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)

Responses of blood pressure to intravenous (i.v.) or intracerebroventricular (i.c.v.) endothelin-1 (ET-1) in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats were investigated. Conscious male SHRs and WKY rats were used for the experiments. ET-1 (300-1,000 ng/kg) was injected intravenously in the i.v. experiments, or 30 and 100 ng/kg of ET-1 were injected into the lateral ventricle in the i.c.v. experiments. The initial depressor response to i.v. ET-1 was greater in SHRs (n = 10) than in WKY rats (n = 10) at 1,000 ng/kg (-54 +/- 6 vs. -41 +/- 3 mm Hg, mean +/- SEM, p less than 0.05). The subsequent pressor response to i.v. ET-1 was smaller in SHRs than in WKY rats (3.5 +/- 0.8 vs. 7.0 +/- 0.9 mm Hg at 300 ng/kg, p less than 0.05, and 11 +/- 2 vs. 17 +/- 2 mm Hg at 1,000 ng/kg, p less than 0.05). Pressor responses to i.c.v. ET-1 were not different in SHRs (n = 8) and WKY rats (n = 8) at both doses (10 +/- 4 vs. 10 +/- 3 mm Hg at 30 ng/kg, and 46 +/- 10 vs. 49 +/- 10 mm Hg at 100 ng/kg). A greater initial depressor response and a smaller subsequent pressor response to i.v. ET-1 were observed in SHRs than in WKY rats. The attenuated pressor response to intravenously administered ET-1 may be unique since vasoconstrictor responses to other known vasoactive substances such as angiotensin, catecholamines, or vasopressin are reportedly augmented in SHRs. We did not find any difference in responsiveness to i.c.v. ET-1 between SHRs and WKY rats.
J Cardiovasc Pharmacol 1991
PMID:Blood pressure responses to intravenous or intracerebroventricular endothelin-1 in spontaneously hypertensive rats. 172 61

Endothelin-3-like immunoreactivity (ET-3-ir) was detected in extracts of rat hypothalamic median eminence, and in the anterior and neurointermediate lobes of the pituitary at levels (ng ET-3/mg protein) exceeding those present in extracts of abdominal aorta. This ET-3-ir appeared authentic because radioimmunoassay (RIA) dose-response curves parallel to those of synthetic ET-3 could be constructed and this ET-3-ir comigrated on C-8 high-pressure liquid chromatography (HPLC) with synthetic ET-3. Endothelin-1-like immunoreactivity, on the other hand, was abundant in extracts of abdominal aorta and cerebral cortex and only minimally present in hypothalamus and anterior pituitary gland. Central administration of 11 and 23 pmol ET-3 resulted in significant (4.2- and 5.7-fold, respectively) elevations of plasma levels of vasopressin. Oxytocin levels were transiently, yet significantly, elevated (1.8-fold) by the higher dose of ET-3. These results, and our findings that central administration of ET-3 inhibits stimulated water drinking, suggest a physiologically important role for endogenously produced endothelin in the central mechanisms regulating fluid and electrolyte homeostasis.
J Cardiovasc Pharmacol 1991
PMID:Hypothalamic endothelin: presence and effects related to fluid and electrolyte homeostasis. 172 77

