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)

The effects of pretreatment with atrial natriuretic factor (ANF) on the pressor responsiveness to injections of angiotensin II (ANGII), arginine vasopressin (AVP), and norepinephrine (NE), as well as the effect of pretreatment with ANGII on the hypotensive responses to ANF injection were studied in conscious sheep. The hemodynamic effects of ANF infusion (100 micrograms/h for 60 min) were also examined in animals pretreated with the angiotensin-converting enzyme (ACE) inhibitor, captopril. Infusion of ANF attenuated the pressor responsiveness to exogenous AII and NE, but caused no significant change in the blood pressure increases produced by vasopressin. In contrast, infusion of AII had no effect on the immediate hypotensive response to ANF injection. Infusion of ANF for 60 min produced similar hemodynamic actions in sheep during ACE inhibition as compared with the responses observed in normal sheep, although the reduction in cardiac output and increase in calculated total peripheral resistance was attenuated. Infusion of captopril increased plasma concentration of renin (PRC), and infusion of ANF produced no further change in PRC. In conclusion, the short-term cardiovascular responses to ANF infusion in conscious sheep are not mediated solely by inhibition of the renin-angiotensin system. However, ANF attenuates the pressor actions of pharmacologic doses of exogenous ANGII and NE. In contrast, the vasodepressor response to exogenous ANF injection was not altered in animals receiving ANGII infusion. This study suggests that ANF may be important in regulating the effects of endogenous vasoconstrictor hormones on blood pressure (BP).
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PMID:Effects of atrial natriuretic factor on pressor responsiveness to angiotensin II, norepinephrine, and vasopressin in conscious sheep. 168 75

The degree of water transport via aquaporin-2 (AQP2) water channels in renal collecting duct principal cells is reflected by the level of the urinary excretion of AQP2 (u-AQP2). In rats, the AQP2 expression varies with sodium intake. In humans, the effect of sodium intake on u-AQP2 and the underlying mechanisms have not previously been studied. We measured the effect of 4 days of high sodium (HS) intake (300 mmol sodium/day; 17.5 g salt/day) and 4 days of low sodium (LS) intake (30 mmol sodium/day; 1.8 g salt/day) on u-AQP2, fractional sodium excretion (FE(Na)), free water clearance (C(H2O)), urinary excretion of PGE(2) (u-PGE(2)) and cAMP (u-cAMP), and plasma concentrations of vasopressin (AVP), renin (PRC), ANG II, aldosterone (Aldo), atrial natriuretic peptide (ANP), and brain natriuretic peptide (BNP) in a randomized, crossover study of 21 healthy subjects, during 24-h urine collection and after hypertonic saline infusion. The 24-h urinary sodium excretion was significantly higher during HS intake (213 vs. 41 mmol/24 h). ANP and BNP were significantly lower and PRC, ANG II, and Aldo were significantly higher during LS intake. AVP, u-cAMP, and u-PGE(2) were similar during HS and LS intake, but u-AQP2 was significantly higher during HS intake. The increases in AVP and u-AQP2 in response to hypertonic saline infusion were similar during HS and LS intake. In conclusion, u-AQP2 was increased during HS intake, indicating that water transport via AQP2 was increased. The effect was mediated by an unknown AVP-independent mechanism.
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PMID:Effect of high and low sodium intake on urinary aquaporin-2 excretion in healthy humans. 2199 90