Effect of nitric oxide on renin secretion. II. Studies in the perfused juxtaglomerular apparatus

He, Xiao-Rui; Greenberg, Suzanne; Briggs, Josie P.; Schnermann, Jürgen

doi:10.1152/ajprenal.1995.268.5.f953

Cited by 38 publications

(36 citation statements)

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“…Some ongoing studies focus on the potential role of cGK II in regulation of renin release. However, in general cGMP regulation of renin release seems to be complex and currently not well understood since studies using different cGMP-elevating agents (ANP, NO, and sodium nitroprusside [SNP]), or different cell or tissue systems (isolated perfused rat kidneys, renal cortex slices or cells, isolated JG cells or JG apparatus), have concluded that cGMP can have stimulatory, inhibitory, or biphasic effects on renin release (10,(29)(30)(31)(32). This may imply that there are cGMP-independent effects of some agonists and that there are different cGMP targets of action or different complexities of regulatory feedback systems present in the various cell/tissue preparations.…”

Section: Discussionmentioning

confidence: 99%

Expression of type II cGMP-dependent protein kinase in rat kidney is regulated by dehydration and correlated with renin gene expression.

Gambaryan¹,

Häusler²,

Markert³

et al. 1996

J. Clin. Invest.

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AbstractcGMP-based regulatory systems are vital for counteracting the renin-angiotensin system (RAS) which promotes volume expansion and high blood pressure. Natriuretic peptides and nitric oxide acting through their second messenger cGMP normally increase natriuresis and diuresis, and regulate renin release; however, the severe pathological state of cardiac heart failure is characterized by elevated levels of atrial natriuretic peptide that are no longer able to effectively oppose exaggerated RAS effects. There is presently limited information on the intracellular effectors of cGMP actions in the kidney. Recently we reported the cloning of the cDNA for type II cGMP-dependent protein kinase (cGK II), which is highly enriched in intestinal mucosa but was also detected for the first time in kidney. In the present study, cGK II was localized to juxtaglomerular (JG) cells, the ascending thin limb (ATL), and to a lesser extent the brush border of proximal tubules. An activator of renin gene expression, the angiotensin II type I receptor inhibitor, losartan, increased cGK II mRNA and protein three to fourfold in JG cells. In other experiments, water deprivation increased cGK II mRNA and protein three to fourfold in the inner medulla where both cGK II, and a kidney specific Cl

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Section: Discussionmentioning

confidence: 99%

Expression of type II cGMP-dependent protein kinase in rat kidney is regulated by dehydration and correlated with renin gene expression.

Gambaryan¹,

Häusler²,

Markert³

et al. 1996

J. Clin. Invest.

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“…As reviewed recently by Liang and Knox (50) and by Ortiz and Garvin (80), there is evidence that NO reduces sodium reabsorption in all tubular segments, including the proximal tubule (50,80), thick ascending limb (78,79), distal tubules, and cortical collecting ducts (80), although medullary nephron segments and collecting ducts remain to be studied in detail. Studies have also demonstrated that tubuloglomerular feedback control of afferent arteriolar resistance is influenced by macula densa NO production, thereby enhancing autoregulation of renal blood flow, GFR, and renin secretion (30,37,53,75,122,128).…”

Section: No Production and The Overall Regulation Of Renal Functionmentioning

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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“…Many investigators have reported that NO stimulates renin secretion, both in vivo (21,25,29) and in the perfused kidney (15,16), while early work reported an inhibitory NO effect on renin secretion (39). Some authors suggest that NO from the macula densa cells may stimulate renin release, while NO derived from the endothelial cells in the afferent arteriole may inhibit renin secretion (2,4,12). Current concepts are seemingly rather complex (30).…”

mentioning

confidence: 99%

Renal nerves and nNOS: roles in natriuresis of acute isovolumetric sodium loading in conscious rats

Kompanowska-Jezierska

Wolff²,

Kuczeriszka³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Kompanowska-Jezierska E, Wolff H, Kuczeriszka M, Gramsbergen JB, Walkowska A, Johns EJ, Bie P. Renal nerves and nNOS: roles in natriuresis of acute isovolumetric sodium loading in conscious rats. Am J Physiol Regul Integr Comp Physiol 294: R1130-R1139, 2008. First published January 30, 2008 doi:10.1152/ajpregu.00908.2007.-It was hypothesized that renal sympathetic nerve activity (RSNA) and neuronal nitric oxide synthase (nNOS) are involved in the acute inhibition of renin secretion and the natriuresis following slow NaCl loading (NaLoad) and that RSNA participates in the regulation of arterial blood pressure (MABP). This was tested by NaLoad after chronic renal denervation with and without inhibition of nNOS by S-methyl-thiocitrulline (SMTC). In addition, the acute effects of renal denervation on MABP and sodium balance were assessed. Rats were investigated in the conscious, catheterized state, in metabolic cages, and acutely during anesthesia. NaLoad was performed over 2 h by intravenous infusion of hypertonic solution (50 mol ⅐ min Ϫ1 ⅐ kg body mass Ϫ1 ) at constant body volume conditions. SMTC was coinfused in amounts (20 g ⅐ min Ϫ1 ⅐ kg Ϫ1 ) reported to selectively inhibit nNOS. Directly measured MABPs of acutely and chronically denervated rats were less than control (15% and 9%, respectively, P Ͻ 0.005). Plasma renin concentration (PRC) was reduced by renal denervation (14.5 Ϯ 0.2 vs. 19.3 Ϯ 1.3 mIU/l, P Ͻ 0.005) and by nNOS inhibition (12.4 Ϯ 2.3 vs. 19.6 Ϯ 1.6 mlU/l, P Ͻ 0.005). NaLoad reduced PRC (P Ͻ 0.05) and elevated MABP modestly (P Ͻ 0.05) and increased sodium excretion six-fold, irrespective of renal denervation and SMTC. The metabolic data demonstrated that renal denervation lowered sodium balance during the first days after denervation (P Ͻ 0.001). These data show that renal denervation decreases MABP and renin secretion. However, neither renal denervation nor nNOS inhibition affects either the renin downregulation or the natriuretic response to acute sodium loading. Acute sodium-driven renin regulation seems independent of RSNA and nNOS under the present conditions. plasma renin concentration; total body sodium; blood pressure; sodium excretion THE INTERRELATIONSHIP BETWEEN blood pressure changes and acute variations in water and sodium excretion is not well defined. Arterial blood pressure is controlled by multiple systems, which differ widely in their time of activation. Neural systems react within seconds, while the hormonal and paracrine systems are more sluggish, requiring minutes to hours, or even days, to respond with full capacity. Neurogenic factors have long been hypothesized to be important in the initiation and maintenance of high blood pressure. There is considerable evidence suggesting that enhanced sympathetic drive to the heart and peripheral circulation is involved in the development of persistent blood pressure elevation or maintains the blood pressure elevation originally induced by nonneurogenic mechanisms (11). Moreover, it is known that electrical stimulation of the renal ...

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Effect of nitric oxide on renin secretion. II. Studies in the perfused juxtaglomerular apparatus

Cited by 38 publications

References 0 publications

Expression of type II cGMP-dependent protein kinase in rat kidney is regulated by dehydration and correlated with renin gene expression.

Expression of type II cGMP-dependent protein kinase in rat kidney is regulated by dehydration and correlated with renin gene expression.

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

Renal nerves and nNOS: roles in natriuresis of acute isovolumetric sodium loading in conscious rats

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