In patients with congenital heart disease two poorly understood postoperative complications are pulmonary hypertensive crises after repair of large atrioventricular or ventricular septal defects and right atrial and pulmonary thrombi after the Fontan operation. In this study we assessed whether cardiopulmonary bypass in these patients is associated with the release of agents that might induce platelet aggregation and vasoconstriction, such as biologically active von Willebrand factor and platelet-activating factor. In addition, we measured levels of anticoagulants such as antithrombin III and proteins C and S. Three groups of patients with congenital heart disease undergoing cardiopulmonary bypass were monitored through the perioperative period for secundum atrial septal defects, large atrioventricular or ventricular septal defects, and tricuspid atresia or univentricular heart (Fontan candidates). Control values were obtained from age-matched patients; patients requiring major noncardiac operations and those with cardiac disease not requiring cardiopulmonary bypass were also studied. After cardiopulmonary bypass in all three groups biologic activity of von Willebrand factor increased markedly in the immediate and early postoperative periods compared with preoperative values, whereas antithrombin III values were decreased. Platelet-activating factor was detected in only two patients with congenital heart disease, both in the early postoperative period. In contrast, patients who did not have cardiopulmonary bypass did not show these abnormalities. All measured parameters normalized at late follow-up (6 to 18 months after operation). Although cardiopulmonary bypass in these patients resulted in increased von Willebrand factor activity and decreased antithrombin III, changes that may predispose the patient to platelet aggregation and thrombus formation, absolute values in individual patients alone were not predictive of pulmonary hypertensive crises or detectable thrombi. This suggests that these hematologic abnormalities may contribute to but are not by themselves a cause of morbidity in the early postoperative period. Moreover, the increased von Willebrand factor biologic activity seen postoperatively in patients with congenital heart disease suggests that use of synthetic vasopressin may be ineffective and potentially detrimental.
J Thorac Cardiovasc Surg 1992 Jan
PMID:Abnormalities in von Willebrand factor and antithrombin III after cardiopulmonary bypass operations for congenital heart disease. 172 19

The Fontan procedure results in right atrial distention and is complicated by fluid retention. Since systemic fluid balance may be hormonally mediated in part and related to right atrium size, we measured plasma atrial natriuretic factor and plasma arginine vasopressin levels in 19 patients undergoing the Fontan procedure and in 12 control patients undergoing other types of heart operations. Preoperative plasma atrial natriuretic factor levels were higher in patients undergoing the Fontan procedure than in control patients (95 +/- 16 pg/ml preoperatively versus 50 +/- 8 pg/ml; p less than 0.05) and increased in patients undergoing the Fontan procedure to 330 +/- 48 pg/ml by postoperative day 2 (p less than 0.05) but not in control patients. Increased plasma atrial natriuretic factor levels could enhance capillary transudation, but elevated plasma atrial natriuretic factor levels should also enhance diuresis and prevent fluid retention. Vasopressin levels, however, were also increased in patients undergoing the Fontan procedure (from 9 +/- 2 pg/ml preoperatively to 144 +/- 37 pg/ml at end of operation) and were higher and remained elevated longer than in control patients undergoing heart operations (37 +/- 7, 20 +/- 4, 16 +/- 6 pg/ml on postoperative days 1, 2, and 3 to 10 for the Fontan group compared with 15 +/- 4, 4 +/- 1, 4 +/- 2 pg/ml for control patients). Vasopressin levels were highest in the Fontan group with the most severe fluid retention and effusions (for example, 51 +/- 10 pg/ml versus 23 +/- 4 pg/ml, on postoperative day 1). Increased vasopressin and atrial natriuretic factor could act synergistically to result in the development of effusions after the Fontan procedure when atrial natriuretic factor-induced capillary transudation is combined with vasopressin-induced antidiuresis.
J Thorac Cardiovasc Surg 1991 Dec
PMID:The role of vasopressin and atrial natriuretic factor in postoperative fluid retention after the Fontan procedure. 183 45

During the past few years more than 30 novel, biologically active peptides have been discovered. Some are produced in endocrine glands and circulate as hormones in the blood; others are contained in the enterochromaffin cells of the gut and may be involved in the regulation of intestinal functions. The vast majority of new peptides, however, have been detected in the central and peripheral nervous systems, where they are synthesized in distinct neurons and stored in neurovesicles. Many of these neuropeptides may be involved in circulatory regulation. There is evidence supporting such a role, especially for centrally located angiotensin, opioid peptides, substance P, neuropeptide Y (NPY), vasopressin, atrial natriuretic peptide (ANP), kinins, corticotropin releasing factor, bombesin, and somatostatin. In this review we discuss the cardiovascular actions of angiotensin, neuropeptide Y, and calcitonin gene related peptide.
Cardiovasc Drugs Ther 1991 Feb
PMID:The role of neuropeptides in cardiovascular regulation. 203 31

