Effects of daily sodium intake and ANG II on cortical  and medullary renal blood flow in conscious rats

Groß, Volkmar; Kurth, Theresa; Skelton, M. M.; Mattson, David L.; Cowley, Allen W.

doi:10.1152/ajpregu.1998.274.5.r1317

Cited by 36 publications

(54 citation statements)

References 14 publications

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“…Rats fed a high-salt diet exhibit a reduction of plasma renin activity (PRA) (22) and ANG II (19,21) and impaired responses to vasodilator stimuli that are similar to those in SS rats in the present study. In a similar fashion, SS rats exhibit significantly lower PRA than SS.13 BN rats (8) and congenic rats having the Dahl R renin BN rats, and BN rats.…”

Section: Discussionsupporting

confidence: 70%

“…Other studies (31,32,34,48) have shown that high-salt diet alone leads to impaired vasodilation in arterioles and resistance arteries of Sprague-Dawley rats, in the absence of a change in blood pressure. Impairment of vascular relaxation in response to vasodilator stimuli during exposure to high-salt diet appears to be caused by the suppression of circulating levels of angiotensin II (ANG II) that occurs in response to elevated dietary salt intake (19,21). The latter hypothesis is supported by recent findings that continuous intravenous infusion of a low dose of ANG II to prevent ANG II suppression with high-salt diet restores the dilation in response to acetylcholine (ACh) and hypoxia that is eliminated with high-salt diet in middle cerebral arteries (MCA) (34).…”

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confidence: 99%

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Restoration of normal vascular relaxation mechanisms in cerebral arteries by chromosomal substitution in consomic SS.13^BNrats

Drenjančević-Perić

Phillips

Falck

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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This study sought to identify the mechanisms of vascular relaxation that are rescued in middle cerebral arteries (MCA) of SS.13 BN consomic rats by substituting chromosome 13 containing the renin gene from Brown Norway (BN) rats into the Dahl salt-sensitive (SS) genetic background. Isolated MCA from SS rats exhibited an indomethacinsensitive constriction in response to acetylcholine (ACh) and hypoxia. ACh-induced dilation was NO dependent and hypoxic dilations were cyclooxygenase (COX) dependent in BN and SS.13 BN rats. In SS rats, hypoxic dilation was restored by indomethacin and abolished by inhibiting cytochrome P-450 epoxygenases, suggesting a role for epoxyeicosatrienoic acids. MCA from SS and SS.13 BN rats constricted and MCA from BN rats dilated in response to the stable prostacyclin analog iloprost. MCA from SS.13 BN and BN rats (but not SS rats) dilated in response to the prostaglandin E2 receptor agonist butaprost. Hypoxia increased prostacyclin release in cerebral arteries from all the strains, whereas thromboxane A 2 production was reduced in BN rat vessels only. These data suggest that SS rats may be less sensitive to vasodilator prostaglandins and that normalization of renin-angiotensin system regulation causes a switch from production of COX-derived vasoconstrictor metabolites (in SS rats) toward NOdependent relaxation in response to ACh-and prostaglandin-dependent dilation in response to hypoxia in SS.13 BN rats.angiotensin II; vasodilation; hypoxia; endothelium; genetic models; physiological genomics; vascular relaxation REGULATION OF THE ACTIVE TONE of resistance vessels is a complex and integrated process that involves multiple mechanisms. Alterations in the function of resistance arteries can have significant pathophysiological consequences. For example, an impaired relaxation in response to vasodilator stimuli has been documented in many experimental animal models of hypertension (9 -11, 15, 32, 35, 39, 53) and in hypertensive humans (3, 13, 42-44, 49, 50). Other studies (31,32,34,48) have shown that high-salt diet alone leads to impaired vasodilation in arterioles and resistance arteries of Sprague-Dawley rats, in the absence of a change in blood pressure. Impairment of vascular relaxation in response to vasodilator stimuli during exposure to high-salt diet appears to be caused by the suppression of circulating levels of angiotensin II (ANG II) that occurs in response to elevated dietary salt intake (19,21). The latter hypothesis is supported by recent findings that continuous intravenous infusion of a low dose of ANG II to prevent ANG II suppression with high-salt diet restores the dilation in response to acetylcholine (ACh) and hypoxia that is eliminated with high-salt diet in middle cerebral arteries (MCA) (34). Other studies have provided evidence that the protective effect of ANG II to maintain normal vasodilator responses in animals on high-salt diet can be prevented by blocking AT 1 receptors with losartan (52).Recent studies have demonstrated that restoration of the normal regulati...

