:Variations in oxytocin, vasopressin and neurophysin concentrations in the bovine ovary during the oestrous cycle and pregnancy. 674 62

1. To determine if increases in plasma sodium concentration P[Na] have any sustained effects of the renin-aldosterone system, P[Na] was increased in a group of six dogs over a period of 6 days by increasing sodium intake from 10 to 200 mmol per day while a fixed 700 ml per day water intake was maintained along with a continuous i.v. infusion of antidiuretic hormone (ADH) at a rate of 2.4 units per day. 2. P[Na] rose from 137.3 +/- 2.0 to 153.6 +/- 6.5 mmol/l during the high intake period. Plasma potassium concentration, 22Na space, and mean arterial pressure all remained near control levels in response to Na loading. 3. Plasma renin activity (PRA) averaged 1.0 +/- 0.1 ngAI/ml per hour on the final low Na day and fell transiently to 0.6 +/- 0.2 ngAI/ml per hour on the first day of sodium loading. For the duration of the study it remained at the control level. Plasma aldosterone concentration fell from the low Na level of 15.4 +/- 2.4 ng/100 ml to 10.5 +/- 1.5 ng/100 ml on the final day of high Na intake. 4. We conclude that increases in P[Na] in the absence of concomitant changes in P[K], 22Na space and MAP do not have a sustained effect on control of renin release but may exert a negative effect on aldosterone secretion.
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PMID:Effect of sustained hypernatraemia on the renin-aldosterone system in the dog. 701 64

NO synthase is present in magnocellular neurons of supraoptic and paraventricular nuclei as well as in the posterior pituitary gland and may participate in control of vasopressin secretion. To test this possibility, experiments were performed in conscious, chronically prepared rabbits to determine the effect of NO synthesis inhibition with NG-nitro-L-arginine methyl ester hydrochloride (L-NAME) on basal vasopressin secretion and vasopressin responses to increased plasma osmolality (hypertonic saline infusion; P osm) and decreased blood pressure (nitroprusside infusion). L-NAME infusion (0.5 mg.kg-1 x min-1 i.v.) increased mean arterial pressure [MAP; 82.6 +/- 3.4 to 93.0 +/- 3.0 mmHg (P < 0.02)], decreased heart rate [HR; 242 +/- 12 to 209 +/- 9 beats/min (P < 0.02)], decreased plasma renin activity [PRA; 3.1 +/- 0.6 to 2.0 +/- 0.6 ng.ml-.2 h-1 (P < 0.001)], and increased plasma vasopressin concentration [P AVP; 2.2 +/- 0.3 to 4.5 +/- 1.0 pg/ml (P < 0.05)]. P(osm) did not change. Hypertonic saline infusion did not change MAP or HR but decreased PRA [4.3 +/- 0.8 to 0.9 +/- 0.2 ng.ml-1 x 2 h-1 (P < 0.01)], increased P(osm) [284 +/- 1 to 305 +/- 2 mosmol/kg H2O (P < 0.001)], and increased PAVP [2.8 +/- 0.3 to 12.7 +/- 2.7 pg/ml (P < 0.01)].(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of inhibition of nitric oxide synthesis on vasopressin secretion in conscious rabbits. 751 50

To determine which ovarian hormone is involved in the sexually dimorphic antidiuretic action of vasopressin, the antidiuretic response to vasopressin was examined in sham-operated nonestrous female rats chronically treated with vehicle and in ovariectomized rats treated with vehicle, progesterone, estradiol, or the combination of estradiol and progesterone, respectively. Three-week-old female rats were sham operated or ovariectomized, and a slow-release hormone pellet was implanted at the 6th wk. The experiment was performed at the 10th to 12th wk in conscious, chronically instrumented rats hydrated with tap water (2% body wt). Infusion of vasopressin at rates of 10-1,000 pg.min-1.kg body wt-1 resulted in a dose-dependent antidiuretic response that was significantly enhanced in ovariectomized rats compared with the intact nonestrous females. Progesterone had no effect, whereas estradiol attenuated and restored the antidiuretic response to vasopressin to a level similar to that in intact nonestrous female rats. These results suggest that it is estrogen, but not progesterone, that reduces the antidiuretic response to vasopressin in the female rat.
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PMID:Estradiol attenuates the antidiuretic action of vasopressin in ovariectomized rats. 773 6

Continuous pump-driven veno-venous hemofiltration (CVVH) has become an established method for treatment of acute renal failure (ARF). Since severe disturbances of (micro-) circulation are intimately involved in the bad outcome of these patients, the profile of endocrinological regulators of circulation was prospectively and serially measured in patients undergoing pump-driven CVVH (n = 15). 15 patients with similar APACHE II score, but without ARF and without CVVH were also studied. Endothelin-1 (ET-1), atrial natriuretic peptide (ANP), vasopressin, renin, and catecholamine (epinephrine, norepinephrine) plasma levels were measured before start of CVVH (= "baseline") (in the non-CVVH patients: admission to intensive care unit) and during the next 5 days. Various hemodynamic parameters were additionally monitored. MAP, HR, PAP, CI, and right ventricular hemodynamics (RVEF, RVEDV, RVESV) remained almost unchanged in the CVVH patients and were without differences to the non-CVVH group within the entire investigation period. PCWP and RAP were higher in the CVVH patients already at baseline (RAP, 17.8 +/- 4.0 mmHg; PCWP, 22.1 +/- 4.5 mmHg) (p < .02) and remained elevated in the further course of the investigation. Renin plasma level was higher already at baseline in the CVVH patients (907 +/- 184 pg/ml) (p < .05) and further increased during CVVH (to 1453 +/- 186 pg/mL). Vasopressin increased only in the CVVH group (from 3.80 +/- .66 to 11.85 +/- 1.05 pg/mL) (p < .01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in regulators of circulation in patients undergoing continuous pump-driven veno-venous hemofiltration. 2597 10


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