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)

We investigated the role of arginine-vasopressin (AVP) in maintaining the blood pressure of spontaneously hypertensive (SH) rats (stroke-prone strain) with established hypertension (22--28 weeks of age). In comparison with normotensive Wistar Kyoto (WKY) rats, plasma AVP concentrations of SH rats with benign hypertension (BH) were elevated twofold and in rats with severe or malignant hypertension (S-MH), fourfold. The height of the blood pressure was quantitatively related to plasma AVP in both BH and S-MH rats, the overall correlation coefficient being 0.66 (p less than 0.001). The intravenous injection of a specific AVP antiserum into conscious and unrestrained rats lowered blood pressure in 4 BH rats by 48 +/- 14 mm Hg and in 4 S-MH rats by 78 +/- 10 mm Hg and had only a marginal effect in 4 normotensive WKY rats. Infusion of saralasin did not lower blood pressure in WKY and BH rats and reduced blood pressure in only 2 of 7 S-MH rats tetsted (by 15 and 20 mm Hg). During AVP infusion the blood pressure of SH rats increased more (p less than 0.001) and heart rate fell much less (p less than 0.001) than in WKY rats. It is concluded that in SH rats with established hypertension, plasma AVP plays an important role in the maintenance of high blood pressure, while the renin-angiotensin system plays a minor or no role.
J Cardiovasc Pharmacol
PMID:Studies on the role of vasopressin in blood pressure control of spontaneously hypertensive rats with established hypertension (SHR, stroke-prone strain). 9 26

Catheter dislodgement is a major cause of technical failures in intraarterial vasopressin therapy for gastrointestinal bleeding. Ten such cases were observed in the past five years. In seven patients catheter dislodgement led to recurrent bleeding during vasopressin infusion. In one patient aortic infusion of vasopressin caused recurrent bleeding and reversible acrocyanosis of the feet, and in two patients vasopressin infusion into the left renal artery resulted in chest pain and hematuria. Catheter dislodgement should be suspected if bleeding that was initially controlled recurs during vasopressin infusion.
Cardiovasc Radiol 1978 Jul 25
PMID:Catheter dislodgement: a cause of failure of intraarterial vasopressin infusions to control gastrointestinal bleeding. 31 Dec 49

The effect of pulsatile flow on plasma vasopressin levels during cardiopulmonary bypass (CPB) was studied in 20 patients undergoing open valve replacement. Routine bypass was used in 10 patients and the AVCO pulsatile bypass pump was utilized in the other 10. In Group I (nonpulsatile) during CPB, the vasopressin level was markedly elevated (3.1 +/- 2 to 80 +/- 22 pg/ml) as was urine flow (0.6 +/- 0.2 to 5.9 +/- 2 ml/min) and urine Na+ concentration (69 +/- 19 to 116 +/- 7 mEq/L). In Group II (pulsatile) during CPB, the vasopressin level (3.8 +/- 3 to 54 +/- 14 pg/ml), urine flow (0.6 +/- 0.1 to 16.2 +/- 4.8 ml/min), and urine Na+ concentrations (61 +/- 13 to 97 +/- 10 mEq/L) were also elevated. The rise in vasopressin and urine Na+ was less in the pulsatile group (p less than 0.05) whereas the urine flow was higher (p less than 0.05). To maintain comparable blood pressure, the pulsatile flow group required significantly higher flows (4.5 +/- 0.2 compared to 3.8 +/- 0.2; p less than 0.05). These data suggest that CPB produces a marked vasopressin stress response which is beyond the physiological range for an antidiuretic effect on the kidney. At these levels vasopressin can exert a vasopressor effect to maintain resistance and affect renal blood flow, as well as producing an Na+ diuresis. The addition of pulsatile flow creates a more physiological situation attenuating the vasopressin response and producing a decrease in systemic resistance and a less pronounced Na+ diuresis.
J Thorac Cardiovasc Surg 1979 Nov
PMID:Plasma vasopressin levels and urinary flow during cardiopulmonary bypass in patients with valvular heart disease: effect of pulsatile flow. 49 33

