Atriopeptin and spontaneous hypertension in rats

Xie, Cui-Wei; Song, D.L.; Ding, Jianbo; Chang, Jaw Kang; Chang, Ding; Tang, Jian

doi:10.1016/0024-3205(86)90238-9

Cited by 18 publications

(4 citation statements)

References 10 publications

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“…18 -20 Similarly, reports on ANF and BNP production and secretion in hypertension are controversial and have been carried out mostly in male SHR at a time when hypertension and left ventricular hypertrophy were already established (Ͼ 17 weeks). 1,4,[21][22][23] In the latter, age-related physiologic and molecular changes in cardiac muscle 24 -27 are difficult to separate from those related to hypertension, ie, increased ANF mRNA and irANF content with age. Despite the fact that gender differences concerning the risk of cardiovascular disease exist, studies similar to those mentioned earlier using female SHR rats have not been forthcoming.…”

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confidence: 99%

Atrial natriuretic factor and brain natriuretic peptide gene expression in the spontaneous hypertensive rat during postnatal development

Bold

1998

American Journal of Hypertension

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The increase in natriuretic peptides (NP), atrial natriuretic factor (ANF), and brain natriuretic peptide (BNP) production and release by cardiocytes that occurs in hypertension has been considered to be a compensatory mechanism against ventricular overload. Studies on NP production in the spontaneously hypertensive rat (SHR), an experimental model of human hypertension, have produced controversial results and were carried out when hypertension was already established (> > 17 weeks). At this time, agerelated physiologic and molecular changes in cardiac muscle are difficult to separate from those related to hypertension, ie, increased ANF production and plasma levels. In addition, most of the studies used male rats because the rate of increase in arterial blood pressure-as well as the level to which it rises-is greater in males than in females. Studies of a similar nature using female SHR are not available. The aim of this work was to determine 1) whether ANF and BNP production and secretion increase with the development of hypertension in genetically hypertensive rats; 2) whether a sexual dimorphism in ANF and BNP production and secretion is present in the genetically hypertensive rat during the development of hypertension; and 3) whether the demand for ANF and BNP is the same from each chamber of the heart under these experimental conditions. Age-matched male and female SHR, Wistar-Kyoto (WKY), and Sprague Dawley (SD) rats at 2, 4, and 8 weeks of age were used. The normotensive SD were included to provide a wider basis for baseline findings, as WKY rats are not always a suitable control for SHR due to genetic variations. Natriuretic peptide plasma levels and tissue content were measured by radioimmunoassay. ANF, BNP, as well as ␣-and ␤-myosin heavy chain (MHC) mRNA were estimated by Northern blot analysis. Blood pressure (BP) of more than 150 mm Hg was found only in 8-week-old male SHR. Plasma immunoreactive (ir)ANF and irBNP increased significantly at puberty (8 weeks) in both male and female SHR. The earliest molecular change encountered during the development of hypertension was a significant increase in BNP mRNA in the right and left atria from both male and female 8-week-old SHR. In the ventricles from both male and female SHR, there was no increase in the ratio of left ventricular wet weight/body weight, no increase in ventricular ANF mRNA transcripts, and no myosin heavy chain isoform switch (a protein marker of hypertrophy). irBNP ventricular concentration, however, increased significantly in both male and female SHR, but only in female SHR was there a concomitant increase in BNP mRNA. These results suggest that 1) ANF and BNP production are not coordinated in all cardiac compartments during the development of hypertension; 2) upregulation of BNP in the atria from male and female SHR is the earliest event detected at 8 weeks; 3) the prehypertensive stage, in the genetically hypertensive female rats, is associated with an increase in ventricular irBNP concentration and BNP mRNA; 4) there is a

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confidence: 99%

Atrial natriuretic factor and brain natriuretic peptide gene expression in the spontaneous hypertensive rat during postnatal development

Bold

1998

American Journal of Hypertension

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“…Considerable variation exists in the literature regarding the resting plasma concentrations of ANP in WKY and SHR. Several authors have reported increased plasma ANP concentrations (Imada et al 1985;Gutkowska et al 1986;Morii et al 1986;Xie et al 1986) while Higa et al (1985) reported decreased plasma ANP concentrations in spontaneously hypertensive rats. The present observation of similar basal levels of plasma ANP in SPR, SHR and WKY is in agreement with results of Haass et al (1986).…”

Section: Discussionmentioning

confidence: 98%

Complementary Changes in Plasma Atrial Natriuretic Peptide and Antidiuretic Hormone Concentrations in Response to Volume Expansion and Haemorrhage: Studies in Conscious Normotensive and Spontaneously Hypertensive Rats

Morris

Cain

Chalmers

1987

Clin Exp Pharma Physio

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1.Plasma concentrations of atrial natriuretic peptide (ANP) and antidiuretic hormone (ADH) were measured in conscious stroke-prone spontaneously hypertensive (SPR), spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats before and after acute volume expansion or haemorrhage.2. Plasma ANP concentration was reduced to one-third of resting values 30 min after a 1.5% haemorrhage (1.5 ml of blood per 100 g bodyweight). Plasma ADH concentration rose immediately 50-fold on haemorrhage and remained elevated at 30 min.3. Plasma ANP concentration increased 2.5-fold relative to resting values 1 min after infusion of 2.0 ml per 100 g 5% dextrose; after 10 min plasma ANP remained elevated. Plasma ADH concentration tended to fall on volume expansion although no significant decrease was observed.4. There was no difference in the basal levels of ANP and ADH, or in the changes produced by alterations in blood volume, in hypertensive SPR and SHR compared with normotensive WKY. 5. Thus, plasma ANP concentrations moved in opposite directions in response to two physiological stimuli: volume expansion and haemorrhage. Reciprocal changes were observed in plasma ADH.

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“…Thus, although plasma ANP levels are elevated in SHR, [17][18][19][20] ANP is not present in culture media (un published observation) and culturing conditions thus favor reversibility of any prior in vivo down-regula tion. Alternatively, receptor desensitization through covalent receptor modification, for example by cyclic AMP-dependent protein kinase or protein kinase C 47/48 may also be considered because in hypertension, abnor malities in both cyclic AMP and phosphoinositide me tabolism occur.…”

Section: 47mentioning

confidence: 99%

Atrial Natriuretic Peptide: Binding and Cyclic GMP Response in Cultured Vascular Smooth Muscle Cells From Spontaneously Hypertensive Rats

Scott‐Burden²,

Cr³

et al. 1989

American Journal of Hypertension

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Atriopeptin and spontaneous hypertension in rats

Cited by 18 publications

References 10 publications

Atrial natriuretic factor and brain natriuretic peptide gene expression in the spontaneous hypertensive rat during postnatal development

Atrial natriuretic factor and brain natriuretic peptide gene expression in the spontaneous hypertensive rat during postnatal development

Complementary Changes in Plasma Atrial Natriuretic Peptide and Antidiuretic Hormone Concentrations in Response to Volume Expansion and Haemorrhage: Studies in Conscious Normotensive and Spontaneously Hypertensive Rats

Atrial Natriuretic Peptide: Binding and Cyclic GMP Response in Cultured Vascular Smooth Muscle Cells From Spontaneously Hypertensive Rats

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