In summary, for reasons that are not clear, some persons seem to be extremely good at retaining sodium on a high-sodium diet or poor at excreting sodium on a high-sodium intake. This is more frequent in Western hemisphere blacks than in whites in the West or in blacks in Africa. These geographic/ethnic differences in sodium handling ability may be related to environmental factors or, more likely, to inherited differences in the ability to conserve sodium based on the evolutionary principle of survival fo the fittest for the ability to conserve sodium. The frequency of this salt-conserving (thrifty) genotype in Western hemisphere blacks may have been further increased as a consequence of severe selection pressures for survival based on the ability to conserve sodium during the slavery period of history in the West. One characteristic of the blood pressure control systems of Western hemisphere blacks is suppression of plasma renin activity without suppression of aldosterone production. In addition there is greater nephrosclerosis in blacks than whites and a more rapid decline in creatinine clearance with age. When more sodium is ingested than the kidneys are able to handle (excrete), there is a (transient) slight positive sodium balance; as a result sodium, chloride, and water are retained, resulting in an expansion of plasma volume (Fig. 7-3). The initial physiologic responses include (increased) secretion of atrial natriuretic peptides and the digitalis-like substance (natriuretic hormone), and inhibition of vasopressin and aldosterone secretion. The net effect is directly enhanced natriuresis and diuresis, and a reduction in plasma volume, with no significant effect on blood pressure. However, if there is a continuing tendency to sodium retention and volume expansion, the capacity of the aforementioned mechanisms to control plasma volume will be exceeded; then, the chronically elevated level of the digitalis-like substance will inhibit the sodium pumps in the arterial and venous smooth muscle cells and in the sympathetic neurons. The increased venous tone will help to reduce plasma volume directly by reducing central venous volume. Arterial tone will be increased by direct action of the digitalis-like substance on the arterial smooth muscle and, indirectly, via the hormone's action on the sympathetic neurons. Initially, of course, blood pressure will be maintained in the normal range (but will be labile) because of the compensating cardiovascular reflexes. Once the capacity of these reflexes to control blood pressure is exceeded, however, the blood pressure will begin to rise; this will induce a pressure natriuresis to help restore plasma volume to normal.(ABSTRACT TRUNCATED AT 400 WORDS)
Cardiovasc Clin 1991
PMID:The pathogenesis of hypertension: black-white differences. 204 19

d(CH2)5Tyr(Me)-AVP is a potent inhibitor of the systemic vasoconstrictor action of vasopressin (AVP). In order to examine the effectiveness of this agent in blocking AVP-induced coronary vasoconstriction, 11 pentobarbital-anesthetized mongrel dogs were instrumented for the measurement of left circumflex (LCX) coronary blood flow, systemic arterial blood pressure, heart rate, lead II electrocardiogram, left ventricular end-diastolic pressure, left ventricular developed pressure, and left ventricular +/- dP/dt. Direct injection of AVP (0.01-1 microgram) into the LCX produced a dose-dependent decrease in coronary artery blood flow (maximum reduction: 60.5 +/- 8.1% after 1 microgram), - dP/dt (maximum reduction: 41.8 +/- 5.3% after 1 microgram), and +dP/dt (maximum reduction: 14.6 +/- 5.3%), whereas a dose-dependent increase in left ventricular end-diastolic pressure was observed (maximum increase: 62.6 +/- 20.2%). No significant changes occurred in heart rate, mean blood pressure, or left ventricular developed pressure. Intravenous administration of d(CH2)5Tyr(Me)-AVP reduced (1 microgram/kg) or abolished (5 micrograms/kg) the effects of AVP on coronary blood flow +/-dP/dt and left ventricular end-diastolic pressure. In addition, doses of 1,2, and 5 micrograms/kg of d(CH2)5Tyr(Me)-AVP alone produced increases of LCX blood flow of 5.1 +/- 1.5, 2.0 +/- 0.7, and 6.8 +/- 1.7 ml/min, respectively (p less than 0.05). We conclude that d(CH2)5Tyr(Me)-AVP is effective in preventing the coronary artery constriction and hemodynamic sequelae of intracoronary administered AVP.
J Cardiovasc Pharmacol
PMID:Antagonism of vasopressin-induced coronary artery constriction by the vasopressin antagonist d(CH2)5Tyr(Me)-AVP. 241 8

