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)

Rats with unilateral nephrectomy were offered 1% sodium chloride as drinking fluid and were injected with desoxycorticosterone trimethylacetate (D.O.C.-T.M.A.) at weekly intervals. During the fourth to seventh week after the start of the experiment, malignant hypertension developed in most of the animals: body weight fell, reflecting volume depletion; serum osmolality and serum sodium and urea concentrations increased; in the kidneys malignant nephrosclerosis occurred. In such animals, plasma concentrations of arginine-vasopressin were increased ten-fold in comparison with control animals; intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood-pressure (B.P.) to normal or subnormal levels, while the injection of an angiotensin-I or angiotensin-II antibody did not affect B.P. In control animals none of the antibodies had an effect on B.P. It is concluded that in the pathogenesis of malignant D.O.C. hypertension vasopressin plays a role similar to that of renin-angiotensin in malignant renal hypertension.
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PMID:Is vasopressin involved in the pathogenesis of malignant desoxycorticosterone hypertension in rats? 5 84

Male Sprague-Dawley rats with unilateral renal artery stenosis and a contralateral untouched kidney develop a malignant hypertension (MH) which is characterized by high blood pressures, sodium and water depletion, and subsequent activation of the renin-angiotensin system. In the present studies we found plasma arginine vasopressin (AVP) concentrations-3-fold higher than those in rats with benign renal hypertension, and 4- to 5-fold higher than those in normotensive control rats. Analysis of individual values showed considerable scatter; about 50% of the values fell in the range of benign hypertensive or control rats. When a specific AVP antiserum was injected, iv, into eight conscious unrestrained MH rats, BP transiently fell toward control values in four; in one, BP fell by only 10 mm Hg, and three other MH rats showed no response. In the same rats, injection of a specific angiotensin II antiserum always induced a transient fall in BP. On the basis of these and previously reported observations, we conclude that, subsequent to sodium and water loss and activation of the renin-angiotensin system, vasopressin release is stimulated in a significant number of MH rats and that, in these rats, vasopressin may cause significant systemic vasoconstriction. Thereby vasopressin may contribute to the development of malignant renal hypertension in rats.
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PMID:Plasma vasopressin concentrations and effects of vasopressin antiserum on blood pressure in rats with malignant two-kidney Goldblatt hypertension. 61 98

1. Blood pressure is controlled by both integrated neurogenic and humoral vasoactive mechanisms. 2. Both vasopressor (angiotensin and vasopressin) and vasodepressor (bradykinin) hormonal peptides have been identified. 3. In acute experimental renal hypertension in the rat plasma renin, angiotensin and vasopressin have all been shown to be elevated. 4. Associated with this increase in vasopressor hormonal peptides, urinary kallikrein excretion has been demonstrated to be reduced during the development of renal hypertension. 5. The level of blood pressure achieved in experimental renal hypertension is probably a summation of these vasoactive peptides as well as other factors.
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PMID:Vasoactive peptides in experimental renal hypertension. 73 55

1. The role of arginine-vasopressin in the pathogenesis of malignant deoxycorticosterone (DOC) hypertension of rats was investigated. 2. In rats with malignant DOC hypertension plasma arginine-vasopressin concentrations increased more than tenfold subsequent to volume depletion and a rise of serum osmolality. 3. The injection of a specific antibody serum for arginine-vasopressin caused a marked fall of blood pressure in rats with malignant DOC hypertension, whereas the injection of angiotensin II antiserum did not affect blood pressure. 4. In rats exhibiting a benign course of DOC hypertension plasma concentrations of arginine-vasopressin were increased threefold in comparison with normotensive control rats; the injection of an arginine-vasopressin antiserum induced a significant but small fall of blood pressure. 5. It is concluded that in the pathogenesis of malignant DOC hypertension arginine-vasopressin might play the role that the renin-angiotensin system plays in the pathogenesis of malignant renal hypertension.
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PMID:Vasopressin and malignant deoxycorticosterone hypertension in rats. 107 63

