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

The concept of depressor reflexes originating in the heart was introduced by von Bezold in 1867 and was later revived by Jarisch. The Bezold-Jarisch reflex originates in cardiac sensory receptors with nonmyelinated vagal afferent pathways. The left ventricle, particularly the inferoposterior wall, is a principal location for these sensory receptors. Stimulation of these inhibitory cardiac receptors by stretch, chemical substances or drugs increases parasympathetic activity and inhibits sympathetic activity. These effects promote reflex bradycardia, vasodilation and hypotension (Bezold-Jarisch reflex) and also modulate renin release and vasopressin secretion. Conversely, decreases in the activity of these inhibitory sensory receptors reflexly increase sympathetic activity, vascular resistance, plasma renin activity and vasopressin. Long regarded as pharmacologic curiosities, it is now clear that reflexes originating in these inhibitory cardiac sensory receptors are important to the pathophysiology of many cardiovascular disorders. This paper reviews the role of inhibitory cardiac sensory receptors in several clinical states including 1) bradycardia, hypotension and gastrointestinal disorders with inferoposterior myocardial ischemia and infarction, 2) bradycardia and hypotension during coronary arteriography, 3) exertional syncope in aortic stenosis, 4) vasovagal syncope, 5) neurohumoral excitation in chronic heart failure, and 6) the therapeutic effects of digitalis.
J Am Coll Cardiol 1983 Jan
PMID:The Bezold-Jarisch reflex revisited: clinical implications of inhibitory reflexes originating in the heart. 682 48

The reasons for the disturbances of electrolyte and water balance in cardiac failure are not yet clarified. The decrease of cardiac output in cardiac insufficiency causes humoral regulatory mechanisms such as increased activity of the renin angiotensin-aldosterone system and increased secretion of antidiuretic hormone. These mechanisms in turn lead to an enhancement of renal sodium and water reabsorption. The humoral disturbances can be interpreted as ineffective regulatory mechanisms for hemodynamic changes in cardiac insufficiency; in fact, the humoral disturbances increase cardiac failure. In addition, an increased sodium content of the arteries may contribute to the hemodynamic changes in cardiac insufficiency.
Basic Res Cardiol
PMID:Electrolyte and water balance in cardiac insufficiency. Recent clinical and experimental data. 699 67

The influence of captopril on pressor responses to exogenously administered vasopressor substances was investigated in normal subjects. Norepinephrine (0.05, 0.1 and 0.2 micrograms/kg . min -1; n = 5), angiotensin II (5, 10 and 20 ng/kg . min -1; n = 5) and vasopressin (2 mU/kg . min -1; n = 5) were infused each for 10 minutes; each infusion was repeated twice. Captopril (50 mg orally) significantly attenuated the pressor response to norepinephrine (0.1 [p less than 0.05], 0.2 [p less than 0.01] micrograms/kg . min -1; n = 7) and to vasopressin (p less than 0.01, n = 5), but not to angiotensin II; these responses were reproducible. Attenuation of the pressor responses to norepinephrine did not occur when a subpressor dose of angiotensin II (ng/kg . min-1) was infused in addition to captopril (n = 5). Infusion of a subpressor dose of bradykinin (0.1 ng/kg . min-1) had no influence on the pressor responses to norepinephrine (n = 5). In the five subjects treated with indomethacin (225 mg/54 hours) captopril still attenuated the pressor responses to norepinephrine. These results suggest that the attenuation by captopril of the pressor responses to norepinephrine and vasopressin might have been due to reduction of endogenous angiotensin II.
Am J Cardiol 1982 Apr 21
PMID:Captopril attenuates pressor responses to norepinephrine and vasopressin through depletion of endogenous angiotensin II. 704 92

Vasovagal syncope is associated with an abnormal reflex and the physiopathological mechanisms of the phenomenon overall are only partially known. Experimental and clinical studies suggest that the main factor which triggers the syncope is the brusque interruption of the alpha-adrenergic tone with marked, sudden peripheral vasodilation. Although documented, vagal hypertony, with consequent bradycardia and asystolia, is only occasional and is almost always a secondary phenomenon. The most commonly suggested cause of vasovagal syncope is a Bezold-Jarish reflex starting from the cardiac receptors in the walls of the ventricle, mediated by the paradoxical activation of afferent vagal fibres. However, recent studies are suggesting that there may be other pathogenetic mechanisms such as the paradoxical activation of the venous-atrial baroceptors and other "extracardiac" vascular receptors. The neuro-endocrine aspect of the vasovagal reaction is very complex and in spite of the many studies carried out on the catecholamine, renal-angiotensive system, arginine-vasopressin, and b-endorphine trends, there are still many points awaiting clarification. The response of the autonomous nervous system linked to age also require further research.
G Ital Cardiol 1995 Jul
PMID:[Physiopathology of vasovagal syncope: review of the most endorsed theories and recent findings]. 755 40

