Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atrial natriuretic factor (ANP) is present in neuronal cells of the locus coeruleus and its vicinity in the pontine tegmentum and moderate amount of ANP is detectable in this area by radioimmunoassay. The ANP (both peripheral and brain-born) is known as a neuropeptide which may influence the body salt and water homeostasis and blood pressure by targeting both central and peripheral regulatory mechanisms. Whether this pontine ANP cell group is involved in any of these regulatory mechanisms, the effect of various types of hypertension and experimental alterations in the salt and water balance on ANP levels was measured by radioimmunoassay in the locus coeruleus of rats. Adrenalectomy, as well as aldosterone and dexamethasone treatments failed to alter ANP levels in the locus coeruleus. Reduced ANP levels were measured in spontaneously hypertensive (both young and adult) rats, and in diabetes insipidus (Brattleboro) rats with vasopressin replacement. In contrast to these situations, elevated ANP levels were found in rats with DOCA-salt or 1-kidney-1-clip hypertension. These data suggest a link between ANP levels in the locus coeruleus and fluid volume homeostasis. Whether this link is causal and connected with the major activity of locus coeruleus neurons (noradrenergic influence on brain regulatory activities) needs further informations.
 ...
PMID:Atrial natriuretic peptide in the locus coeruleus and its possible role in the regulation of arterial blood pressure, fluid and electrolyte homeostasis. 183 23

This study examined the contribution of the main pressor systems to the residual hypertension exhibited by genetically hypertensive (LH) rats of the Lyon strain after early chronic sympathectomy with guanethidine. Blood pressure (BP) was recorded in conscious LH and normotensive control (LN) rats, either intact or sympathectomized, during sequential blockade of the renin-angiotensin system, vasopressin receptors, the autonomic nervous system, and finally after maximal vasodilation with hydralazine. In sympathectomized rats 1) renin-angiotensin system blockade equally reduced BP in both strains, whether it was realized before (-20%) or after (-30%) vasopressin antagonism; 2) isolated vasopressin antagonism decreased BP in LH (-8%) but not in LN rats; 3) autonomic blockade and hydralazine induced additional decreases in BP that were similar in both strains; and 4) intermediate and final levels of BP remained always higher in LH than in LN rats. It is concluded that, after sympathectomy, BP is maintained primarily by the renin-angiotensin system. In sympathectomized LH rats, the maintenance of hypertension does not depend on hyperactivity of the main pressor systems but rather on an increase in the intrinsic vascular resistance that develops in the absence of the sympathetic innervation of the vessels.
 ...
PMID:Blood pressure maintenance in hypertensive sympathectomized rats. II. Renin-angiotensin system and vasopressin. 183 88

In the past several years great progress has been made in the understanding of the (patho) physiology of ANP. Because an inhibitor of ANP is not available for human use, there is still discussion about the physiological role of ANP. Nevertheless, from the studies described above the evidence is accumulating that ANP has a role in protecting against fluid overload and hypertension by means of inducing natriuresis, inhibition of the renin-angiotensin-aldosterone system and vasopressin and by vasodilation. The therapeutic potential of modulation of the ANP system seems promising, but must await further research.
 ...
PMID:Atrial natriuretic peptide. 183 64

In the first part of the text the main elements of renal physiology are mentioned as well as the role played by sodium-modulating hormones in the preservation of sodium and water homeostasis. A personal contribution concerns the release as well as the circadian rhythm of atrial natriuretic peptide (ANP) and of the digitalis-like substance (DLS). In the second part, the problem is dealt with from a pathophysiologic point of view, with reference made to the literature, and to our own data. In particular, the problem of essential hypertension with reduced levels of plasma renin activity (PRA) is thoroughly analyzed. As is well known, this kind of hypertension is characterized by normal plasma aldosterone levels associated with reduced kallikrein urinary excretion. The data we gathered not only confirmed these findings but also enabled us to point out other typical features of this particular kind of hypertension: normal values of vasopressin, elevation of ANP and DLS, hyperactivity of Na+/K+ cotransport. The introduction of a single variant in the sodium-modulating systems confirmed that the low PRA patient also behaves distinctively from a dynamic point of view. In fact, prostaglandin inhibition determines hypertension only in these patients, while both oral kallikrein administration and intravenous ANP administration were particularly effective because of a primitive deficit of the natriuretic paracrine systems paralleled by a compensatory increase of ANP. After identifying this group of hypertensive patients we intended to ascertain whether, even in the normal or high PRA patients, it was possible to identify a sub-group of subjects with altered sodium-modulation. The patients we examined were subdivided according to their hormonal and renal response to a saline load, and to angiotensin II, into "modulators" (with normal) and "nonmodulators" (with reduced sodium excretion capacity). An analysis of the hormonal characteristics of non-modulators identified an increased responsiveness of all sodium-modulation systems and not only of the renin-angiotensin-aldosterone system as pointed out by some other authors. The last part of the text is devoted to clinical and therapeutic problems. The behaviour of the daily blood pressure profile in patients with essential hypertension, and then the influence that sodium-modulating systems may have on pressure are discussed. The consequences of a progressive reduction in renal function on the circadian rhythm of arterial pressure are then assessed, and, at the same time, how renal impairment parallels the flattening of the daily pressure rate is observed.
 ...
PMID:The kidney and essential hypertension. 183 73

