scholarly journals Role of Renal Nerves in the Stimulation of the Renin System by Reduced Renal Arterial Pressure

Hypertension ◽  
1999 ◽  
Vol 34 (5) ◽  
pp. 1101-1105 ◽  
Author(s):  
Charlotte Wagner ◽  
Markus Hinder ◽  
Bernhard K. Krämer ◽  
Armin Kurtz
Keyword(s):  
Arterial Pressure ◽  
Renal Nerves ◽  
Stimulation Of

Hypothalamic projections of renal afferent nerves in the cat

1980 ◽  
Vol 58 (5) ◽  
pp. 574-576 ◽  
Author(s):  
J. Ciriello ◽  
F. R. Calaresu
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Fluid Balance ◽  
Lateral Hypothalamus ◽  
Discharge Rate ◽  
Renal Nerves ◽  
Preoptic Nucleus ◽  
Afferent Nerves ◽  
Stimulation Of

In 10 cats anaesthetized with chloralose the electrical activity of spontaneously active hypothalamic units was recorded for changes in discharge rate during electrical stimulation of renal afferent nerves. The discharge rate of 141 single units was altered by stimulation of either the ipsilateral or contralateral renal nerves. Most of the responsive units were located in the regions of lateral preoptic nucleus, lateral hypothalamus, and paraventricular nucleus. These results demonstrate that renal afferent nerves provide information to hypothalamic structures known to be involved in the regulation of arterial pressure and fluid balance.

Role of renal nerves in onset and maintenance of spontaneous hypertension

1982 ◽  
Vol 243 (2) ◽  
pp. H284-H288 ◽  
Author(s):  
R. A. Norman ◽  
D. J. Dzielak
Keyword(s):  
Arterial Pressure ◽  
Renal Denervation ◽  
Indirect Measurement ◽  
Renal Nerves ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Norepinephrine Content ◽  
Wistar Kyoto

Renal denervation has been reported to delay development of hypertension in Okamoto spontaneously hypertensive rats (SHR) but to have no effect on the final hypertensive state. However, functional reinnervation begins to occur about 1 mo after renal denervation. The arterial pressure of SHR undergoing repeated bilateral renal denervations at the age of 4, 7, 10, 13, and 16 wk was compared with that in sham-operated SHR. In addition, the effect of successive renal denervations at 4, 7, and 10 wk of age in Wistar-Kyoto (WKY) control rats was determined. Both indirect measurement of pressure by the tail-cuff technique and mean arterial pressure (MAP) measurement indicated that renal denervation prevents full expression of hypertension in SHR. MAP in 19-wk-old renal-denervation SHR averaged 159 +/- 5.1 mmHg (SE) vs. 178 +/-0 4.2 mmHg in sham-operated SHR. Renal denervation had no effect on arterial pressure of WKY rats. Renal norepinephrine content in the renal-denervated WKY rats and SHR was less than 20% of that in the sham-operated groups. Successive bilateral renal denervations every 3 wk blocks 30-40% of the expected progressive elevation of arterial pressure in aging SHR.

Role of atrial peptide in the acute natriuretic response to uninephrectomy

1990 ◽  
Vol 258 (4) ◽  
pp. F1054-F1060
Author(s):  
J. P. Valentin ◽  
J. Ribstein ◽  
E. Pussard ◽  
A. Mimran
Keyword(s):  
Arterial Pressure ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Right Atrial ◽  
Important Mediator ◽  
Renal Ablation ◽  
Anaesthetized Rats ◽  
Sodium And Potassium ◽  
Stimulation Of

Unilateral nephrectomy (UNX) is associated with an immediate natriuretic response of the remaining kidney. The role of atrial natriuretic peptide (ANP), as assessed by right atrial appendectomy (APX), was investigated in euvolemic anaesthetized rats. In sham APX rats, UNX resulted in a twofold increase in urinary sodium and potassium excretion (1.03 +/- 0.11 to 2.08 +/- 0.17 and 1.39 +/- 0.05 to 2.26 +/- 0.08 mueq/min, respectively) and a doubling of urinary excretion of guanosine 3',5'-cyclic monophosphate (cGMP). No significant change in glomerular filtration rate, renal plasma flow, and lithium clearance occurred in response to UNX. APX totally prevented the UNX-induced natriuresis and diuresis as well as the rise in urinary cGMP. Post-UNX plasma concentration of ANP was higher in sham-operated compared with APX rats (45 +/- 9 vs. 20 +/- 2 fmol/ml). In sham APX rats, UNX was associated with a transient (less than 15 min) rise in arterial pressure; in APX rats, this immediate increase in arterial pressure was of similar magnitude but of longer (greater than 30 min) duration. The observed stimulation of ANP release after UNX and the blunting of the natriuretic response to UNX by APX suggest that ANP may be an important mediator of the renal response to contralateral renal ablation.