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Section: Discussionsupporting

confidence: 70%

mentioning

confidence: 99%

Restoration of normal vascular relaxation mechanisms in cerebral arteries by chromosomal substitution in consomic SS.13^BNrats

Drenjančević-Perić

Phillips

Falck

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…NO is also an important modulator of the vasoconstrictor influence of AngII in the renal cortical circulation (26,42). Furthermore, changes in renal cortical blood flow appear to play an important role in the chronic regulation of sodium excretion and BP (43). This result could be important considering that in AT 2 Ϫ/Ϫ mice the AT 1 receptor is upregulated in cortical structures (16).…”

Section: Discussionmentioning

confidence: 99%

Pressure Natriuresis in AT2 Receptor–Deficient Mice with L-NAME Hypertension

Obst¹,

Groß²,

Janke

et al. 2003

Journal of the American Society of Nephrology

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Abstract. AT 2 receptor-disrupted (AT 2 Ϫ/Ϫ) mice provide a unique opportunity to investigate the cardiovascular and BP-related effects of NO depletion. This study compared the pressure-diuresis-natriuresis relationship in (AT 2 Ϫ/Ϫ) and wild-type (AT 2 ϩ/ϩ) mice after treating the animals with L-NAME (130 mg/kg body wt per day) for 1 wk. L-NAME increased mean arterial pressure (MAP) more in AT 2 Ϫ/Ϫ than in AT 2 ϩ/ϩ mice (118 Ϯ 2 versus 108 Ϯ 4 mmHg). This difference occurred even though L-NAME-treated AT 2 ϩ/ϩ mice had a greater sodium excretion than AT 2 Ϫ/Ϫ mice (10.9 Ϯ 0.5 versus 8.0 Ϯ 1.0 mol/h). The pressurenatriuresis relationship in conscious AT 2 Ϫ/Ϫ mice was shifted rightward compared with controls. RBF was decreased in AT 2 Ϫ/Ϫ compared with AT 2 ϩ/ϩ mice. L-NAME decreased RBF in these mice further from 4.08 Ϯ 0.43 to 2.79 Ϯ 0.15 ml/min per g of kidney wt. GFR was not significantly different between AT 2 ϩ/ϩ and AT 2 Ϫ/Ϫ mice (1.09 Ϯ 0.08 versus 1.21 Ϯ 0.09 ml/min per g of kidney wt). L-NAME reduced GFR in AT 2 Ϫ/Ϫ to 0.87 Ϯ 0.07 ml/min per g of kidney wt. Fractional sodium (FE Na ) and water (FE H2O ) curves were shifted more strongly to the right by L-NAME in AT 2 Ϫ/Ϫ mice than in AT 2 ϩ/ϩ mice. AT 1 receptor blocker treatment lowered BP in both L-NAME-treated strains to basal values. It is concluded that the AT 1 receptor plays a key role in the impaired renal sodium and water excretion induced by NO synthesis blockade. Changes in RBF, GFR, and tubular sodium and water reabsorption are involved and may be also responsible for the greater BP increase in L-NAME-treated AT 2 Ϫ/Ϫ mice.Nitric oxide (NO) and angiotensin II (AngII) are integrated in homeostatic mechanisms regulating renal function and BP. The effects of AngII are mediated by at least two receptor isoforms (AT 1 and AT 2 ). AngII stimulates proximal tubular sodium reabsorption and decreases sodium excretion by reducing renal medullary blood flow via the AT 1 receptor. AngII also enhances sodium reabsorption indirectly by stimulating aldosterone release through the AT 1 receptor. There is evidence that the AT 2 receptor serves a counter-regulatory protective role (1). Tonically secreted intrarenal NO is also involved in the control of glomerular hemodynamics, tubuloglomerular feedback, renin release, and sodium and water excretion (2). NOsynthesis blockade by L-NAME lowers renal blood flow, reduces sodium and water excretion, shifts pressure-natriuresis curves toward the right (2-5), and increases BP (6 -8). The renin-angiotensin system participates in the renal and systemic alterations induced by NO synthesis blockade (9). Chronic AT 1 receptor or converting enzyme blockade prevents the development of L-NAME hypertension (6,10). However, pretreatment with losartan had no effect on the impaired pressure natriuresis produced by NO-synthesis blockade in another study (11), suggesting that the AT 1 receptor may not or only partially be involved in L-NAME-induced changes. This suggestion is underscored by results suggesting that AT 2 receptor ...