Postsynaptic binding sites for alpha 1 and alpha 2 adrenoceptor ligands are found in abundance in the renal cortex of several species, with reports of 2-3 times as many alpha 2 as alpha 1 sites. These alpha adrenoceptor subtypes can potentially influence salt and water excretion through both vascular and tubular effects. Renal vascular resistance in dogs is increased by both alpha adrenoceptor subtype agonists but alpha 1 agonists are more potent. In rats, alpha 2, agonists have almost no effect on the renal circulation whereas alpha 1 agonists are capable of intense renal vasoconstriction. The mechanisms by which alpha 2 agonists increase glomerular filtration rate are not yet clear and may involve the secondary release of hormones affecting glomerular dynamics and permeability. Thus, an abundance of alpha 2 adrenoceptor binding sites in whole cortical homogenate of rat kidneys with little demonstrable vascular effect of alpha 2 agonist suggests that the preponderance of these receptors lies instead on the tubular epithelium. Alpha-1 adrenoceptors are probably responsible for the increased Na reabsorption from the proximal tubule and the anti-natriuresis following low level renal nerve stimulation. In contrast, an alpha 2 agonist such as guanabenz produces a diuresis by reducing the release of vasopressin and by antagonizing its hydrosmotic effect on the nephron, and a modest natriuresis by decreasing medullary interstitial osmolality and reducing passive Na reabsorption.
J Cardiovasc Pharmacol 1985
PMID:Role of alpha-2 receptors in the regulation of renal function. 241 45

Central alpha-adrenoceptor agonists (methyldopa, clonidine, guanabenz) decrease sympathetic outflow and renin and vasopressin secretion as well as increase parasympathetic activity. These drugs are commonly employed as antihypertensives. Two other conditions, chronic heart failure and ischemic heart disease, may also benefit from central alpha-adrenergic stimulation. In both acute and chronic heart failure, central alpha-adrenoceptor agonists reduced cardiac work load by decreasing heart rate, systemic arterial pressure and reducing venous tone. Also, plasma catecholamines were decreased. Exercise at comparable work loads was achieved at a lower pressure-rate product and effort capacity was sometimes increased. Central alpha-adrenoceptor agonists increased effort capacity in patients with ischemic heart disease and angina pectoris. Again, the benefits are thought to be decreased heart rate, systemic arterial blood pressure and rate-pressure products during exercise; catecholamines are reduced in these patients as well. Central alpha-adrenoceptor agonists offer another avenue of approach to alter neurohumoral factors in congestive heart failure and ischemic heart disease and thereby produce beneficial hemodynamic response.
J Cardiovasc Pharmacol 1985
PMID:Central alpha-adrenergic agonists in chronic heart failure and ischemic heart disease. 241 48

The renin-angiotensin system has a range of physiological actions concerned with the control of the circulation. Angiotensin II has both an immediate and a delayed pressor effect; it stimulates the secretion of aldosterone and antidiuretic hormone, promotes thirst, stimulates the sympathetic nervous system at various sites while inhibiting vagal tone, and has a range of direct effects on the kidney. Several aspects of this range of actions can become deranged in a number of forms of hypertension as well as in congestive cardiac failure. Hence much effort has been directed in recent years to the development of agents designed to interfere with the renin-angiotensin system and to apply these clinically in the treatment of hypertension and congestive cardiac failure. Orally active converting enzyme inhibitors are of proven benefit not only in renovascular hypertension, but also, when combined with loop diuretics, in the treatment of intractable hypertension as well as, both alone and in combination with thiazide diuretics, in the treatment of essential hypertension. In congestive cardiac failure controlled trials have shown that converting enzyme inhibitors can improve exercise tolerance while diminishing lassitude, correct potassium deficiency, and limit ventricular arrhythmias. Energetic efforts are being made to develop orally active inhibitors of the enzyme renin itself, since these should be more specific in action than the presently available and very successful converting enzyme inhibitors.
J Cardiovasc Pharmacol 1986
PMID:Circulatory basis for the use of angiotensin converting enzyme inhibitors in hypertension and cardiac failure. 242 88


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