Studies were performed to characterize the regulation of central vasopressin (AVP) receptors in deoxycorticosterone acetate (DOCA)-NaCl-treated and control rats, and in DOCA-treated primary neuronal enriched cell cultures. Uninephrectomized rats were given NaCl to drink and implanted subcutaneously with a silastic implant containing 200 mg/kg DOCA. [3H]AVP binding to a diencephalic block of tissue was examined. Whereas DOCA-NaCl treatment did not affect the affinity of [3H]AVP binding, the total number of AVP receptors was increased between 3 and 14 days following DOCA-NaCl administration. No differences in the number of binding sites were present in the established (35-56 days after DOCA-NaCl administration) stages of hypertension. To determine whether the increase in [3H]AVP binding was a direct effect of DOCA on neurons or related to the hormonal, volume or other physiologic changes that DOCA-NaCl treatment causes in the whole animal, [3H]AVP binding was examined in neurons grown in culture that was treated with DOCA. Scatchard analysis demonstrated that DOCA treatment (compared to control) produced an increase in the number but no change in the affinity of the AVP binding sites in primary neuron-enriched cultures. Treatment of cultured neurons with other steroids (estrogen, corticosterone, or aldosterone), did not change the kinetics of [3H]AVP binding, suggesting that the effects of DOCA on the AVP receptor were specific for this steroid. These data indicate that, in comparison to control rats, DOCA-NaCl hypertensive rats, have an enhanced number of AVP receptors in the diencephalon, perhaps as a direct result of an interaction between DOCA and AVP receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Central vasopressin receptors are upregulated by deoxycorticosterone acetate. 183 96

In man, cardiac receptors exert a continuous restraint on sympathetic activity. Reflexes originating from the heart also restrain renin and vasopressin secretion, thereby being involved both in blood pressure and in blood volume homeostasis. We have shown that these reflexes are markedly depressed in subjects with left ventricular hypertrophy (LVH) due to hypertension and that this is also the case when, in normotensive subjects, LVH is caused by prolonged physical training. In both instances, the cardiogenic reflex impairment is associated with derangement of blood pressure homeostasis. Either spontaneous regression of LVH by physical training cessation or antihypertensive treatment is followed by a marked improvement of the cardiogenic reflex. Thus, LVH also affects the 'afferent' function of the heart. 'Physiological', as well as pathological, hypertrophy has a similar adverse effect. This effect is reversible, however, and the reflex function can be restored by regression of hypertrophy.
 ...
PMID:Left ventricular hypertrophy and the 'cardiogenic reflex' in man. 183 67

The aim of the present study was to compare effects of intravenous infusion of vasopressin AVP and V1 receptors blockade on blood pressure and heart rate in normotensive (WKY) and spontaneously hypertensive (SHR) rats. A 20 min vasopressin infusion (1.2 ng/kg/min) elicited significantly greater increase in mean blood pressure (MP) in SHR than in WKY. Heart rate was significantly reduced in SHR while nonsignificantly in WKY. A 20 min dEt2 AVP (V1 antagonist) infusion (0.5 microgram/kg/min) elicited significant decrease in MP and increase in heart rate (HR) in SHR, but produced no effect in WKY. The data indicate that SHR are more susceptible to pressor and hypotensive effects of sustained elevation of AVP and AVP antagonist. The results support the hypothesis that AVP may contribute to pathogenesis of hypertension.
 ...
PMID:Effects of vasopressin and V1 receptors blockade on blood pressure and heart rate in spontaneously hypertensive rats. 184 Mar 31