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“…Studies in chronically instrumented Sprague-Dawley rats in our laboratory found no changes in MBF as daily sodium intake was increased from 0.4 to 4.0% (27). However, rats fed a high-sodium diet (4.0%) exhibited an increase in NOS-immunoreactive protein for all isoforms in the medullary tissue (58).…”

Section: Influence Of Medullary No Production On Blood Pressure Salt mentioning

confidence: 99%

Role of renal NO production in the regulation of medullary blood flow

Cowley

Mori

Mattson

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

176

202

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. Role of renal NO production in the regulation of medullary blood flow. Am J Physiol Regul Integr Comp Physiol 284: R1355-R1369, 2003 10.1152/ajpregu.00701.2002The unique role of nitric oxide (NO) in the regulation of renal medullary function is supported by the evidence summarized in this review. The impact of reduced production of NO within the renal medulla on the delivery of blood to the medulla and on the long-term regulation of sodium excretion and blood pressure is described. It is evident that medullary NO production serves as an important counterregulatory factor to buffer vasoconstrictor hormoneinduced reduction of medullary blood flow and tissue oxygen levels. When NO synthase (NOS) activity is reduced within the renal medulla, either pharmacologically or genetically [Dahl salt-sensitive (S) rats], a super sensitivity to vasoconstrictors develops with ensuing hypertension. Reduced NO production may also result from reduced cellular uptake of L-arginine in the medullary tissue, resulting in hypertension. It is concluded that NO production in the renal medulla plays a very important role in sodium and water homeostasis and the long-term control of arterial pressure. renal medulla; Dahl salt-sensitive rats; hypertension; L-arginine THE RENAL MEDULLARY CIRCULATION is now recognized to be of importance for reasons that extend far beyond providing the economy of countercurrent exchange to concentrate large volumes of filtrate to produce small volumes of concentrated urine. It is now recognized that medullary blood flow (MBF) can play an important role in determining long-term levels of arterial pressure and that 15-30% reductions of blood flow to the renal medulla in the face of imperceptibly small changes of total renal blood flow can lead to the development of hypertension (16,21). Evidence is reviewed showing that nitric oxide (NO) plays a unique role in the acute and chronic regulation of renal MBF, sodium homeostasis, and arterial pressure. More specifically, the role of NO in the regulation of MBF, in linking tubular metabolic needs with delivery of nutrients and as a counterregulatory system to protect the medulla from the consequences of underperfusion, are the focus of this review. The influence of NO on the renal cortex and such issues that relate to pressure-natriuresis, autoregulation of total renal blood flow, tubuloglomerular feedback, and glomerular filtration rate (GFR) regulation are important subjects of renal function that either have been reviewed by others (2,29,43,55,96) or are beyond the scope of this relatively brief review.

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Effects of daily sodium intake and ANG II on cortical and medullary renal blood flow in conscious rats

Cited by 36 publications

References 14 publications

Restoration of normal vascular relaxation mechanisms in cerebral arteries by chromosomal substitution in consomic SS.13^BNrats

Restoration of normal vascular relaxation mechanisms in cerebral arteries by chromosomal substitution in consomic SS.13^BNrats

Pressure Natriuresis in AT2 Receptor–Deficient Mice with L-NAME Hypertension

Role of renal NO production in the regulation of medullary blood flow

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Effects of daily sodium intake and ANG II on cortical and medullary renal blood flow in conscious rats

Cited by 36 publications

References 14 publications

Restoration of normal vascular relaxation mechanisms in cerebral arteries by chromosomal substitution in consomic SS.13BNrats

Restoration of normal vascular relaxation mechanisms in cerebral arteries by chromosomal substitution in consomic SS.13BNrats

Pressure Natriuresis in AT2 Receptor–Deficient Mice with L-NAME Hypertension

Role of renal NO production in the regulation of medullary blood flow

Contact Info

Product

Resources

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Restoration of normal vascular relaxation mechanisms in cerebral arteries by chromosomal substitution in consomic SS.13^BNrats

Restoration of normal vascular relaxation mechanisms in cerebral arteries by chromosomal substitution in consomic SS.13^BNrats