Heart failure is a pathophysiological state resulting from disturbed cardiac function. It is based on complex molecular processes, many of which are not fully understood. During heart failure adaptive mechanisms, that reinstall altered cardiac function, are activated. The main mechanisms are: a) Alteration of the structure and composition of myocytes by myocardial hypertrophy, reexpression of fetal and neo-natal proteins and the expression of certain proto-oncogenes; b) Activation of the neuroendocrinal system, specifically the sympathetic nervous system, renin-angiotensin-aldosterone system and vasopressin release; c) Activation of autocrine and paracrine systems. However, when these systems are activated beyond a certain limit they contribute to heart failure aggravation. This can also be promoted by alteration of the calcium metabolism inherent in heart failure. The synthesis of the counterregulator atrial natriuretic factor is also increased.
Rev Port Cardiol 1994 Nov
PMID:[Molecular pathobiology in heart failure]. 784 57

Rilmenidine binds to alpha 2-adrenoceptors and imidazoline receptors in the central nervous system and the kidney. To test the hypothesis that rilmenidine would increase sodium excretion, renal function was studied in rats with innervated and denervated kidneys to distinguish between indirect (via renal sympathetic nerves) and direct effects of rilmenidine on the kidney. Standard clearance techniques were used in Wistar rats anesthetized with thiobutabarbital to measure renal function during 80 minutes of infusion of 0.9% NaCl or rilmenidine (20 or 50 micrograms.kg-1.min-1 intravenously). Snares on abdominal arteries were used to offset hypotension induced by rilmenidine. Heart rate decreased by 80-120 beats/min with either dose of rilmenidine. At 20 micrograms.kg-1.min-1, rilmenidine increased total and fractional excretion of sodium and clearance of osmoles while decreasing free water clearance from innervated kidneys. There were no changes in these variables in chronically denervated kidneys. Direct recording of renal sympathetic nerve activity showed a progressive, marked decrease in nerve activity during the low-dose infusion of rilmenidine. At 50 micrograms.kg-1.min-1, rilmenidine produced a differential effect on the clearance of osmoles by innervated and denervated kidneys but both kidneys had an increase in free water clearance. The data indicate that rilmenidine increases sodium excretion indirectly in anesthetized rats by decreasing renal sympathetic nerve activity. At doses and infusion periods used in these studies, there was no evidence for a direct effect of rilmenidine on sodium excretion. The increase in free water clearance seen with the high dose of rilmenidine suggests that the inhibitory effect of alpha 2-adrenoceptor activation on vasopressin is involved at this dose.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1994 Dec 22
PMID:Natriuretic effect of rilmenidine in anesthetized rats. 799 80

Heart failure is a syndrome characterized by the activation of neurohumoral mechanisms (sympathoadrenergic, renin-angiotensin, vasopressin) which cause peripheral vasoconstriction, sodium retention and myocardial hypertrophy. In acute myocardial disfunction these systems can play a critical role in patient survival, however, they can directly worsen myocardial function and patient prognosis on a long-term basis. Other neurohumoral systems activated in heart failure (atrial natriuretic factor, prostaglandins, dopamine) tend to counterbalance the vasoconstrictive, sodium retentive mechanisms. Though their secretion is increased in heart failure, it is however not sufficient, and peripheral vasoconstriction and sodium retention prevail. Moreover the role of local factors, such as tissue renin-angiotensin system, EDRF and endothelin secretion has been recently pointed out. Neurohumoral activation is directly related to the severity of the clinical and hemodynamic impairment and prognosis of the patient with heart failure. A thorough evaluation of the neurohumoral mechanisms is therefore of paramount importance for the assessment of patients with heart failure. Neurohumoral activation can be roughly assessed using some simple laboratory measurements: plasma sodium concentration, for example, is inversely related to the degree of activation of many neurohormones such as norepinephrine, angiotensin II, vasopressin and atrial natriuretic factor. The method most commonly used to assess neurohumoral activity relies on the direct measurement of the plasma concentrations. It must be noted, however, that plasma levels are critically dependent on many factors besides hormone secretion and metabolism. For example, 3-4 days on a low sodium diet or standing for at least 2 hours can increase plasma renin activity in a normal subject from 1.5 to 5-10 pg/ml/hr. Plasma concentrations of neurohormones are related to the factors controlling their secretion: for example, "normal" values of plasma renin activity in presence of fluid retention and edema are to be judged as excessively elevated. Autonomic nervous system activity can also be assessed studying reflexes in which this system is involved (orthostasis, cold pressor test, phenylephrine test...). Another method consists in the study of the spontaneous variability of some parameters controlled by this system, such as heart rate and blood pressure. The most reliable method is based on the power spectral analysis of heart rate variability. With this last method, a low frequency component depending mainly on sympathetic activity and an high frequency component depending on vagal activity can be identified in heart rate variability. Thus, complex phenomena such as sympatho-vagal balance can be easily studied through simple noninvasive tools.
G Ital Cardiol 1993 Feb
PMID:[Neurohormonal assessment in heart failure: from the sophisticated laboratory to practical indications]. 809 6

