Renal adrenoceptor mediation of antinatriuretic and renin secretion responses to low frequency renal nerve stimulation in the dog.

Osborn, Jeffrey L.; Holdaas, Hallvard; Thames, Marc D.; DiBona, G. F.

doi:10.1161/01.res.53.3.298

Cited by 147 publications

(81 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, there is evidence that at vascular smooth musclejunctions, foi example rat aorta and rabbit coronary artery (Vanhoutte & Rimele, 1982), and in spontaneously hypertensive rat models (Kazda et al, 1985), that a1-adren-oceptor-mediated vasoconstrictor responses can be dependent on inward movement of calcium. Renal nerve-induced increases in tubular sodium reabsorption appear to be mediated by oxi-adrenoceptors in the dog (Osborn et al, 1983), the rabbit (Hesse & Johns, 1985) as well as the rat (Johns & Manitius, 1986b) and the possibility existed that calcium channel blockers could interfere with neurotransmission at this specialized junction. However, the magnitude of the reduction in the calcium excretion due to the low frequency renal nerve stimulation was not altered by either dose of drug.…”

Section: Discussionmentioning

confidence: 99%

A study in the rat of the renal actions of nitrendipine and diltiazem on the adrenergic regulation of calcium and sodium reabsorption

Johns

Manitius

1986

British J Pharmacology

View full text Add to dashboard Cite

1In pentobarbitone-anaesthetized rats, intravenous administration of diltiazem at 5 g kg-' min -' did not change blood pressure or renal blood flow but increased glomerular filtration rate by approximately 16%, urine flow by 85%, calcium excretion by 151% and absolute and fractional sodium excretions by 100% and 69%, respectively. A similar pattern of responses was obtained in renally denervated animals, except that calcium excretion did not change statistically. Diltiazem given at 20 pg kg'1 min-' into renally innervated and denervated groups of animals depressed blood pressure between 15-17 mmHg but had no effect on renal haemodynamic or tubular function. 2 Nitrendipine administered at 0.5 ig kg-' min-' to renally innervated and denervated animals significantly depressed blood pressure in intact animals by 6 mmHg and in both groups did not change renal haemodynamics but caused similar increases in urine flow ofbetween 79-98%, calcium excretion of between 87 and 125%, absolute sodium excretion of between 108 and 140% and fractional sodium excretion of between 83 and 170%. Infusion of nitrendipine at 1.0 jig kg-' min' into intact or renally denervated animals decreased blood pressure by 18-20 mmHg and increased urine flow by 84-111 %, calcium excretion by 85%, absolute sodium excretion by 81-137% and fractional sodium excretion by 52-102%. 3 Stimulation of the renal nerves at low frequencies (0.8 to 1.5 Hz) caused minimal changes in renal haemodynamics but decreased urine flow by 27%, calcium excretion by 35%, absolute and fractional sodium excretions 32% and 36%, respectively. In different groups of animals given either diltiazem at 20 pg kg-I min' or nitrendipine at 0.5 pg kg'-min' or 1.0 fg kg'-min' , a similar degree of renal nerve stimulation caused an identical pattern of excretory responses of similar magnitude to those obtained in the absence of drug. 4 The calciuretic, diuretic and natriuretic activities of diltiazem and nitrendipine were not dependent on renal nerves and probably represented a direct action on the tubular reabsorptive processes of these ions. The renal nerve-induced increases in tubular calcium and sodium reabsorption indicate that these a-adrenoceptor-mediated responses are not dependent on the inward movement of calcium

show abstract

Section: Discussionmentioning

confidence: 99%

A study in the rat of the renal actions of nitrendipine and diltiazem on the adrenergic regulation of calcium and sodium reabsorption

Johns

Manitius

1986

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…13 -15 This adrenergic stimulation of renin release will consequently increase circulating Ang II and aldosterone and subsequently decrease urinary sodium excretion by the mechanisms previously discussed. Second, renal sympathetic outflow also directly stimulates renal tubular sodium reabsorption at the proximal convoluted tubule 16 " 18 or at the thick ascending limb of the loop of Henle. 16 Direct sympathetic innervation of these tubular structures has been identified, 19 and the adrenergic receptor mediating these responses has been described by several investigators as a.…”

Section: Renal Sympathetic Nerves Renal Function and Arterial Pressurementioning

confidence: 99%

“…16 Direct sympathetic innervation of these tubular structures has been identified, 19 and the adrenergic receptor mediating these responses has been described by several investigators as a. 16 - 18 Recent evidence indicates that a-adrenergic receptor activation of renal tubular structures increases sodium reabsorption by activation of sodium-hydrogen exchange, eliciting net increases in renal sodium bicarbonate reabsorption. 20 It is important to note that direct neurogenic activation of tubular sodium reabsorption will concomitantly decrease the distal delivery of sodium chloride, leading to further activation of renin release via the macula densa.…”

Section: Renal Sympathetic Nerves Renal Function and Arterial Pressurementioning

confidence: 99%

Relation between sodium intake, renal function, and the regulation of arterial pressure.

