Exaggerated natriuretic response to atrial natriuretic factor in rats developing spontaneous hypertension.

Pollock, David M.; Arendshorst, William J.

doi:10.1161/01.hyp.16.1.72

Cited by 11 publications

(4 citation statements)

References 28 publications

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“…Indeed, ANP appears to be a key candidate among potential factors involved in the pathogenesis of hypertension -likely due to the essential role of the kidney and renal function in the development of hypertension, and the effects of ANP on natriuresis, diuresis and hypertension itself [9]. Animal models have demonstrated an exaggerated diuretic and natriuretic response to exogenously administered ANP in spontaneously hypertensive rats compared with normotensive strains [82]. Furthermore, genetically reduced production of ANP has been shown to lead to salt-sensitive hypertension in mice [83].…”

Section: Hypertensionmentioning

confidence: 99%

Natriuretic peptides and cardio-renal disease

Volpe¹

2014

International Journal of Cardiology

103

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The natriuretic peptide (NP) system is an important endocrine, autocrine and paracrine system, consisting of a family of peptides which provide cardiac, renal and vascular effects that, through their beneficial physiological actions, play a key role in maintaining overall cardiovascular health. Traditionally, the pathophysiological origins of cardio-renal disease have been viewed as the domain of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (SNS), with inappropriate activation of both systems leading to deleterious changes in cardio-renal function and structure. Therapies designed to suppress the RAAS and the SNS have been routinely employed to address the consequences of cardio-renal disease. However, it is now becoming increasingly apparent that enhancing the beneficial physiological effects of the NP system may represent an attractive alternative therapeutic approach to counter the pathophysiological effects of disease. In particular, innovative therapeutic strategies aimed at enhancing the physiological benefits afforded by NPs while simultaneously suppressing the RAAS are generating increasing interest as potential treatment options for the management of cardio-renal disease.

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Section: Hypertensionmentioning

confidence: 99%

Natriuretic peptides and cardio-renal disease

Volpe¹

2014

International Journal of Cardiology

103

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“…SHR have been shown to exhibit higher systolic blood pressure (BP) than Wistar-Kyoto rats (WKY) at 3 weeks, 6 4 1 ⁄2 weeks, 7 and 5 weeks of age 8 -10 ; SHR have also shown higher systolic BP than at 6 weeks, [11][12][13] 7 weeks, 14,15 9 weeks, 14 -16 10 weeks, 17 and 12 weeks of age. 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).…”

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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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“…However, in kidneys from young prehypertensive SHRs (3-4 wk), renal GLP-1R expression was significantly diminished, as judged by immunohistochemistry, despite normal expression in the pancreas. At 6 wk of age, arterial blood pressure in SHRs was slightly increased compared with agematched WKY rats (31), and no differences were found in RBF and GFR, suggesting that at this young age, the SHR is hemodynamically comparable to the WKY rat. However, another study (13) showed that at 6 wk of age, SHRs had significantly decreased RBF and GFR, which could contribute to the development of hypertension in these animals.…”

Section: Discussionmentioning

confidence: 80%

GLP-1-induced renal vasodilation in rodents depends exclusively on the known GLP-1 receptor and is lost in prehypertensive rats

Jensen

Møller

Hviid

et al. 2020

American Journal of Physiology-Renal Physiology

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Glucagon-like peptide-1 (GLP-1) is an incretin hormone known to stimulate postprandial insulin release. However, GLP-1 also exerts extrapancreatic effects, including renal effects. Some of these renal effects are attenuated in hypertensive rats, where renal expression of GLP-1 receptors is reduced. Here, we assessed the expression and vascular function of GLP-1 receptors in kidneys from young prehypertensive rats. We also examined GLP-1-induced vasodilation in the renal vasculature in wild-type (WT) and GLP-1 receptor knockout mice using wire and pressure myography and the isolated perfused juxtamedullary nephron preparation. We investigated whether GLP-1 and the metabolite GLP-1(9–36)amide had renal vascular effects independent of the known GLP-1 receptor. We hypothesized that hypertension decreased expression of renal GLP-1 receptors. We also hypothesized that GLP-1-induced renal vasodilatation depended on expression of the known GLP-1 receptor. In contrast to normotensive rats, no immunohistochemical staining or vasodilatory function of GLP-1 receptors was found in kidneys from prehypertensive rats. In WT mice, GLP-1 induced renal vasodilation and reduced the renal autoregulatory response. The GLP-1 receptor antagonist exendin 9–39 inhibited relaxation, and GLP-1(9–36)amide had no vasodilatory effect. In GLP-1 receptor knockout mice, no relaxation induced by GLP-1 or GLP-1(9–36)amide was found, the autoregulatory response in afferent arterioles was normal, and no GLP-1-induced reduction of autoregulation was found. We conclude that in prehypertensive kidneys, expression and function of GLP-1 receptors is lost. The renal vasodilatory effect of GLP-1 is mediated exclusively by the known GLP-1 receptor. GLP-1(9–36)amide has no renal vasodilatory effect. GLP-1 attenuates renal autoregulation by reducing the myogenic response.

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Exaggerated natriuretic response to atrial natriuretic factor in rats developing spontaneous hypertension.

Cited by 11 publications

References 28 publications

Natriuretic peptides and cardio-renal disease

Natriuretic peptides and cardio-renal disease

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

GLP-1-induced renal vasodilation in rodents depends exclusively on the known GLP-1 receptor and is lost in prehypertensive rats

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