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)

Previous studies have implicated a functionally defined area of the forebrain, the anteroventral third ventricle (AV3V) region as being involved in the regulation of blood pressure and required for the expression of neurogenic hypertension. The present study re-examined the effect of AV3V lesion on hypertension caused by the destruction of the nucleus tractus solitarius (NTS), focussing on whether ablation of the AV3V region altered either the sympathoadrenal or vasopressin (VP) components of NTS hypertension. Bilateral electrolytic lesions of the NTS elicited acute severe hypertension in conscious, freely moving rats whether or not the animals had received AV3V or Sham lesions 14 days previously. Mean arterial pressure (MAP) measured 45 min following NTS lesion was 157 +/- 6 mm Hg in AV3V + NTS lesioned rats and 161 +/- 7 mm Hg in SHAM + NTS lesioned rats. Plasma VP levels were similarly elevated in the two groups of NTS lesioned animals, and the contribution of VP to the hypertensive response (as assessed by the decrease in arterial pressure in response to a VP pressor antagonist) was the same in both groups. In contrast, NTS lesion appeared to produce a lesser degree of sympathetic nervous system activation in AV3V lesioned rats, as evidenced by a substantially smaller increase in plasma norepinephrine (NE) levels. These results demonstrate that AV3V lesions do not attenuate or prevent NTS hypertension. However, AV3V lesions do appear to attenuate the sympathoadrenal activation caused by NTS lesions.
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PMID:Lesions of the AV3V region attenuate sympathetic activation but not the hypertension elicited by destruction of the nucleus tractus solitarius. 335 92

The purpose of this study was to examine, using pentobarbital-anesthetized rats, whether vasopressin contributes to hypertension caused by denervation of baroreceptors, in comparison to the contribution of vasopressin to hypertension caused by nucleus tractus solitarius (NTS) lesions. Bilateral baroreceptor denervation caused acute hypertension which was inhibited by intravenous injection of an antagonist of the vasoconstrictor action of vasopressin. Lesions of the NTS also produced an increased in blood pressure which was reduced by the vasopressin antagonist. The magnitude of the antagonist-induced hypotension was significantly greater in NTS hypertension than that in baroreceptor denervation hypertension. It is concluded, that in rats, vasopressin contributes to the neurogenic hypertension caused by baroreceptor denervation and NTS lesions. Thus, it appears that interruption of baroreceptor afferents at the NTS level is responsible for the vasopressin-mediated hypertension caused by NTS lesions but that it is not the only factor involved.
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PMID:Contribution of vasopressin to hypertension caused by baroreceptor denervation and nucleus tractus solitarius lesions in rats. 377 19

1. The responses of the mean arterial pressure to (-)-noradrenaline, tyramine, angiotensin II-val(5)-amide, vasopressin and rat renin have been contrasted in renal hypertensive and in salt plus desoxycorticosterone hypertensive rats. The responses were measured in rats both unanaesthetized and rats anaesthetized with pentobarbitone.2. Responses of unanaesthetized, ganglion blocked renal hypertensive rats to noradrenaline, tyramine and vasopressin markedly exceeded, and to angiotensin II and renin were markedly smaller than, those of unanaesthetized ganglion blocked salt + DOC hypertensive animals. Responses to angiotensin and to renin were apparently enhanced in the latter animals.3. Hydrochlorothiazide and frusemide markedly reduced mean arterial pressure in salt + DOC hypertensive rats before and after ganglionic blockade.4. Neither diuretic caused significant reduction in the mean arterial pressures of unanaesthetized, renal hypertensive rats in the absence of ganglionic blockade: frusemide did so in anaesthetized and unanaesthetized rats after ganglionic blockade.5. Whereas the diuretics did not affect the responses of the renal hypertensive rats to pressor agents, frusemide and to a lesser extent hydrochlorothiazide tended to depress the responses to pressor agents in salt induced hypertension.6. Hydrochlorothiazide did not influence mean arterial pressure in unanaesthetized rats with neurogenic hypertension.
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PMID:Responses of mean arterial pressure to pressor agents and diuretics in renal hypertensive and salt hypertensive rats. 432 21

