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

The kidney is a complex endocrine organ, and many of the renal hormones have actions that help regulate renal function. Although we have much more to learn about the role of most of these hormones in the regulation of renal function in both the newborn and adult kidney, there are some important aspects to keep in mind as we approach therapeutic interventions in sick newborn and premature infants. Because of the many interactions between hormonal systems, drugs that we may use for specific actions on one system may have effects on others as well (ACE inhibitors, cyclooxygenase inhibitors, dopamine antagonists). In addition, it is clear that the state of the organism may play a role in which of the renal hormones is active. Finally, the nonrenal hormonal systems that affect renal function (aldosterone, atrial natriuretic peptide, vasopressin, etc) may interact to change further expected results of any therapeutic intervention. Therefore, it behooves the clinician to monitor carefully renal function whenever modifications in therapy are made, whether it is a change in mechanical or pharmacologic intervention.
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PMID:Development of the endocrine function of the kidney. 157 74

Experimental myocardial infarction is a model of cardiac overload due to amputation of part of the cardiac muscle. The development of cardiac failure depends on the size of the infarct and the time factor. This model of overload is associated with changes of the phenotype of the remaining healthy muscle and with peripheral vascular modifications partially dependent of the activation of pressor and/or deactivation of dilator systems. These changes are proportional to the size of the infarction at a given time after induction of the model. The degree of right ventricular hypertrophy and the decrease in blood pressure reflect the severity of infarction and the deterioration of the remaining myocardial function, affecting the haemodynamics both before and after the left ventricle. The increases in the 1/3 forms of isomyosins, the amount of subendocardial collagen, the biosynthesis, stocking and secretion of ANF are related to the infarct size and degree of overload. Similarly, the concentration of cyclic GMP is proportional to the infarct size. These parameters reflect ventricular overload, the increase of stress and energy deprivation of the remaining healthy muscle. The activation of peripheral pressor systems is also dependent on the infarct size reflects the effect of cardiac pump dysfunction on the kidney, liver, brain and endothelium. Large infarcts are associated with increased circulating renin and renal concentrations, with a decrease in angiotensinogen levels related to its consumption by the renin and to reduced hepatic synthesis and also with increased secretion and biosynthesis of vasopressin by the hypothalamus. In this model, Perindopril is beneficial by decreasing the cardiac load. It reduces the blood pressure, causes regression of bi-auricular and right ventricular hypertrophy. Changes in myosin isoenzyme configuration regress and subendocardial fibrosis and ANF concentrations are normalised. The effects of ACE inhibitors in this context, though very beneficial, are limited by the impossibility of normalising cardiac load and stress when the initial amputation of cardiac contractile mass exceeds 40%.
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PMID:[Experimental myocardial infarction in the rat. Effect of perindopril]. 166 27

The antihypertensive effect of inhibitors of the angiotensin I-converting enzyme (ACE = kininase II) results from their vasodilatory and natriuretic effects as well as their effect on baroreceptor function. In addition to the inhibition of systemic and local angiotensin II formation, other local hormonal systems may also be involved in this effect at multiple target sites. Thus, potentiation of the vasodilator and natriuretic kinin system following inhibition of kininase II is thought to contribute to the persistent hypotensive effect of ACE inhibitors despite normalization of circulating ACE activity. Although increased plasma bradykinin levels cannot be detected, we found that the enhanced kinin-dependent local vascular prostacyclin production can be blunted in vitro by aprotinin, a kallikrein inhibitor. ACE inhibition may affect the atrial natriuretic peptide (ANP) system as the renin-angiotensin system and ANP appear to play antagonistic roles at the peripheral and central nervous system levels. Inhibition of kallikrein or of kininase II were both shown to modulate the natriuretic and vasorelaxant effects of ANP. In hypertensive subjects, we found that ACE inhibition with blood pressure normalization reduces basal and stimulated plasma ANP and blunts the renal sodium excretion in response to saline loading. In contrast, we did not observe effects of acute ACE inhibition in healthy sodium-depleted volunteers on plasma vasopressin under basal conditions or in response to passive tilt. Finally, we investigated the interaction of ACE inhibition with substance P, a powerful endogenous diuretic and natriuretic peptide that may have a transmitter function in the baroreceptor reflex arch.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kinin- and non-kinin-mediated interactions of converting enzyme inhibitors with vasoactive hormones. 169 69