Intravenous infusion of vasopressin decreased mesenteric arterial- and portal venous flow in dogs. In 4 of 5 high-risk patients, in whom acu te portosystemic shunting was performed, the peroperative intravenous infusion of vasopressin facilitated the surgical procedure by reducing portal pressure and peroperative bleeding from venous collaterals. In 1 patient with reversed portal flow, the portal pressure and flow were not affected by the vasopressin infusion. No undesirable effects of vasopressin were encountered and all patients survived surgery and the early postoperative period.
Scand J Thorac Cardiovasc Surg 1977
PMID:Peroperative vasopressin infusion during portocaval shunt surgery. 59 19

The effect of CPB on plasma ADH levels, urine flow, and urine osmolality was studied in nine patients. All patients received morphine, 1 mg. per kilogram, and 50 per cent nitrous oxide-50 per cent oxygen for anesthesia. CPB utilized a Travenol disposable bubble oxygenator and the prime consisted of 3 L. of Ringer's lactate. Measurements were made prior to induction of anesthesia , at 30 minutes following surgical incision, and at 15, 30, and 45 minutes during CPB. There were no statistically significant changes in mean arterial BP, cardiac index, serum sodium, or serum osmolality in any period. Urine flow increased from 0.99 +/- 0.3 ml. per minute to a high of 6.13 +/- 2.0 ml. per minute at 30 minute at 30 minutes on CPB (P less than 0.02). Urine osmolality declined from a control value of 691 +/- 142 mOsm. per kilogram to a low of 425 +/- 48 mOsm. per kilogram at 45 minutes on CPB (p less than 0.05). ADH levels rose from a control value of 4.3 +/- 1.5 to 13.0 +/- 3.3 pg. per milliliter with surgical stimulatiion (p less than 0.05). During CPB the ADH levels rose to a peak of 23.7 +/- 3.6 pg. per milliliter at 30 minutes (p less than 0.01) and were declining at 45 minutes. These data suggest that the stress of CPB results in an outpouring of ADH (or vasopressin) to function as a pressor to produce an increase in peripheral resistance. The ADH concentrations far exceed those required for normal physiologic control of water excretion and the urineflow will thus vary more with the hemodynamic changes than with the ADH levels.
J Thorac Cardiovasc Surg 1977 Jan
PMID:Antidiuretic hormone levels during cardiopulmonary bypass. 83 Oct 6

Hemodynamic effects of the kallikrein-kinin system can be investigated by experimental administration of specific kinin antagonists and by measurement of kinin levels in the circulating blood. In conscious normal rats, the bradykinin analog B4162 blunts the hypotensive effect of exogenous bradykinin. This kinin antagonist has no blood pressure effect in control rats, but it enhances the pressor effect of vasoconstrictor substances such as vasopressin or angiotensin II when they are infused at subpressor doses. Endogenous kinins may therefore participate in blood pressure regulation by antagonizing pressor substances. Plasma levels of endogenous kinins are normally in the low picomolar range. They are rapidly generated and destroyed in biological fluids. Thus, measurement of plasma kinins requires sensitive assays based on high-affinity antibodies and careful sample-handling techniques. Nonpolar solid-phase extraction on phenylsilylsilica provides a rapid, reliable, and easy extraction of kinins from plasma with constant and high recoveries.
J Cardiovasc Pharmacol 1992
PMID:Antagonizing and measurement: approaches to understanding of hemodynamic effects of kinins. 128 26

We studied the effects of nifedipine on blood pressure and on clinical and analytical parameters in hypertensive patients. Seven male and eight female subjects (mean age of 46.27 +/- 5.38 years, range of 41-56 years) with essential arterial hypertension were given nifedipine (20 mg b.i.d.) for 3 months. Before and after treatment, history, blood pressure, and biochemical values were recorded [blood: Na, K, Ca, creatinine, uric acid, triglycerides, cholesterol, HDL cholesterol, antidiuretic hormone (ADH), and aldosterone; urine: Na, K, Ca, creatinine, ADH, aldosterone, and percentage fraction of Na, K, and Ca excreted]. After 3 months of treatment, we found (a) significant decreases in systolic (147 +/- 18 vs. 166 +/- 16 mm Hg, p less than 0.001) and diastolic blood pressure (90 +/- 8 vs. 107 +/- 8 mm Hg, p less than 0.0007), triglycerides (107 +/- 47 vs. 120 +/- 49 mg/dl, p less than 0.0007), and cholesterol (236 +/- 4 vs. 257 +/- 44 mg/dl, p less than 0.00075) in blood, and in K excretion (50 +/- 19 vs. 46 +/- 19 mEq/g of creatinine, p less than 0.0007) and excreted fraction of K (49 +/- 6% vs. 8 +/- 5%, p less than 0.0012) in urine; (b) significant increases in HDL cholesterol (65 +/- 13 vs. 58 +/- 13 mg/dl, p less than 0.001) in blood, and in Na (115 +/- 73 vs. 109 +/- 69 mEq/g of creatinine, p less than 0.0007) in urine; and (c) no significant change in the remaining biochemical parameters, or in heart rate. Secondary effects included flushing (34%), headache (20%), ankle swelling (17%), dizziness (13%), palpitations (4%), and pruritus (4%).(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1992
PMID:Metabolic and antihypertensive effects of nifedipine in hypertensive patients. 137 8