Cardiac atria and, under certain circumstances, also ventricles produce and secrete into the circulation atrial natriuretic factor (ANF). ANF exerts a significantly natriuretic, myorelaxant, renin-, aldosterone-, and vasopressin-inhibiting effect and acts as a neurotransmitter in the central and autonomous nervous systems. Expansion of the extracellular volume stimulates secretion of ANF which consequently contributes to renal excretion of sodium and water. The renal effect of ANF is apparently modulated by interaction with other mechanisms. ANF concentration in peripheral blood is the product of its secretion by the heart and degradation by peripheral tissues. In ascitic liver cirrhosis, the decreased splanchnic bed uptake may contribute to the increase in plasma ANF concentration observed. Insufficient production or secretion of ANF are not likely to be the primary etiopathogenic mechanism of arterial hypertension. In the course of development of hypertension, ANF is mobilized as a corrective-adaptive mechanism in an effort to normalize the raised BP, extracellular volume or circulating pressor agents. Through its production of ANF, the heart possess an important endocrine function markedly affecting pressure, electrolyte and volume homeostasis.
 ...
PMID:Role of the heart as an endocrine organ. 184 37

In previous studies we found that vasopressin stimulation of both cyclic AMP (cAMP) formation in cortical collecting tubules (CCT) and sodium reabsorption in isolated perfused kidneys was markedly exaggerated in rats with mineralocorticoid hypertension. In the present study, we tested the response (cAMP accumulation) of cortical and outer medullary collecting tubules (OMCT) to vasopressin in two rat models that are resistant to deoxycorticosterone acetate (DOCA)-induced hypertension, the Wistar-Furth strain and NaCl-deficient rats. The blood pressure of normal outbred Wistar rats rose to hypertensive levels (systolic pressure more than 165 mm Hg) during a 5-week treatment with DOCA (10 mg/week) and 1% saline to drink. Significant hypertrophy of the heart and kidneys was also observed. Vasopressin (10(-8) M)-induced cAMP formation was enhanced 3.4-fold in the CCT (OMCT unchanged) of hypertensive rats compared with normotensive controls. Significant hypertrophy (as indexed by tubule diameter) of the CCT but not the OMCT was also observed in DOCA-salt hypertensive rats. Restriction of dietary NaCl (0.13% in chow, tap water to drink) completely prevented DOCA-induced hypertension, organ and CCT hypertrophy, and enhancement of vasopressin-stimulated cAMP formation in the CCT. In Wistar-Furth rats, DOCA-salt treatment did not alter blood pressure or cause significant organ hypertrophy. However, DOCA-salt treatment enhanced vasopressin-stimulated cAMP formation by 4.1-fold in CCT of Wistar-Furth rats, with significant tubular hypertrophy in the CCT but not the OMCT. We conclude that DOCA-induced hypertension and changes in CCT function are dependent on excess dietary NaCl.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Jan
PMID:Vasopressin response in collecting ducts of rats resistant to mineralocorticoid hypertension. 184 20

An endogenous ouabain-like sodium pump inhibitor was demonstrated originally in serum or plasma of acutely extracellular fluid volume (ECFV) expanded animals and humans. Since then numerous studies have confirmed the presence of ouabain-like factor(s) (OLF) in blood, urine, cerebrospinal fluid, and various tissues including the heart and hypothalamus. Some of these OLFs represent well-known endogenous compounds, eg, free unsaturated fatty acids, which in vitro exhibit inhibition of transepithelial sodium transport, direct inhibition of the Na-K-ATPase enzyme, displacement of 3H-ouabain from its membrane receptor, and crossreaction with a digoxin antibody. Small molecular weight (MW) OLFs of yet unknown peptidic or nonpeptidic nature, which may be of hypothalamic origin, were also detected in various animal models of hypertension and in hypertensive patients. They may play a pathophysiological role especially in salt- and volume-dependent forms of hypertension. Our results show that OLFs increase basal and vasopressin-stimulated intracellular Ca2+ release in rat vascular smooth muscle cells in culture and in human platelets similar to the newly discovered endothelin. In addition, a natriuretic factor (natriuretic hormone) was detected by bioassay in plasma and urine, whose activity changes in parallel with sodium intake. We found that this natriuretic factor is associated with small peptides with a MW of less than 1,000. It is, however, unlikely that the two biological properties, ie, the ouabain-like and natriuretic activities, reside in a single compound. A number of circulating OLFs is certainly not identical with a humoral natriuretic factor. Nevertheless, there is increasing evidence for multiple interactions between OLF and the atrial natriuretic peptide (ANP).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Endogenous natriuretic and ouabain-like factors. Their roles in body fluid volume and blood pressure regulation. 184 64


<< Previous 1 2 3 4 5 6 7 8 9 10