In 1984 we demonstrated in an animal model of chronic congestive heart failure due to rapid right ventricular pacing in chronically instrumented dogs, that the inhibition of the renin-angiotensin-aldosterone system by captopril from the onset of pacing has beneficial effects on hemodynamic and neurohumoral mechanisms. In contrast to control animals, dogs on a chronic therapy with the ACE-inhibitor showed no significant increase in peripheral vascular resistance, a reduced decline of cardiac output and no significant increase of mean pulmonary arterial pressure. Chronic ACE-inhibition led to a significant reduction of the secretion of aldosterone, to an attenuation of the activation of the sympathetic activity and to a prevention of inappropriate stimulation of vasopressin secretion. This was associated with a reduction in symptoms and a lack of fluid retention, whereas control animals developed pleural infusions and ascites. Similar beneficial effects have been demonstrated in rats following myocardial infarction during a long-term therapy with captopril on hemodynamic parameters, heart size, and survival. Thus, early inhibition of the renin-angiotensin-aldosterone system in heart failure may be an attractive approach for treatment in patients with ventricular dysfunction even before symptoms develop.
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PMID:[ACE inhibition: mechanisms of cardioprotection in chronic experimental heart failure]. 183 Sep 9

Early chronic sympathectomy does not normalize blood pressure (BP) in genetically hypertensive rats of the Lyon strain (LH). The purpose of this study was to examine the role of the renin angiotensin system (RAS) and vasopressin in the residual hypertension exhibited by LH sympathectomized rats. Chronic sympathectomy was achieved by treating male LH and control normotensive LN rats with guanethidine sulfate between 1 and 13 weeks of age (60 mg/kg daily from day 7 after birth to day 25, 30 mg/kg daily from day 26 to day 70 and 30 mg/kg every other day from day 71 to day 90). At 14 weeks of age, catheters were inserted into the lower abdominal aorta and inferior vena cava via the left femoral artery and vein. After 2 days of recovery, BP was continuously recorded in the conscious freely moving animals during 3 consecutive 1-hour periods: before and after administration of either an angiotensin converting enzyme inhibitor (perindopril 2 mg/kg i.v.) or a selective vascular vasopressin antagonist [beta-mercapto- beta,beta-cyclopentamethylenepropionyl1, O-Me-Tyr2, Arg8-vasopressin, AVPX 10 micrograms/kg i.v.) and finally after conjoint administration of both drugs. At the end of each period, the efficacy of blockade was verified by the disappearance of pressor responses to respective agonists (angiotensin I 150 ng/kg i.v., Arg8-vasopressin 10 ng/kg i.v.). Chronic treatment with guanethidine resulted in the disappearance of pressor responses to tyramine (250 micrograms/kg i.v.) indicating complete functional denervation of the vessels. Under basal conditions, the 1-hour average value of mean BP (MBP) was higher in LH than in LN sympathectomized rats (134 +/- 3 vs 104 +/- 2 mmHg, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Role of renin-angiotensin system and vasopressin in the control of blood pressure in genetically hypertensive rats after sympathectomy]. 212 62

A decrease in cardiac output in patients with congestive heart failure due to dilated cardiomyopathy is compensated by stimulation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. The increase in plasma norepinephrine and depletion of norepinephrine in the myocardium as well as the disturbance of beta-adrenal and baroreceptor function reflect the limits of the sympathetic nervous stimulation. Together with augmented levels of angiotensin II and vasopressin, this stimulation leads to a significant increase in systemic vascular resistance. Sustained stimulation of at least one of these mechanisms can cause further impairment of the left ventricular function. The severity and prognosis of congestive heart failure due to dilated cardiomyopathy is expressed by the plasma norepinephrine concentration and by its myocardial depletion. Ultimately, activation of the compensatory mechanisms provides the basis for therapeutic approaches: 1. reduction of afterload and systemic vascular resistance and/or 2. diminution of the sympathetic nervous activity. For about the last ten years, ACE inhibitors have been used as pharmacological treatment in addition to positive inotropic and vasodilating substances. Captopril, one of the first orally applicable drugs, reduces left ventricular filling pressure, pulmonary capillary pressure, systemic vascular resistance and increases the cardiac output. Beside the hemodynamic improvement, a decrease in plasma norepinephrine and aldosterone can be observed. Vasodilators and alpha-blocking agents can also reduce afterload and systemic vascular resistance in patients with congestive heart failure due to dilated cardiomyopathy, and may lead to hemodynamic improvement. The main limitations of their long-term application are relatively short duration of action, reflex activation of the renin-angiotensin system due to vasodilation and induction of tolerance.
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PMID:[Sympathetic activity in patients with heart failure due to idiopathic dilated cardiomyopathy: effect of ACE inhibitors and other vasodilators]. 219 17

Stimulation of the renin angiotensin system, catecholamines and antidiuretic hormone causes prominent vasoconstriction in severe heart failure. Angiotensin converting enzyme inhibitors reverse these effects, and thus ameliorate cardiac function and reduce mortality in severe heart failure. Angiotensin II is an important regulator of renal function in diseases with renal hypoperfusion, and treatment with angiotensin converting enzyme inhibitors may cause a serious decrease in glomerular filtration and hyperkalemia. Asymptomatic heart failure, acute heart failure and acute myocardial infarction are areas where angiotensin converting enzyme inhibitors may prove beneficial in the future.
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PMID:[Treatment of heart failure with angiotensin converting enzyme inhibitors]. 221 71