Osborn

1991

Hypertension

Self Cite

View full text Add to dashboard Cite

The long-term regulation of arterial pressure requires the maintenance of a balance between sodium and water intake and sodium and water excretion. Normal salt and water balance leads to stable body fluid volumes and the maintenance of normal renal function is critical to establishing extracellular fluid volume homeostasis. This review focuses on the role of the kidney in the long-term control of salt and water balance with particular emphasis on the relations between sodium intake, the renin-angiotensin-aldosterone system, renal sympathetic nerve activity, and the regulation of arterial pressure via renal sodium and water excretion. T he regulation of the extracellular fluid volume encompasses the continuous, ongoing maintenance of normal sodium and water balance as a relation between sodium intake and excretion. As humans, we exist as intermittent sodium and water consumers, leaving the bulk of the task of regulating our constant expansion of extracellular fluid volumes to the renal excretory processes. There are many factors that influence renal sodium excretion and thereby participate in this regulatory process. These factors can be subdivided into extrinsic and intrinsic mechanisms. Extrinsic mechanisms include the production of angiotensin II (Ang II) and aldosterone, the release of atrial natriuretic factor, and the alterations of renal sympathetic outflow; some intrinsic mechanisms are the regulation of glomerular filtration rate, renal hemodynamics, intrarenal physical forces controlling tubular reabsorp- Supported by an American Heart Association Established Investigator Award, by an American Heart Association Grant-inAid, and by National Heart, Lung, and Blood Institute grants HL-40137 and HL-29587.Address for correspondence: Jeffrey L. Osborn, PhD, Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226. tion, and intrarenal hormonal systems such as kinins, Ang n, and prostaglandins. Renal Function and Arterial PressureA close correlation between normal kidney function and blood pressure control has been demonstrated in several experimental forms of hypertension including the spontaneously hypertensive rat (SHR) 1 and the Dahl salt-sensitive (DS) rat.2 The spontaneously hypertensive strain of rats develops elevated arterial pressure spontaneously with age, and in some strains this hypertension is exacerbated with elevated sodium chloride intake. Kawabe et al 3 have shown that in this strain, replacement at an early age of the SHR kidneys by transplantation with kidneys from age-matched normotensive control rats results in a substantial diminution of the blood pressure. This same response has been shown in other genetic models of hypertension including the Milan hypertensive strain 4 and the DS rat. 5 Thus, a direct correlation has been documented between renal function and arterial pressure in several genetic models of hypertension, and in some strains a critical interaction exists between sodium intake and the magnitude of the hypertension.The complex relations between the natriu...

show abstract

“…16 A slightly higher frequency of RNS, 0.5 Hz, increased RSR without affecting U Na V, RBF, or GFR; this was attributed to direct activation of ␤ 1 -adrenoceptors on juxtaglomerular granular cells, as it was inhibited by ␤ 1 -adrenoceptor antagonists. 17 At progressively higher frequencies of RNS, associated initially with antinatriuresis and then renal vasoconstriction, the macula densa receptor and baroreceptor mechanisms became engaged. 18,19 On examining the stimulus response curve of the frequency of RNS versus both renin secretion rate and RBF, it is important to note that a large portion of the maximum RSR response is achieved with frequencies of RNS that do not substantially affect RBF.…”

mentioning

confidence: 99%

Neural Control of the Kidney

DiBona

2003

Hypertension

158

View full text Add to dashboard Cite

Abstract-This article provides a chronological perspective on the development of knowledge concerning the neural control of renal function and is divided into three parts: the past, the present, and the future. The PastResearch in the area of the neural control of renal function was not very active for the first half of the 20th century. This can be attributed to 2 factors. First, the renowned renal physiologist, Homer Smith, rendered an opinion that the renal nerves were of little functional consequence. [1][2][3] This was based on his interpretation of experiments involving renal denervation in anesthetized and surgically operated animals. He criticized this approach, as he believed that the starting level of renal sympathetic nerve activity (RSNA) would be quite elevated, owing to the associated stress, so that "denervation hyperemia and diuresis appear to be a release from enhanced vasoconstriction engendered by anesthesia and traumatic operative procedures." 3 Second, there was a lack of convincing evidence that the renal innervation extended beyond the renal vasculature to either the tubules or the juxtaglomerular apparatus. The demonstration by Luciano Barajas 4 that all segments of the renal tubule (as well as the juxtaglomerular apparatus) were innervated by norepinephrine-containing renal sympathetic nerve terminals that make contact with the renal tubular epithelial cell basement membrane paved the way for increased research activity in this area. This critical observation reconfirmed once again the important relationship between structure and function.Given the powerful influence of changes in renal hemodynamics (ie, arterial pressure, glomerular filtration rate [GFR] and renal blood flow [RBF]) on urinary sodium excretion (U Na V), it was evident that the influence of changes in RSNA on U Na V must be examined in experimental protocols in which these variables remained constant. By using electrical stimulation of the efferent renal sympathetic nerves at frequencies just subthreshold for decreases in RBF, it was shown that a reversible decrease in U Na V occurred in the absence of changes in GFR (ie, filtered sodium load), RBF, and arterial pressure. 5 These results indicated that lowfrequency renal sympathetic nerve stimulation increased overall renal tubular sodium reabsorption via a direct action on the renal tubule, independent of changes in renal hemodynamics. Additional experiments demonstrated that this effect occurred in the proximal convoluted tubule, the thick ascending limb of Henle's loop, the distal convoluted tubule, and the collecting duct. 6,7 Subsequent work (reviewed in DiBona and Kopp 8 ) showed that this was owing to the release of norepinephrine from renal sympathetic nerve terminals with stimulation of postsynaptic ␣ 1 -adrenoceptors located on the basolateral membrane of renal tubular epithelial cells throughout the nephron. Subsequent intracellular signaling events resulted in an increase in activity of the sodium pump (Na ϩ ,K ϩ -ATPase), with increased transepithelial sod...

show abstract

Renal adrenoceptor mediation of antinatriuretic and renin secretion responses to low frequency renal nerve stimulation in the dog.

Cited by 147 publications

References 20 publications

A study in the rat of the renal actions of nitrendipine and diltiazem on the adrenergic regulation of calcium and sodium reabsorption

A study in the rat of the renal actions of nitrendipine and diltiazem on the adrenergic regulation of calcium and sodium reabsorption

Relation between sodium intake, renal function, and the regulation of arterial pressure.

Neural Control of the Kidney

Contact Info

Product

Resources

About