Plasma osmolality is maintained within very narrow limits by the control of water intake via thirst and water output via secretion of vasopressin. Osmoreceptors are situated in the brain, but on the blood side of the blood-brain barrier in a circumventricular organ. These regions are stimulated by an increase in plasma osmolality and form the most important input to cause thirst and drinking. Cardiopulmonary and arterial baroreceptors sensitive to blood volume and blood pressure also can be important, so hypovolaemic events such as haemorrhage can stimulate thirst. Both raised plasma osmolality and reduced blood volume contribute to thirst and vasopressin secretion following water deprivation. The importance of the nucleus medianus in the neural circuitary involved in integrating thirst should be emphasized. Mechanisms which stop drinking are different from those which initiate it, and oropharyngeal metering of the volume of fluid consumed provides the important input. There are a number of situations in humans where thirst thresholds and sensitivities are altered. The elderly have higher thirst thresholds and this can cause symptoms of dehydration. Increased drinking is seen in congestive heart failure, renal hypertension and certain cerebral lesions. Thirst thresholds are set at lower levels in pregnancy and in the luteal phase of the menstrual cycle and may contribute to fluid retention in these situations.
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PMID:The importance of thirst in maintenance of fluid balance. 269 42

Studies in sodium-dependent models of hypertension have shown that arginine-vasopressin (AVP) plays an important role in the maintenance of blood pressure, predominantly through its vasoconstrictor action. In addition to AVP, the sympathetic nervous system (SNS) also acts to maintain blood pressure in high sodium one-kidney, figure-8 renal wrap hypertension. The purpose of this study was to determine if chronic blockade of vascular AVP (V1) receptors affected the induction of high sodium renal hypertension and the contribution of the SNS to the maintenance of blood pressure. Rats receiving chronic s.c. administration of a V1 antagonist, d(CH2)5Tyr(Me)AVP, or vehicle were subjected to renal wrapping or sham surgery, V1 receptor blockade was confirmed periodically by an 80 +/- 3% reduction of the pressor response to a bolus injection of 10 mU/kg of AVP. d(CH2)5Tyr(Me)AVP did not affect the development of hypertension or the associated changes in plasma sodium, potassium, osmolality and hematocrit. In renal-wrapped rats, ganglionic blockade caused a greater fall in blood pressure in animals treated with d(CH2)5Tyr(Me)AVP than in vehicle-treated animals. However, this apparent increase in SNS function was not responsible for the hypertension in d(CH2)5Tyr(Me)AVP-treated, renal-wrapped rats, inasmuch as ganglionic blockade lowered blood pressure a similar amount in normotensive d(CH2)5Tyr(Me)AVP-treated, sham-operated rats and blood pressure remained elevated after combined blockade of the SNS, AVP and the renin-angiotensin systems. These results indicated that chronic blockade of V1 receptors did not alter the induction of high sodium renal hypertension and the mechanism of the elevated blood pressure was not through an activation of the SNS or other neurohumoral mechanisms.
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PMID:Development of high sodium renal hypertension during chronic blockade of the vascular effects of vasopressin. 287 11

We investigated the plasma concentration of [Arg8]-vasopressin (AVP), the density of AVP-binding sites on membranes from the mesenteric vascular bed, and the pressor response to AVP of the perfused mesenteric vasculature in vitro from one-kidney, one-clip (1K, 1C) and two-kidney, one-clip (2K, 1C) Goldblatt hypertensive rats. The plasma concentration of AVP was increased in 1K, 1C hypertensive rats. The density of AVP-binding sites was similar in sham-operated normotensive, in 2K, 1C hypertensive, and in uninephrectomized rats but was significantly decreased in 1K, 1C hypertensive rats (P less than 0.05). The binding affinity of AVP was similar in all experimental groups. Vasoconstrictor response to AVP was increased in 2K, 1C hypertensive rats (27% higher than sham-operated normotensive rats, P less than 0.05). Responses in 1K, 1C hypertensive rats were similar to those of uninephrectomized rats. Our results indicate that together with an increased concentration of AVP in plasma the number of vascular AVP-binding sites is decreased in 1K, 1C hypertensive rats, whereas both are unaltered in 2K, 1C hypertensive rats. Vascular AVP receptors appear to be regulated inversely to plasma AVP concentrations. Pressor responsiveness to AVP is normal in 1K, 1C hypertensive rats and exaggerated in 2K, 1C hypertensive rats. Increased vascular responsiveness to AVP may occur independently of the regulation of AVP receptors and may contribute to elevation of blood pressure in renal hypertension in the rat.
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PMID:Vascular vasopressin receptors in renal hypertensive rats. 297 16

