Radioimmunoassay of angiotensin II in rat plasma

Oster, P.; Hackenthal, E.; Hepp, Rebecca

doi:10.1007/bf01926526

Cited by 50 publications

(27 citation statements)

References 4 publications

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“…AII is elevated in sodium-depleted rats (16) and could have contributed significantly to alterations in a number of the factors affecting both sngfr and APR. The potential influences of All upon sngfr have been delineated with infusion studies, demonstrating that AII can decrease rpf, increase PG, Pt, and AP, increase AR and ER, and decrease LpA and sngfr (2,3).…”

Section: Resultsmentioning

confidence: 99%

“…Infusion of AII has been shown to reduce LpA (2), and the elevated plasma AII found in sodium depletion (16) (19). It is also possible that either high levels of antidiuretic hormone associated with volume contraction or other regulatory systems, e.g., prostaglandin synthesis (21) and release (22), mediated the reduction in LpA (10,11), and that Saralasin infusion does not acutely reverse the effects of such systems.…”

Section: Resultsmentioning

confidence: 99%

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Glomerular Hemodynamics in Rats with Chronic Sodium Depletion

Steiner¹,

Tucker²,

Blantz³

1979

J. Clin. Invest.

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A B S T R A C T In chronic sodium depletion the glomerular filtration rate may be reduced, and alterations in proximal tubular function may contribute to the maintenance of antinatriuresis. Measurements were made by micropuncture technique in superficial nephrons of the Munich-Wistar rat of (a) the determinants of glomerular filtration rate, (b) peritubular capillary hydrostatic and oncotic pressure, and (c) proximal tubular fractional and absolute reabsorption in both a control group (group 1, n = 12) and a group of chronically sodium-depleted rats (group 2, n = 12). Single nephron filtration rate (sngfr) was 37.2±1.2 in group 1 and 31.6 ± 1.0 nl/min/g kidney wt (P < 0.05) in group 2. Of the factors potentially responsible for the observed reduction in sngfr, there was no change in systemic oncotic pressure or the transglomerular hydrostatic pressure gradient. Sngfr was lower in group 2 because of both a reduced single nephron plasma flow (rpf) (128±6 vs. 112+5 nl/min per g kidney wt, P < 0.05) and additionally to a decrease in the glomerular permeability coefficient, LPA, from a minimum value of 0. 105+0.012 in group 1 to 0.054±0.01 nl/s per g kidney wt per mm Hg (P < 0.01) after chronic sodium depletion. There was no difference in fractional proximal tubular reabsorption between group 1 and group 2. Absolute proximal reabsorption (APR) was reduced from 20.8±1.3 in group 1 to 16.3±0.9 nl/min per g kidney wt in group 2.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Glomerular Hemodynamics in Rats with Chronic Sodium Depletion

Steiner¹,

Tucker²,

Blantz³

1979

J. Clin. Invest.

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“…For angiotensin II determinations, the plasma samples were processed by SepPak elution (Walter GmbH, Eschborn, Germany) and were then analyzed by radioimmunoassay for Ang II (19). The cross-reactivity of angiotensin antibodies are as follows: Ang II with Ang I, 0.02%; Ang I with Ang II, Ͻ0.01%; and Ang I with angiotensinogen, Ͻ0.2%.…”

Section: Plasma Aldosterone Angiotensin I and Angiotensin Iimentioning

confidence: 99%

Controlled Hypertension, a Transgenic Toggle Switch Reveals Differential Mechanisms Underlying Vascular Disease