Pressor and bradycardiac responses induced by electrical stimulation of the mesencephalic reticular formation in urethane-anesthetized rats were used as model of neurogenic hypertension. Oxytocin (OXT) and prolyl-leucyl-glycinamide (OXT-(7-9] administered into the fourth cerebral ventricle markedly attenuated the magnitude of the pressor response. OXT-(7-9) was somewhat more potent than OXT and its effect was dose-dependent. Microinjection of OXT-(7-9) into the dorsal raphe nucleus reduced the pressor response as well. [Arg8]vasopressin (AVP) did not affect the pressor response when administered via this route, while prolyl-arginyl-glycinamide (AVP-(7-9] had an action that was similar to that of OXT-(7-9). None of these peptides affected the magnitude of the bradycardiac response. It is suggested that OXT and related fragments modulate neurogenic hypertensive responses through lower brainstem mechanisms.
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PMID:Reduction of a centrally induced pressor response by neurohypophyseal peptides: the involvement of lower brainstem mechanisms. 614 Jan 70

Experimental hypertensions following sino-aortic deafferentation or manoeuvres not involving initially the baroreceptor reflexes are discussed in relation with a simple graphical analysis of these reflexes. Blood pressure increases only slightly as a result of interruption of the sino-aortic afferences, but its variability is markedly enhanced. On the other hand, the final level of arterial pressure in various forms and non-neurogenic hypertension appears independent from the presence of the baroreceptor reflexes ("resetting"). Thus, the baroreceptor reflexes are of primary importance in limiting variations around a given level of arterial pressure, but they do not really set this level since it can be modified easily by other blood pressure control systems. In order to emphasize the role of the baroreflex in the short-term regulation of blood pressure and other haemodynamic variables, its significance in "whole-body autoregulation" and in the cardiovascular effects of vasopressin is discussed.
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PMID:The baroreceptor reflexes in experimental hypertension. 700 Apr 59

1. Arginine vasopressin (AVP) is synthesized in specific brain regions including the magnocellular and parvocellular divisions of the paraventricular nucleus (PVN). Whereas magnocellular AVP responds to osmotic stimuli and functions mainly--although not exclusively--as an antidiuretic hormone, that produced in the parvocellular region controls the hypothalamus-pituitary-adrenal (HPA) axis, in conjunction with CRF. 2. In view of the reported sex differences in control of the HPA axis, we studied if these also pertain to AVP mRNA in the PVN of ovariectomized-estrogenized female rats and male rats determined by in situ hybridization. AVP mRNA was measured in intact rats, adrenalectomized (ADX) rats and ADX receiving dexamethasone (DEX) of both sexes. 3. Computerized autoradiography showed that in both sexes, AVP mRNA levels in the parvocellular division of the PVN increased after adrenalectomy and decreased following DEX. However, the reduction by DEX was more pronounced in female rats. No changes were found for the magnocellular region. Grain counting analysis of the medial-medial (MMP) and medial-lateral (MLP) subdivisions of the parvocellular region showed that the average number of grains per cell area in the MMP region of adrenally intact female rats was higher than that in males. However, in females there was no clear-cut effect of adrenalectomy on AVP mRNA levels, although the reduction after DEX treatment was again greater than that in male rats. Frequency histograms constructed by plotting the number of cells vs the number of grains per area substantiated the enhanced glucocorticoid negative control of AVP mRNA in the MMP and MLP of female rats. 4. The results indicated a sexual dimorphism in the glucocorticoid-dependent plasticity of AVP mRNA levels in the PVN. Because AVP mRNA expression differs between sexes under basal levels, after adrenalectomy, and after DEX treatment, these plastic changes may differentially condition the response to stress. Taking into consideration that stress and AVP may play a role in neurogenic hypertension, the possibility of sexual dimorphisms in AVP control may be important to assess the role of sex hormones in stress and steroid-derived hypertension.
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PMID:Sex difference in glucocorticoid regulation of vasopressin mRNA in the paraventricular hypothalamic nucleus. 944 52