Effect of Sodium Nitroprusside on Norepinephrine Overflow and Antidiuresis Induced by Stimulation of Renal Nerves in Anesthetized Dogs

Maekawa, Hiromi; Matsumura, Yasuo; Matsuo, Gen; Morimoto, Shiro

doi:10.1097/00005344-199602000-00006

Cited by 24 publications

(6 citation statements)

References 26 publications

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“…Yamamoto et al 17 found that field stimulation of rat mesenteric arteries caused noradrenaline release, which was decreased by some 50% in the presence of N-nitro-L-arginine (30 mol/L), suggesting NO was necessary for effective neurotransmission. Conversely, Egi et al 18 and Maekawa et al, 19 using the dog, found that intrarenal blockade of NO generation was associated with an increase, whereas NO donors led to a suppression of noradrenaline spillover from the kidney. Despite these diverse reports, there is a view that NO released from the nerve terminals can act presynaptically to exert a tonic inhibitory action on transmitter release.…”

Section: Discussionmentioning

confidence: 94%

Nitric Oxide Modulation of Neurally Induced Proximal Tubular Fluid Reabsorption in the Rat

Johns

2002

Hypertension

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Abstract-This study investigated the role of NO in mediating the renal sympathetic nerve-mediated increases in proximal tubular fluid reabsorption (Jva). In inactin-anesthetized Wistar rats, renal sympathetic nerve stimulation (15 V, 2 ms) at 0.75 and 1.0 Hz did not change blood pressure or glomerular filtration rate but did decrease urine flow and sodium excretion in a frequency-related fashion by 40% to 50% at 1.0 Hz (both, PϽ0.01). Renal nerve stimulation in control animals increased Jva by 11% at 0.75 Hz (PϽ0.05) and 31% at 1.0 Hz (PϽ0.01). Intraluminal N-nitro-L-arginine methyl ester (L-NAME) resulted in a higher basal Jva (19%, PϽ0.05), and renal nerve stimulation had no effect on Jva. When L-NAME plus sodium nitroprusside was present intraluminally, however, there were frequency-dependent increases in Jva that were similar in pattern and magnitude to the control rats. Introduction of the relatively selective nNOS blocker 7-nitroindazole intraluminally, at 10 Ϫ6 and 10 Ϫ4 M, raised basal Jva by 18% and 24%, respectively (PϽ0.01), and renal nerve stimulation did not change Jva. Intraluminal aminoguanidine (10 Ϫ4 M), a relatively selective iNOS blocker, did not affect basal Jva, which remained unchanged during renal nerve stimulation. These data are consistent with NO exerting a tonic inhibitory action on the basal levels of Jva, which, in part, is caused by NO generated by the nNOS isoform. Moreover, the findings have revealed that the presence of NO is necessary to ensure that renal nerves can stimulate fluid reabsorption by the proximal tubules, requiring NO generated from both nNOS and iNOS. Key Words: nitric oxide Ⅲ renal nerves Ⅲ antinatriuresis Ⅲ sodium Ⅲ kidney T he renal sympathetic nerves play an important role in regulating renin release, tubular sodium and water reabsorption, and renal vascular resistance. Increasing levels of renal nerve activity progressively recruit these functions; that is, at low frequencies there is renin release. Thereafter, increased tubular reabsorption of fluid becomes apparent, and it is only at the higher frequencies that there are reductions in renal blood flow and glomerular filtration rate. 1,2 Noradrenaline is released from the renal sympathetic nerve endings and, as at other sympathetic neuroeffector junctions, has an autoinhibitory feedback action, mediated via presynaptic ␣ 2 -adrenoceptors, to attenuate the level of neurotransmitter release. 3 At the postsynaptic level, noradrenaline acts on the ␣ 1 -adrenoceptors of the epithelial cells to stimulate sodium, and hence water, transport by activation of the Na ϩ /K ϩ -ATPase at the basolateral membrane and the Na ϩ /H ϩ -exchanger at the apical membrane. 4,5 Recently, there has been increasing interest in the role of NO in the control of renal function. NO synthase (NOS) catalyzes the generation of NO, which stimulates cyclic GMP production to modify specific aspects of renal function. 6 At least 3 isoforms of NOS have been identified so far: inducible NOS (iNOS), endothelial NOS (eNOS), and neuronal NOS (nNOS),...