Renal prostaglandins (PGs) help maintain renal blood flow and glomerular filtration rate when the kidney is exposed to a vasoconstrictor stress. In addition, they aid pressure natriuresis and blunt the antidiuretic effect of vasopressin. Angiotensin-converting enzyme (ACE) inhibitors could decrease renal PG synthesis by reducing angiotensin II (Ang II) formation or increase it by preventing kinin inactivation. Additionally, they could affect PG synthesis or catabolism directly. The effects of ACE inhibitors on blood pressure and renal hemodynamics appear to be largely independent of changes in renal PG synthesis. Similarly, there is no evidence that pressure natriuresis is modified by ACE inhibitors. A kinin induced increase in collecting duct PG synthesis may account for the water diuresis seen clinically with ACE inhibitors. A possible beneficial interaction between thromboxane synthesis inhibitors and ACE inhibitors may exist. Thromboxane synthetase inhibitors can reduce renal vascular resistance by redirecting PG endoperoxide synthesis toward prostacyclin. This effect may be offset by a prostaglandin-induced increase in renin release and Ang II formation. ACE inhibitors, by preventing Ang II synthesis, may increase the vasodilation due to thromboxane synthesis inhibition.
J Cardiovasc Pharmacol 1992
PMID:Renal prostaglandin synthesis and angiotensin-converting enzyme inhibition. 138 64

The brain is one of the organs where an intrinsic renin-angiotensin system (RAS) has been described. Stimulation of circumventricular or brainstem angiotensin II (Ang II) receptors engenders a distinct pattern of cardiovascular, endocrine, and behavioral responses featuring blood pressure increase, attenuation of the baroreceptor reflex, drinking, release of pituitary hormones such as vasopressin, oxytocin, and ACTH, and natriuresis. In contrast to most of the other central actions of Ang II, the natriuretic effect cannot be elicited by Ang II as a circulating hormone. Recently, we have shown that stimulation of Ang II AT-1 receptors in the circumventricular organs causes a selective release of norepinephrine (NE) in the paraventricular nucleus (PVN) and in the supraoptic nucleus (SON). As vasopressin is also released from the PVN and SON, it is possible that the Ang II-NE interaction is involved in the release of vasopressin, thereby contributing to central blood pressure regulation and volume control. Finally, a substantial body of results suggests that an overactivity of the brain renin-angiotensin system is one of the contributors to genetic hypertension. However, this idea needs further confirmation.
J Cardiovasc Pharmacol 1992
PMID:Role of brain angiotensin in cardiovascular regulation. 138 68

The venous system is supremely important in the control of cardiac output. Drugs which affect the venous system have profound effects on haemodynamics. This review comments on the methods available for the determination of venous compliance, resistance, and unstressed volume and describes the mean circulatory filling pressure (MCFP) technique, its usefulness and limitations. The MCFP technique involves the measurement of central venous pressure during brief (5-7 s) circulatory arrest. Mathematically, MCFP is inversely proportional to vascular compliance while experimentally, it is a primary determinant of venous return. The MCFP technique provides a reproducible and relatively non-traumatic means for the estimation of body venous tone in conscious and anaesthetised animals. Drugs examined by this technique include alpha and beta adrenoceptor agonists and antagonists, ganglionic blockers, vasoactive peptides (endothelin, vasopressin, angiotensin, neuropeptide Y), and vasodilators (hydralazine, nitroprusside, glyceryl trinitrate, calcium antagonists, and MCI-154).
Cardiovasc Res 1992 May
PMID:Effects of drugs on body venous tone, as reflected by mean circulatory filling pressure. 144 14


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