Elevated peripheral vascular resistance, which characterizes hypertension and congestive heart failure (the latter regardless of absolute blood pressure level) is maintained to a large extent by the combined effects of three major neurohormonal pressor mechanisms: the renin-angiotensin system, the sympathoadrenal system, and arginine vasopressin. Blockade of one of these mechanisms may lead to compensatory stimulation of the others, thus offsetting in part the hemodynamic benefits of a specific intervention. Combination therapy, designed to attack all three systems (with use of an angiotensin converting enzyme inhibitor, a sympathetic blocker such as clonidine, and an antagonist of the vasopressor action of vasopressin), may help in the treatment of such cases. To illustrate this strategy, two experimental studies, one case of malignant hypertension, and one case of congestive heart failure are presented.
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PMID:Pressor systems in hypertension and congestive heart failure. Role of vasopressin. 222 58

1. A new isolated perfused preparation is described that allows a direct comparison to be made of the responses of the perfused arterial and retrogradely perfused venous circulations of the rat superior mesenteric vascular bed. 2. In experiments comparing the responses of the intact arterially perfused mesentery and small intestine to those of the same preparation following removal of the intestine and division of the circulations, the increases in perfusion pressure produced by arginine-vasopressin (30 pmol) and noradrenaline (1 nmol) were retained by the arterial circulation and those induced by angiotensin II (30 pmol) by the venous circulation. Endothelin-1 (30 pmol) constricted both portions of the vasculature but the prolonged nature of its response was associated with only the venous vessels. 3. In the simultaneously perfused arterial and venous preparation arginine vasopressin (3-100 pmol) was a selective constrictor of the arterial circulation and angiotensin II (3-100 pmol) of the venous circulation. In addition, noradrenaline (0.3-10 nmol), 5-hydroxytryptamine (0.3-10 nmol) and KCl (1-60 micromol) were more active as constrictors of the arterial than the venous vessels, and U46619 (10-300 pmol) a more active constrictor of the venous than the arterial vessels. Endothelin-1 (3-100 pmol) constricted both the arterial and venous portions of the vasculature but was significantly longer acting as a venoconstrictor than an arterioconstrictor. 4. Angiotensin I (300 pmol) caused constrictions of the venous circulation which were dependent upon the presence of angiotensin converting enzyme for captopril (10 microM) abolished constrictions caused by angiotensin I but not by angiotensin II. 5. In preparations preconstricted by U46619 (0.3-3 microM), acetylcholine (0.01-100 nmol), bradykinin (0.001-nmol), sodium nitroprusside (0.01-lOnmol) or isoprenaline (1-l00pmol) produced dose-related dilatations of both the arterial and the venous vasculatures, whereas adenosine diphosphate (ADP, 0.01-lOOnmol) caused dose-dependent dilatations of the arterial circulation but principally constrictions of the venous circulation. The dilatations caused by acetylcholine and bradykinin in both portions of the circulation, and by ADP in the arterial circulation, were endothelium-dependent as they were inhibited by gossypol (3 microM), whereas dilatations to sodium nitroprusside were not. 6. This preparation allows the responses of the arteries and veins of a single perfused mesenteric bed to be compared. In addition, with this preparation it is possible to demonstrate that veins, as well as arteries, show significant endothelium-dependent relaxations. It is concluded that the venous portion of the vasculature is significantly involved in the responses of the intact circulation.
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PMID:Simultaneous perfusion of rat isolated superior mesenteric arterial and venous beds: comparison of their vasoconstrictor and vasodilator responses to agonists. 232 5

New findings from this laboratory suggest that fragments of angiotensin derived from the amino (N-)terminus are biologically active end products of the renin-angiotensin system. In vitro and in vivo experiments revealed that the heptapeptide angiotensin-(1-7) [Ang-(1-7)] is a major endogenous product of the renin-angiotensin system cascade in the brains of rats and dogs. Additional studies with enzyme inhibitors showed that Ang-(1-7) is produced directly from angiotensin I by an enzyme other than the angiotensin converting enzyme. Immunocytochemical fibers within the hypothalamo-neurohypophyseal vasopressinergic system of the rat. Although Ang-(1-7) is as potent as angiotensin II (Ang II) in stimulating release of vasopressin from superperfused hypothalamo-neurohypophyseal explants, the heptapeptide has no dipsogenic or vasoconstrictor activity. In contrast, Ang-(1-7) mimics the effects of Ang II in augmenting the intrinsic discharge rate of neurons within the vagal-solitary complex and in causing monophasic depressor responses after microinjection into the medial region of the nucleus tractus solitarii. The evidence obtained in these experiments suggests novel mechanisms for the generation of angiotensin peptides in the brain. Additionally, the findings suggest that some of the biological actions ascribed to Ang II might be conveyed by the endogenous production of other angiotensin peptides that are generated by enzymatic pathways alternate to those described in the peripheral circulation.
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PMID:Pathways of angiotensin formation and function in the brain. 240 55


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