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Section: Discussionmentioning

confidence: 94%

Nitric Oxide Modulation of Neurally Induced Proximal Tubular Fluid Reabsorption in the Rat

Johns

2002

Hypertension

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“…However, most evidence suggests that changes in medullary perfusion are due mainly to changes in blood velocity within vasa recta capillaries rather than vasa recta recruitment (see [7] for discussion). A second limitation relates to the fact that NO can affect responses to RNS at pre-junctional sites [20]. Our present experimental approach does not allow us to study separately the impacts of treatments on pre-and post-junctional aspects of sympathetic neuroeffector function.…”

Section: Discussionmentioning

confidence: 98%

Prostaglandins and nitric oxide in regional kidney blood flow responses to renal nerve stimulation

Rajapakse

Flower

Eppel

et al. 2004

Pflugers Arch - Eur J Physiol

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We examined the roles of cyclooxygenase products and of interactions between the cyclooxygenase and nitric oxide systems in the mechanisms underlying the relative insensitivity of medullary perfusion to renal nerve stimulation (RNS) in anaesthetized rabbits. To this end we examined the effects of ibuprofen and N(G)-nitro-L: -arginine (L-NNA), both alone and in combination, on the responses of regional kidney perfusion to RNS. Under control conditions, RNS produced frequency-dependent reductions in total renal blood flow (RBF; -82+/-3% at 6 Hz), cortical laser-Doppler flux (CLDF; -84+/-4% at 6 Hz) and, to a lesser extent, medullary laser-Doppler flux (MLDF; -46+/-7% at 6 Hz). Ibuprofen did not affect these responses significantly, suggesting that cyclooxygenase products have little net role in modulating renal vascular responses to RNS. L-NNA enhanced RBF (P=0.002), CLDF (P=0.03) and MLDF (P=0.03) responses to RNS. As we have shown previously, this effect of L-NNA was particularly prominent for MLDF at RNS frequencies < or = 1.5 Hz. Subsequent administration of ibuprofen, in L-NNA-pretreated rabbits, did not affect responses to RNS significantly. We conclude that counter-regulatory actions of NO, but not of prostaglandins, partly underlie the relative insensitivity of medullary perfusion to renal nerve activation.

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“…First, there is evidence that NO can inhibit release of norepinephrine from prejunctional sites in response to RNS (28). Thus enhanced responses of RBF, CLDF, and MLDF to RNS in rabbits pretreated with L-NNA could be due to facilitated release of norepinephrine, to a postjunctional effect to enhance responses to norepinephrine, or to both.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II and nitric oxide in neural control of intrarenal blood flow

Rajapakse¹,

Sampson²,

Eppel³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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We investigated the roles of the renin-angiotensin system and the significance of interactions between angiotensin II and nitric oxide, in responses of regional kidney perfusion to electrical renal nerve stimulation (RNS) in pentobarbital sodium-anesthetized rabbits. Under control conditions, RNS (0.5-8 Hz) reduced total renal blood flow (RBF; -89 +/- 3% at 8 Hz) and cortical perfusion (CBF; -90 +/- 2% at 8 Hz) more than medullary perfusion (MBF; -55 +/- 5% at 8 Hz). Angiotensin II type 1 (AT(1))-receptor antagonism (candesartan) blunted RNS-induced reductions in RBF (P = 0.03), CBF (P = 0.007), and MBF (P = 0.04), particularly at 4 and 8 Hz. Nitric oxide synthase inhibition with N(G)-nitro-L-arginine (L-NNA) enhanced RBF (P = 0.003), CBF (P = 0.001), and MBF (P = 0.03) responses to RNS, particularly at frequencies of 2 Hz and less. After candesartan pretreatment, L-NNA significantly enhanced RNS-induced reductions in RBF (P = 0.04) and CBF (P = 0.007) but not MBF (P = 0.66). Renal arterial infusion of angiotensin II (5 ng.kg(-1).min(-1)) selectively enhanced responses of MBF to RNS in L-NNA-pretreated but not in vehicle-pretreated rabbits. In contrast, greater doses of angiotensin II (5-15 ng.kg(-1).min(-1)) blunted responses of MBF to RNS in rabbits with intact nitric oxide synthase. These results suggest that endogenous angiotensin II enhances, whereas nitric oxide blunts, neurally mediated vasoconstriction in the renal cortical and medullary circulations. In the renal medulla, but not the cortex, angiotensin II also appears to be able to blunt neurally mediated vasoconstriction.

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Effect of Sodium Nitroprusside on Norepinephrine Overflow and Antidiuresis Induced by Stimulation of Renal Nerves in Anesthetized Dogs

Cited by 24 publications

References 26 publications

Nitric Oxide Modulation of Neurally Induced Proximal Tubular Fluid Reabsorption in the Rat

Nitric Oxide Modulation of Neurally Induced Proximal Tubular Fluid Reabsorption in the Rat

Prostaglandins and nitric oxide in regional kidney blood flow responses to renal nerve stimulation

Angiotensin II and nitric oxide in neural control of intrarenal blood flow

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