The purpose of this study was to investigate whether neurohumoral activation occurs in asymptomatic patients with acute myocardial infarction (AMI) and without clinical signs of heart failure. During the early phase of AMI (mean 8 days), the neurohumoral profiles of 60 patients (mean age 59 range 37 to 70) were examined. Blood levels of the following humoral parameters were measured: atrial natriuretic peptide (ANP), plasma renin activity, aldosterone and vasopressin. All patients underwent cardiac catheterization during hospitalization. Baseline hemodynamic characteristics identified left ventricular dysfunction (ejection fraction < or = 45% and/or left ventricular end-diastolic pressure > or = 15 mmHg) in 32 patients; the remaining 28 patients had normal hemodynamic parameters. In patients with AMI, plasma ANP levels differed significantly from control subjects (111 +/- 74 pg/ml vs. 53 +/- 18 pg/ml; P < 0.001). In patients with AMI and mild left ventricular dysfunction ANP levels were significantly increased when compared to patients with AMI and normal left ventricular function (129 +/- 73 pg/ml vs. 82 +/- 69 pg/ml; P < 0.001). The hemodynamic data showed a significant correlation with ANP only in patients with AMI and left ventricular dysfunction (EF% r = 0.42; LVEDP r = 0.44; P < 0.001). These data show that in patients with myocardial infarction and without heart failure, the atrial natriuretic peptide is the only neurohumoral system activated out of all neurohumoral systems tested in this population and its circulating levels are strictly related to the degree of left ventricular dysfunction.
Int J Cardiol 1993 Dec 15
PMID:Selective activation of atrial natriuretic peptide in patients with myocardial infarction and mild left ventricular dysfunction. 811 15

In healthy humans, the increase in arterial blood pressure seen in patients with autonomic dysfunction in response to exogenous vasopressin (AVP) is abolished. We tested the hypothesis that redistribution of blood from the intra- to the extrathoracic vascular compartment might contribute to this buffer response. Regional distribution of 99mTc labeled autologous red cells was assessed in healthy supine volunteers (n = 7) during arginine-vasopressin administration (1 ng.kg-1 bolus i.v. followed by a 14-min infusion of 3 ng.kg-1 x min-1), along with arterial and central venous pressures, and heart rate. Exogenous vasopressin increased plasma vasopressin concentration from 4.0 +/- 1.4 SEM to 91 pg.ml-1 +/- 12. Thoracic counts increased slightly but significantly by 2.2% +/- 0.9, while global abdominal counts remained unchanged. Most surprisingly, counts in the liver markedly increased (+8.1% +/- 1.8, p = 0.02), but significantly decreased in the spleen (-3.1% +/- 1.4). Intestinal (-2.5% +/- 2.4) and limb counts did not change significantly. Consistent with the increase in thoracic counts central venous pressure increased from 3.6 mmHg +/- 1 to 4.7 +/- 1 (p = 0.02), while arterial pressure and heart rate did not change. All changes reversed towards baseline when vasopressin administration ceased. Thus, in humans with an intact autonomic system, vasopressin, at concentrations observed during hypotension, increases liver and, albeit to a small extent, also thoracic blood volume, but decreases splenic blood content. These results: 1) are incompatible with the hypothesis that AVP induces a shift of blood from intra- to extrathoracic capacitance vessels, and 2) show that AVP increases rather than decreases central blood volume.
Basic Res Cardiol
PMID:Effects of arginine-vasopressin on regional blood volume distribution in supine humans. 821 79

The powerful local metabolic regulation adjusting coronary blood flow to myocardial oxygen consumption under normal conditions is beyond doubt. However, despite substantial experimental efforts the responsible mediators are still largely unknown. Adenosine, a purported mediator of local metabolic control of coronary blood flow, is probably only involved in transient flow adaptations, but not in steady-state coronary autoregulation. Even below the autoregulatory range a substantial vasodilator reserve persists. Recruitment of such vasodilator reserve results in improved regional myocardial blood flow and attenuated regional ischemic dysfunction. beta-adrenergic coronary dilation is of minor functional importance. alpha-adrenergic coronary constriction acts to attenuate increases in coronary blood flow during sympathetic activation under normal conditions, such that myocardial oxygen extraction increases to match the increased oxygen consumption. alpha-adrenergic coronary constriction remains operative in ischemic myocardium, thus precipitating or contributing to acute myocardial ischemia during sympathetic activation and exercise in experimental animals as well as in patients with stable angina. The vagal transmitter acetylcholine--upon exogenous intracoronary infusion--induces critical constriction of epicardial coronary arteries with endothelial dysfunction and atherosclerosis. However, a vagal initiation of coronary spasm or myocardial ischemia has not been documented so far. Similarly, peptide hormones/transmitters such as NPY, vasopressin, and angiotensin can induce myocardial ischemia upon exogenous administration. Their pathophysiological role in myocardial ischemia and reperfusion, however, remains to be established.
Basic Res Cardiol 1993
PMID:Local and neurohumoral control of coronary blood flow. 839 71


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