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)

Endothelin-3-like immunoreactivity (ET-3-ir) was detected in extracts of rat hypothalamic median eminence, and in the anterior and neurointermediate lobes of the pituitary at levels (ng ET-3/mg protein) exceeding those present in extracts of abdominal aorta. This ET-3-ir appeared authentic because radioimmunoassay (RIA) dose-response curves parallel to those of synthetic ET-3 could be constructed and this ET-3-ir comigrated on C-8 high-pressure liquid chromatography (HPLC) with synthetic ET-3. Endothelin-1-like immunoreactivity, on the other hand, was abundant in extracts of abdominal aorta and cerebral cortex and only minimally present in hypothalamus and anterior pituitary gland. Central administration of 11 and 23 pmol ET-3 resulted in significant (4.2- and 5.7-fold, respectively) elevations of plasma levels of vasopressin. Oxytocin levels were transiently, yet significantly, elevated (1.8-fold) by the higher dose of ET-3. These results, and our findings that central administration of ET-3 inhibits stimulated water drinking, suggest a physiologically important role for endogenously produced endothelin in the central mechanisms regulating fluid and electrolyte homeostasis.
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PMID:Hypothalamic endothelin: presence and effects related to fluid and electrolyte homeostasis. 172 77

1. The regional haemodynamic effects of bolus doses (4 and 40 pmol) and infusions (12 and 120 pmol h-1) of endothelin-1 and endothelin-3 were assessed in conscious, Long Evans and Brattleboro (i.e. vasopressin-deficient) rats, chronically-instrumented with pulsed Doppler flow probes. 2. In both strains of rat the lower bolus dose of endothelin-1 caused only a slight pressor effect, but there were marked renal and mesenteric vasoconstrictions and hindquarters vasodilatation. 3. The lower bolus dose of endothelin-3 did not affect blood pressure significantly, although the changes in regional haemodynamics were qualitatively similar to those seen following endothelin-1 in Long Evans and Brattleboro rats. 4. The higher dose of endothelin-1 caused an initial hypotension accompanied by substantial hindquarters vasodilatations in Long Evans and Brattleboro rats. Subsequently, in both strains, there was a rise in blood pressure accompanied by renal, mesenteric and hindquarters vasoconstrictions. 5. The higher bolus dose of endothelin-3 caused initial hypotension and hindquarters vasodilatation similar to those seen with endothelin-1. However, the subsequent pressor effect was less with endothelin-3, as was the renal vasoconstriction, and it did not cause any increase in hindquarters vascular resistance. 6. Infusion of endothelin-1 at the lower rate (12 pmol h-1) caused renal and mesenteric vasoconstrictions in both strains of rat, whereas endothelin-3 at this rate caused only mesenteric vasoconstriction. 7. Infusion of endothelin-1 at the higher rate (120 pmol h-1) caused progressive hypertension and vasoconstrictions in all three vascular beds studied; these were similar in both strains of rat. Endothelin-3 had a smaller pressor effect and a lesser constrictor action on the renal and mesenteric vascular beds; it did not constrict the hindquarters vascular bed. 8. These results show, that in conscious Long Evans and Brattleboro rats, the initial depressor effects of the higher bolus doses of endothelin-1 and -3 were similar, and, hence, not influenced by the absence of endogenous vasopressin. Endothelin-1 and -3 appear equipotent in their initial hyperaemic vasodilator effects in the hindquarters vasculature in both strains, making it unlikely that this effect is dependent on the release of atrial natriuretic peptide (ANP), since ANP does not cause significant increases in hindquarters blood flow in Brattleboro rats. The greater delayed pressor effect of endothelin-1 is associated with its more marked vasoconstrictor effects on renal and mesenteric vascular beds and is accentuated, relative to endothelin-3, by the lack of a constrictor effect of endothelin-3 in the hindquarters vasculature.
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PMID:Regional haemodynamic effects of endothelin-1 and endothelin-3 in conscious Long Evans and Brattleboro rats. 213 84

Since endothelin has been localized in neurons in areas involved in water and electrolyte metabolism, areas which also contain atrial natriuretic peptide (ANP) neurons, we determined whether endothelin would release ANP and induce natriuresis. Endothelin-3 (ET-3) in doses ranging from 38 to 760 pmol was microinjected into the third ventricle (3V) of conscious, water-loaded male rats, and the effect on natriuresis and plasma ANP was determined. ET-3 evoked a dose-related natriuresis beginning within 20 min of injection. Even the lowest dose tested (38 pmol) was effective. At a dose of 95 pmol, it produced a rapid increase of plasma ANP within 5 min peaking at 20 min. A slight kaliuresis and antidiuresis was observed at the 2 highest doses of 380 and 760 pmol. The urinary changes following 3V injection of ET-3 were similar to those evoked by ANP, except for the antidiuresis with increased sodium concentration which followed injection of the 2 higher doses. These results suggest that these 2 higher doses also released vasopressin. Alternatively, activation of the sympathetic nervous system by these higher doses may have decreased glomerular filtration rate and been in part responsible for the antidiuresis. The results with 3V injection of ET-3 contrasted sharply with those obtained following intravenous injection of the 95-pmol dose injected intraventricularly. This intravenous dose of ANP induced a transient decrease in sodium and potassium excretion and urine volume, maximal at 20 min, and had no effect on plasma ANP concentrations at 5 or 20 min after injection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Possible role of endothelin acting within the hypothalamus to induce the release of atrial natriuretic peptide and natriuresis. 812 97