Cholinergic stimulation of the hypothalamus and natriuresis in rats: role of the renal nerves

1986 ◽  
Vol 250 (2) ◽  
pp. F322-F328 ◽  
Author(s):  
C. R. Silva-Netto ◽  
R. H. Jackson ◽  
R. E. Colindres
Keyword(s):  
Renal Plasma Flow ◽  
Isotonic Saline ◽  
Renal Perfusion ◽  
Renal Nerves ◽  
Cholinergic Stimulation ◽  
Renal Nerve ◽  
Water Excretion ◽  
Before And After ◽  
Stimulation Of

The role of the renal nerves in the natriuresis seen after cholinergic stimulation of the hypothalamus was studied in anesthetized rats treated with injection into the lateral hypothalamus (LH) of 1 microgram of carbamylcholine chloride (carbachol) in 1 microliter of 0.15 M NaCl or NaCl alone. Injection of carbachol exhibited diuresis and natriuresis both in acutely denervated kidneys (P less than 0.01) and in contralateral innervated kidneys (P less than 0.01) without changes in glomerular filtration rate (GFR) or renal plasma flow (RPF) (n = 10). Salt and water excretion was unchanged in 10 rats after injection of NaCl. Micropuncture studies in denervated kidneys showed that, after carbachol injection, tubular fluid-to-plasma inulin concentration ratio [(F/P)In] in the late proximal tubule fell from 1.86 +/- 0.08 to 1.64 +/- 0.07 (P less than 0.01) without changes in single-nephron GFR. In nine other carbachol-treated rats in which renal perfusion pressure was maintained low and constant, diuresis and natriuresis, although attenuated, were again observed both in denervated (P less than 0.01) and in contralateral innervated kidneys (P less than 0.05). In another group of 11 animals, efferent renal nerve activity (ERNA) was recorded before and after LH injection of carbachol and isotonic saline. ERNA was significantly depressed for 30 min, only after carbachol injection. Our results suggest that the renal nerves, although involved, are not essential for the natriuretic response after cholinergic stimulation of LH. By exclusion, other factors, presumably hormones, must contribute to the response.

The Role of Endogenous Angiotensin II in Antidiuresis and Norepinephrine Overflow Induced by Stimulation of Renal Nerves in Anesthetized Dogs

1991 ◽  
Vol 17 (5) ◽  
pp. 807-813 ◽  
Author(s):  
Kazutaka Hayashi ◽  
Yasuo Matsumura ◽  
Yasushi Yoshida ◽  
Yasunori Suzuki ◽  
Shiro Morimoto
Keyword(s):  
Angiotensin Ii ◽  
Renal Nerves ◽  
Anesthetized Dogs ◽  
Stimulation Of

scholarly journals Differential role of afferent and efferent renal nerves in the maintenance of early- and late-phase Dahl S hypertension

2016 ◽  
Vol 310 (3) ◽  
pp. R262-R267 ◽  
Author(s):  
Jason D. Foss ◽  
Gregory D. Fink ◽  
John W. Osborn
Keyword(s):  
Arterial Pressure ◽  
Renal Denervation ◽  
Antihypertensive Effect ◽  
Late Phase ◽  
Renal Nerves ◽  
Similar Degree ◽  
Sham Surgery ◽  
Selective Ablation ◽  
Two Phases

Clinical data suggest that renal denervation (RDNX) may be an effective treatment for human hypertension; however, it is unclear whether this therapeutic effect is due to ablation of afferent or efferent renal nerves. We have previously shown that RDNX lowers arterial pressure in hypertensive Dahl salt-sensitive (S) rats to a similar degree observed in clinical trials. In addition, we have recently developed a method for selective ablation of afferent renal nerves (renal-CAP). In the present study, we tested the hypothesis that the antihypertensive effect of RDNX in the Dahl S rat is due to ablation of afferent renal nerves by comparing the effect of complete RDNX to renal-CAP during two phases of hypertension in the Dahl S rat. In the early phase, rats underwent treatment after 3 wk of high-NaCl feeding when mean arterial pressure (MAP) was ∼140 mmHg. In the late phase, rats underwent treatment after 9 wk of high NaCl feeding, when MAP was ∼170 mmHg. RDNX reduced MAP ∼10 mmHg compared with sham surgery in both the early and late phase, whereas renal-CAP had no antihypertensive effect. These results suggest that, in the Dahl S rat, the antihypertensive effect of RDNX is not dependent on pretreatment arterial pressure, nor is it due to ablation of afferent renal nerves.