There are several mechanisms by which the central nervous system participates in the neural and humoral alterations associated with various forms of experimental hypertension. Structures in forebrain with multiple integrative roles in neuroendocrine control of the circulation are involved. Tissue surrounding the anteroventral region of the third cerebral ventricle (AV3V region) is involved physiologically in thirst, sodium homeostasis, osmoreception, secretion of vasopressin and natriuretic factor and sympathetic discharge to blood vessels. Destruction of this tissue prevents or reverses many forms of hypertension. In genetically based spontaneous hypertension, limbic structures such as the central nucleus of the amygdala rather than the AV3V region are the necessary neuroanatomic substrate. Recent evidence suggests that a circumventricular organ in brain stem, the area postrema, is also involved in the mediation of several forms of experimental hypertension. In renin- and nonrenin-dependent forms of renal hypertension, two major factors activate central mechanisms. First, direct central actions of angiotensin, acting through receptors in the subfornical organ and organum vasculosum of the lamina terminalis, increase sympathetic discharge and secretion of vasopressin through mechanisms integrated at the level of the AV3V region. Second, sensory systems originating in the kidney can activate increased sympathetic discharge through complex projection pathways involving forebrain systems. Mineralocorticoid hypertension appears to involve enhanced secretion of vasopressin and central vasopressinergic mechanisms also dependent on the AV3V region. Reciprocal connections between key central areas involved in control of arterial pressure provide the neuroanatomical basis for central nervous system participation in hypertension.
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PMID:Central nervous system and mechanisms of hypertension. 306 Feb 99

The anteroventral third ventricle (AV3V) region plays an important role in fluid and electrolyte balance and cardiovascular control in the rat; however, experiments in other species have raised questions about the universality of findings in the rat. The effects of discrete lesions placed within the AV3V area on hydromineral balance, the pressor response to angiotensin II given intravenously, and the initiation of a renin-dependent model of hypertension were examined in the dog. A transpharyngeal approach to the optic chiasm enabled us to destroy only the anterior aspects of the AV3V region (aAV3V group) or to include the entire nucleus medianus (NM) as well (aAV3V + NM group). Lesions of the aAV3V caused polydipsia and transient hypernatremia and hyperosmolality. In contrast, adipsia and a sustained increase in plasma sodium levels and osmolality were observed in dogs with lesions of the aAV3V plus the entire NM. Neither lesion altered baseline arterial pressure, heart rate, plasma levels of catecholamines and vasopressin, or total plasma protein levels. Only in aAV3V + NM lesioned dogs was there a tendency for plasma angiotensin II immunoreactivity to be elevated above control values at 2 and 4 days after operation. Neither lesion attenuated the pressor response to intravenous angiotension II or the initiation of renal hypertension induced by aortic coarctation. As observed in other species, structures within the AV3V region participate in hydromineral balance in the dog; however, in the dog portions of the NM dorsal to the AV3V region are essential for the mediation of drinking behavior.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The anteroventral third ventricle region. Participation in the regulation of blood pressure in conscious dogs. 399 35

This study assessed the contributions of the sympathetic nervous system and arginine vasopressin to the onset of one-kidney, one-wrap (1K1W) renal hypertension in rats fed a high sodium diet. Two weeks before renal wrap or sham wrap, rats were given a high sodium diet and water ad libitum. At 3 days postwrap, resting mean arterial pressure (MAP) was significantly greater in renal-wrapped rats. The contributions of the sympathetic nervous system and vasopressin to blood pressure (BP) were assessed by ganglionic blockade and vascular vasopressin receptor antagonism, respectively. Depressor responses to ganglionic blockade were significantly greater in the normotensive rats as compared to the hypertensive rats. Administration of vasopressin antagonist caused a significant fall in pressure only in wrapped rats. In addition, enhanced pressor responses to bolus injections of vasopressin were observed in hypertensive rats. These results indicate that during this phase of the hypertension there is an activation of the vasopressin pressor system without an increase in neurogenic function. Equalization of arterial pressure occurred only when both systems were blocked, regardless of the order of blockade, which indicated that the sympathetic nervous system and vasopressin interact to maintain the hypertension. Comparison of depressor responses to the blocking agents revealed that the interaction is compensatory in nature since the contributions of the sympathetic nervous system and vasopressin to the maintenance of arterial pressure were greater when the other system was blocked.
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PMID:Contribution of vasopressin and the sympathetic nervous system in the early phase of high sodium one-kidney renal hypertension. 624 Apr 42


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