Kantachuvesiri¹,

Fleming²,

Peters³

et al. 2001

Journal of Biological Chemistry

142

297

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A novel inbred rat model with inducible hypertension has been generated using a renin transgene under the transcriptional control of the cytochrome P450, Cyp1a1 promoter. The degree and duration of hypertension are regulated tightly by administration of the natural xenobiotic indole-3 carbinol and can be readily reversed. Induction experiments reveal distinct temporal and mechanistic responses to hypertensive injury in different vascular beds, which is indicative of differential susceptibility of organs to a hypertensive stimulus. The mesentery and heart exhibited the greatest sensitivity to damage, and the kidney showed an adaptive response prior to the development of malignant hypertensive injury. Quantitative analysis of morphological changes induced in mesenteric resistance arteries suggest eutrophic remodeling of the vessels. Kinetic evidence suggests that locally activated plasma prorenin may play a critical role in mediating vascular injury. This model will facilitate studies of the cellular and genetic mechanisms underlying vascular injury and repair and provide a basis for the identification of novel therapeutic targets for vascular disease.Essential hypertension has a complex multifactorial phenotype. Both genetic and environmental factors influence its development, and understanding the pathogenesis of complications such as vascular lesions and end-organ damage may lead to more specific treatment and targeted intervention.We have identified candidate loci in rats that may contribute to target organ damage and mortality in malignant hypertension (MH), 1 a condition characterized by an accelerated rise in blood pressure, endothelial injury, activation of the reninangiotensin system, and microangiopathy (1). Several animal models have been generated to investigate the pathophysiology of hypertensive vascular injury. Most animal models of MH to date require surgical or pharmacological intervention to precipitate onset or depend on the constitutive expression of endogenous genes or heterologous transgenes (2-5). In rats doubly transgenic for human renin and angiotensinogen genes, hypertension and fibrinoid vasculitis (5) accompanied by alteration in surface adhesion molecules, proinflammatory cytokines, fibrogenic mediators and leukocyte infiltration (6) have been reported. In most of these models, the onset of disease cannot be determined precisely.The initiation events of pathological processes can only be studied in an animal model in which hypertension is induced by tightly temporally regulated gene expression. If the onset and level of hypertension can be controlled, then the cellular and molecular events during initiation of the vascular and organ injury can be identified unequivocally. Reversibility of the gene expression provides an opportunity to study the molecular and cellular basis of repair. We therefore have generated inbred transgenic rats with inducible hypertension using the cytochrome P450 promoter, Cyp1a1, to drive expression of the mouse Ren-2 gene. The transgene is expressed primarily ...

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“…The detection limit was 50 ng 1-1. Plasma angiotensin I and II were analyzed by radioimmunoassay after solid liquid extraction (C 18 bondapack, Millipore, Molsheim) according to the methods described by Ganten et al (1983), Morton & Webb, (1985), Oster et al (1973), and Hackenthal et al (1977).…”

Section: Determination Of Biochemical Parametersmentioning

confidence: 99%

Interactions between cilazapril and propranolol in man; plasma drug concentrations, hormone and enzyme responses, haemodynamics, agonist dose‐effect curves and baroreceptor reflex.

Belz¹,

Essig²,

Kleinbloesem³

et al. 1988

Brit J Clinical Pharma

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1. The pharmacokinetics, hormonal and haemodynamic responses at rest and during challenges with angiotensin I (blood pressure), isoprenaline (heart rate), and noradrenaline (blood pressure) were investigated in six healthy male volunteers following a 1 week treatment with placebo, propranolol (120 mg day‐1), cilazapril (2, 5 mg day‐1), and a combination of both in a double‐blind cross‐over design. 2. Both drugs reduced systolic and diastolic blood pressure by about 7 mm Hg as compared with placebo. After coadministration, this drop in blood pressure was doubled and lasted longer than after the administration of the individual components. 3. Following cilazapril, a pronounced increase in plasma renin activity (PRA) was found (factor approximately 10 at drug peak concentrations). Coadministration of both drugs resulted only in a moderate increase in the PRA (factor approximately 3). Significant changes in plasma catecholamines were not observed. 4. Propranolol shifted the isoprenaline dose‐effect curve to the right, and cilazapril that of angiotensin I, irrespective of the presence of the other drug. Cilazapril tended to shift the noradrenaline dose‐ effect curve somewhat to the right. 5. The gain of the baroreceptor reflex (angiotensin‐stimulation) was not influenced by cilazapril but was lowered by propranolol, irrespective of the presence of the ACE inhibitor. 6. Except for a statistically not significant decrease in the peak concentrations of each drug during the combined therapy, a pharmacokinetic interaction between the two drugs was not found.

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Radioimmunoassay of angiotensin II in rat plasma

Cited by 50 publications

References 4 publications

Glomerular Hemodynamics in Rats with Chronic Sodium Depletion

Glomerular Hemodynamics in Rats with Chronic Sodium Depletion

Controlled Hypertension, a Transgenic Toggle Switch Reveals Differential Mechanisms Underlying Vascular Disease

Interactions between cilazapril and propranolol in man; plasma drug concentrations, hormone and enzyme responses, haemodynamics, agonist dose‐effect curves and baroreceptor reflex.

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