Role of plasma ANG II in the excretion of acute sodium load in a bird with salt glands (<i>Anas platyrhynchos</i>)

Heinz, Myriam K.; Gray, David A.

doi:10.1152/ajpregu.2001.281.1.r346

Cited by 4 publications

(2 citation statements)

References 33 publications

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“…While salt-induced suppression of PRA and ANG II is indisputable in larger animals (26, 27, 36), rats (23, 53, 72), and humans (24, 57–59), plasma ANG II levels are notoriously affected by blood loss, stress, and anesthesia. Because the small size of the hamster, obtaining an arterial blood sample of adequate size for ANG II measurements is impossible in conscious animals, and anesthesia and sampling of trunk blood cause dramatic increases in plasma ANG II that obscure physiological differences.…”

Section: Discussionmentioning

confidence: 99%

Reduced angiotensin II levels cause generalized vascular dysfunction via oxidant stress in hamster cheek pouch arterioles

Priestley¹,

Buelow²,

McEwen³

et al. 2013

Microvascular Research

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Objectives We investigated the effect of suppressing plasma angiotensin II (ANG II) levels on arteriolar relaxation in the hamster cheek pouch. Methods Arteriolar diameters were measured via television microscopy during short-term (3–6 days) high salt (HS; 4% NaCl) diet and angiotensin converting enzyme (ACE) inhibition with captopril (100 mg/kg/day). Results ACE inhibition and/or HS diet eliminated endothelium-dependent arteriolar dilation to acetylcholine, endothelium-independent dilation to the NO donor sodium nitroprusside, the prostacyclin analogues carbacyclin and iloprost, and the KATP channel opener cromakalim; and eliminated arteriolar constriction during KATP channel blockade with glibenclamide. Scavenging of superoxide radicals and low dose ANG II infusion (25 ng/kg/min, subcutaneous) reduced oxidant stress and restored arteriolar dilation in arterioles of HS-fed hamsters. Vasoconstriction to topically-applied ANG II was unaffected by HS diet while arteriolar responses to elevation of superfusion solution PO2 were unaffected (5% O2, 10% O2) or reduced (21% O2) by HS diet. Conclusions These findings indicate that sustained exposure to low levels of circulating ANG II leads to widespread dysfunction in endothelium-dependent and independent vascular relaxation mechanisms in cheek pouch arterioles by increasing vascular oxidant stress, but does not potentiate O2- or ANG II-induced constriction of arterioles in the distal microcirculation of normotensive hamsters.

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Section: Discussionmentioning

confidence: 99%

Reduced angiotensin II levels cause generalized vascular dysfunction via oxidant stress in hamster cheek pouch arterioles

Priestley¹,

Buelow²,

McEwen³

et al. 2013

Microvascular Research

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show abstract

“…However, total urine excretion remained similar before and after brain-targeted PRR knock down, possibly due to the reduction in water intake in RA mice after PRR knock down. Sodium excretion is regulated by intrarenal pressure, the intrarenal RAS, and the renal sympathetic system [27,29,30]. Interestingly, we unexpectedly found a reduction in plasma Ang II levels following PRR knockdown with no alteration in kidney Ang II levels.…”

Section: Discussionmentioning

confidence: 59%

Brain-Targeted (Pro) Renin Receptor Knockdown Modulates Body Fluid Homeostasis

Cao¹,

Li²,

Seth³

et al. 2013

J Hypertens

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Objectives: The (pro) renin receptor (PRR) is highly expressed in the brain and is involved in the central regulation of blood pressure. However, the role of the brain PRR in regulating body fluid homeostasis in hypertension remains unclear. We hypothesized that the brain PRR knockdown modulates water intake, urine, and urinary sodium excretion in the context of angiotensin II (Ang II)-induced hypertension. Methods and Results: Brain PRR was knocked down in non-transgenic (NT) normotensive and human reninangiotensinogen double-transgenic (RA) mice by intracerebroventricular (ICV) injection of adeno-associated virus expressing short hairpin RNA targeting the PRR (AAV-PRR-shRNA). Water and food intake, and urinary excretion were recorded using metabolic cages. At baseline, RA mice exhibited higher water intake, food intake, urine excretion, urinary sodium excretion and potassium excretion compared to NT mice. PRR knockdown in the brain significantly decreased water and food intake, and urinary potassium and sodium excretion in RA mice, but had no such effects in NT mice. PRR knock down also decreased reactive oxygen species generation and plasma Ang II concentration in RA mice. Conclusion: PRR knockdown modulates body fluid homeostasis in hypertensive RA mice, suggesting that the brain PRR plays a role in regulating body fluid homeostasis during Ang II-dependent hypertension.

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ANG II-induced attenuation of salt gland function in Pekin ducks is not catecholamine-dependent

Butler

2007

J Comp Physiol B

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Pekin ducks (Anas platyrhynchos) were bilaterally adrenalectomized (biADX), injected with 1 mg of triamcinolone (TRIAM) kg bw(-1) im and given 0.9% saline drinking water during a 24 h recovery period followed by chemical sympathectomy with 6OH DOPA 3 h before the start of experimental observations. Baseline plasma dopamine (DA) concentrations decreased from 283 +/- 88.5 pmol ml(-1) to 42.4 +/- 11.1 pmol ml(-1); epinephrine (E) from 142 +/- 46 pmol ml(-1) to 18.4 +/- 9.2 pmol ml(-1) and norepinephrine (NE) from 742 +/- 84 pmol ml(-1) to 406 +/- 38 pmol ml(-1) 1 day after biADX + TRIAM but before chemical sympathectomy. Baseline MABP increased from 132 +/- 3.2 mmHg to 209 +/- 14.3 mmHg (P < 0.05) in response to TRIAM. After chemical sympathectomy with 6OH DOPA there was an additional 90% decrease in plasma NE to 42 +/- 9.4 pmol ml(-1) and a concurrent 60% decrease in MABP to 83.4 +/- 6.9 mmHg (P < 0.05). Nasal fluid secretion was maintained by the continuous infusion of hypertonic saline (1,000 mosmol kg H(2)O(-1) at a rate of 0.3 ml kg(-1) min(-1)). Rates of nasal fluid secretion and fluid electrolyte concentrations were unchanged following biADX + TRIAM + 6OH DOPA. Angiotensin II (ANG II; dose 1 microg kg bw(-1) i.v.), attenuated nasal fluid secretion showing that the response to ANG II was not NE- dependent. Plasma NE concentrations decreased following Tyramine i.v. (33 +/- 8.5 pmol ml(-1)) there being no vasopressor response. This is the first report of the ANG II induced attenuation of duck salt gland secretion in the absence of measurable E and NE.

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Role of plasma ANG II in the excretion of acute sodium load in a bird with salt glands (Anas platyrhynchos)

Cited by 4 publications

References 33 publications

Reduced angiotensin II levels cause generalized vascular dysfunction via oxidant stress in hamster cheek pouch arterioles

Reduced angiotensin II levels cause generalized vascular dysfunction via oxidant stress in hamster cheek pouch arterioles

Brain-Targeted (Pro) Renin Receptor Knockdown Modulates Body Fluid Homeostasis

ANG II-induced attenuation of salt gland function in Pekin ducks is not catecholamine-dependent

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