Enhanced effects of central angiotensin II on cardiovascular and drinking responses in inbred polydipsic (STR/N) mice
ABSTRACT STR/N, an inbred strain of mice, is known to exhibit extreme polydipsia and polyuria. The objective of this study was to investigate the possible reasons for polydipsia. First, comparisons were made between STR/N mice and control mice from the Institute of Cancer Research (ICR) concerning daily drinking, urinary excretion, and basal cardiovascular function. Then, since angiotensin II (ANG II) is a potent stimulus for drinking behavior, we investigated the effects of intracerebroventricular (i.c.v.) administration of ANG II on cardiovascular and water intake responses. Daily water intake, food intake, urinary volume, and urinary electrolytes (Na and K) excretion were larger in STR/N mice than in ICR mice, and the basal blood pressure was significantly lower in STR/N mice than in ICR mice. The i.c.v. administration of ANG II (10 pmol/per mouse) resulted in increased mean arterial blood pressure (MAP) and water intake in both STR/N and ICR mice, but the changes in MAP were significantly larger in STR/N mice than in ICR mice. These results suggest that polydipsia in STR/N mice is at least partially attributable to high sensitivity of central ANG II receptors and low MAP.
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- "Post-operatively, mice were singlyhoused and given 1 week to recover. Cannula placement was confirmed by a positive dipsogenic response (persistent drinking response within 2 min) following ICV administration of 1 μl angiotensin II (10 ng/μl) . ICV injection of the Y2R antagonist or vehicle was administered 30 min before an IPGTT test was performed with either glucose or glucose containing PYY3-36 (5 μg/100 g of bodyweight). "
ABSTRACT: The effect of peptide tyrosine-tyrosine (PYY) on feeding is well established but currently its role in glucose homeostasis is poorly defined. Here we show in mice, that intraperitoneal (ip) injection of PYY3-36 or Y2R agonist improves nutrient-stimulated glucose tolerance and enhances insulin secretion; an effect blocked by peripheral, but not central, Y2R antagonist administration. Studies on isolated mouse islets revealed no direct effect of PYY3-36 on insulin secretion. Bariatric surgery in mice, enterogastric anastomosis (EGA), improved glucose tolerance in wild-type mice and increased circulating PYY and active GLP-1. In contrast, in Pyy-null mice, post-operative glucose tolerance and active GLP-1 levels were similar in EGA and sham-operated groups. PYY3-36 ip increased hepato-portal active GLP-1 plasma levels, an effect blocked by ip Y2R antagonist. Collectively, these data suggest that PYY3-36 therefore acting via peripheral Y2R increases hepato-portal active GLP-1 plasma levels and improves nutrient-stimulated glucose tolerance.08/2013; 2(3):142-52. DOI:10.1016/j.molmet.2013.03.001
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ABSTRACT: To characterize the involvement of specific alpha(1)-adrenergic receptor (alpha(1)-AR) subtypes in hypertension, parameters related to central salt- or angiotensin II (ANG II)-induced hypertension were investigated in alpha(1D)-AR-deficient mice (knockout). Baseline daily water intake and food intake were larger in alpha(1D)(-/-) mice than in alpha(1D)(+/+) mice. Intracerebroventricular (i.c.v.) administration of NaCl (0.67 M NaCl, 1 microl) elicited smaller increases in mean arterial blood pressure (MABP), heart rate, and water intake in alpha(1D)(-/-) mice than it did in alpha(1D)(+/+) mice. I.c.v. administration of ANG II (10 pmol) resulted in increases in MABP and water intake that were similar in alpha(1D)(-/-) mice and alpha(1D)(+/+) mice. These results suggest that alpha(1D)-AR is, at least in part, involved in central salt-induced but not ANG II-induced hypertension and water intake.Neuroscience Letters 03/2004; 356(1):33-6. DOI:10.1016/j.neulet.2003.11.014 · 2.06 Impact Factor