Stimulatory and inhibitory reflexes from somatic receptors: effect on renin release

1984 ◽  
Vol 246 (6) ◽  
pp. R1005-R1010 ◽  
Author(s):  
H. Holdaas ◽  
G. F. DiBona
Keyword(s):  
Sciatic Nerve ◽  
Arterial Pressure ◽  
Nerve Stimulation ◽  
Cardiovascular Responses ◽  
Renin Release ◽  
Renal Nerves ◽  
Pressor Responses ◽  
Bilateral Carotid ◽  
Sciatic Nerve Stimulation ◽  
Stimulation Of

The effect of stimulation of skeletal muscle somatic receptor afferents on renal function and renin release was examined in anesthetized dogs (bilateral carotid occlusion and vagotomy) with controlled renal arterial pressure. Afferent sciatic nerve stimulation (20–40 V, 1 ms) at 0.6–1.5 Hz elicited cardiovascular pressor responses, renal vasoconstriction, and stimulation of renin release, whereas at 0.3–0.8 Hz cardiovascular depressor responses and inhibition of renin release without changes in renal blood flow were found. Renal denervation abolished the inhibition of renin release but not the cardiovascular depressor response to afferent sciatic nerve stimulation at 20–40 V, 1 ms, and 0.3–0.8 Hz. Peripheral somatic afferent nerves contain fibers which, when appropriately stimulated, produce either pressor or depressor cardiovascular responses. At constant renal arterial pressure, increases in renin release occur with pressor responses, whereas decreases in renin release, mediated by the renal nerves, occur with depressor responses.

Ventrolateral medullary neurons modulate pressor reflex to muscular contraction

1989 ◽  
Vol 257 (5) ◽  
pp. R1154-R1161 ◽  
Author(s):  
R. M. Bauer ◽  
G. A. Iwamoto ◽  
T. G. Waldrop
Keyword(s):  
Arterial Pressure ◽  
Excitatory Amino Acid ◽  
Pressor Response ◽  
Minute Ventilation ◽  
Muscular Contraction ◽  
Posterior Hypothalamus ◽  
Ventrolateral Medulla ◽  
Pressor Reflex ◽  
Stimulation Of

Cardiorespiratory alterations during exercise are mediated through feedback from contracting muscles and descending drive from rostral brain sites such as the posterior hypothalamus. The role of medullary sites, which process this information, was examined in this study. In anesthetized cats, muscular contraction elicited by stimulation of L7 and S1 ventral roots and electrical stimulation of sites in the posterior hypothalamus both evoked increases in arterial pressure, heart rate, and minute ventilation. The reflex increase in arterial pressure produced by muscular contraction was attenuated significantly 15-20 min after bilateral microinjections of an excitatory amino acid (EAA) receptor antagonist, kynurenic acid (KYN), into the ventrolateral medulla (VLM). The reflex increase in arterial pressure evoked by muscular contraction returned to control levels 90 min after VLM microinjections of KYN. Microinjection of KYN into the VLM had no effect on the cardiorespiratory responses to posterior hypothalamic stimulation. These findings suggest that neurons in the VLM modulate the reflex pressor response evoked by muscular contraction. This reflex may be mediated through an interaction with EAA receptors on neurons in the VLM.

Recent insights into the interactions between the baroreflex and the kidneys in hypertension

2005 ◽  
Vol 288 (4) ◽  
pp. R828-R836 ◽  
Author(s):  
Thomas E. Lohmeier ◽  
Drew A. Hildebrandt ◽  
Susan Warren ◽  
Paul J. May ◽  
J. Thomas Cunningham
Keyword(s):  
Arterial Pressure ◽  
Experimental Studies ◽  
Secondary Hypertension ◽  
Experimental Models ◽  
Renal Nerves ◽  
Excretory Function ◽  
Clinical Hypertension ◽  
Theoretical Evidence

Recent findings in chronically instrumented animals challenge the classic concept that baroreflexes do not play a role in the chronic regulation of arterial pressure. As alterations in renal excretory function are of paramount importance in the chronic regulation of arterial pressure, several of these recent studies have focused on the long-term interactions between the baroreflex and the kidneys during chronic perturbations in arterial pressure and body fluid volumes. An emerging body of evidence indicates that the baroreflex is chronically activated in several experimental models of hypertension, but in most cases, the duration of these studies has not exceeded 2 wk. Although these studies suggest that the baroreflex may play a compensatory role in attenuating the severity of the hypertension, possibly even in primary hypertension with uncertain causes of sympathetic activation, there has been only limited assessment of the quantitative importance of this interaction in the regulation of arterial pressure. In experimental models of secondary hypertension, baroreflex suppression of renal sympathetic nerve activity is sustained and chronically promotes sodium excretion. This raises the possibility that the renal nerves may be the critical efferent link for baroreceptor-induced suppression of central sympathetic output through which long-term compensatory reductions in arterial pressure are produced. This contention is supported by strong theoretical evidence but must be corroborated by experimental studies. Finally, although it is now clear that pressure-induced increases in baroreflex activity persist for longer periods of time than previously suggested, studies using new tools and novel approaches and extending beyond 2 wk of hypertension are needed to elucidate the true role of the baroreflex in the pathogenesis of clinical hypertension.

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