Role of renal nerves, angiotensin II, and prostaglandins in the antinatriuretic response to acute hypercapnic acidosis in the dog.

Henrich, William L.; Groß, Peter; Dillingham, Mark A.

doi:10.1161/01.res.50.2.294

Cited by 13 publications

(8 citation statements)

References 20 publications

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“…Several investigators reported that renal blood flow decreased during hypercapnia (STONE et al, 1958;BERSENTES and SIMMONS, 1967;NORMAN et al, 1970;FABER et al, 1976;ANDERSON et a!.,1983) and this decrease was attenuated after renal denervation. Other studies showed that hypercapnia decreased urinary sodium excretion (ANDERSON et al, 1982) and increased renin secretion (Fuii Jand ZEHR, 1975;MORITA, 1976;KURTZ and ZEHR, 1978;STASZEWSKA-BARCZAK, 1978). These observations together with our present results suggest that an increase in RNA during hypercapnia might contribute to maintain arterial blood pressure by counteracting the direct vasodilating effect of hypercapnia and by exerting antinatriuretic and antidiuretic actions.…”

Section: Effectssupporting

confidence: 82%

Effects of hypercapnia on renal nerve activity.

Shirahata¹,

Nishino²,

Honda

et al. 1985

Jpn.J.Physiol

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We investigated the response of renal nerve activity (RNA) to hypercapnia and assessed the contribution of the peripheral chemoreceptors to the response of RNA in anesthetized and artificially ventilated cats. RNA and arterial pressure were recorded at four levels of PETC0, with hyperoxia in intact and in peripheral chemoreceptor denervated cats. In intact cats, RNA increased progressively with increasing PETC02, while no consistent change in arterial pressure was observed. In peripheral chemoreceptor denervated cats, the response of RNA to increasing PETca2 was totally abolished. These results suggest that the peripheral chemoreceptors play an important role in increasing RNA during hypercapnia.

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Section: Effectssupporting

confidence: 82%

Effects of hypercapnia on renal nerve activity.

Shirahata¹,

Nishino²,

Honda

et al. 1985

Jpn.J.Physiol

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“…Indirect support for this contention has been provided by studies which have demonstrated that a-adrenoceptor antagonists inhibited the angiotensin II-induced increase in active sodium transport in rat kidney cortical slices (Brunton, Parsons & Poat, 1978) and the angiotensin II-induced antinatriuresis in intact rats (Radhi, Chapman & Munday, 1982), implying that angiotensin II exerted its effect indirectly through the release of noradrenaline from sympathetic nerve endings. Two studies in the dog have also shown that captopril or angiotensin II receptor antagonists attenuated the renal nerve-mediated antinatriuresis during hypercapnic acidosis (Anderson, Henrich, Gross & Dillingham, 1982) or shock avoidance (Koepke & Obrist, 1983), in the absence of changes in renal haemodynamics. Together these data would establish that angiotensin II plays an important role in modulating neurotransmission at the level of the renal tubule comparable to that exhibited at neurovascular junctions within the sympathetic nervous system.…”

Section: Low-level Renal Nerve 8timulationmentioning

confidence: 97%

Interaction of the renin‐angiotensin system and the renal nerves in the regulation of rat kidney function.

Handa¹,

Johns²

1985

The Journal of Physiology

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SUMMARY1. Stimulation of the renal sympathetic nerves in pentobarbitone anaesthetized rats achieved a 13 % reduction in renal blood flow, did not change glomerular filtration rate, but reduced urine flow by 37 %, absolute sodium excretion by 37 %, and fractional sodium excretion by 34 %. Following inhibition of converting enzyme with captopril (0-38 mmol kg-' h-1), similar nerve stimulation reduced both renal blood flow and glomerular filtration rate by 16 %, and although urine flow and absolute sodium excretion fell by 32 and 31 %, respectively, the 18 % fall in fractional sodium excretion was significantly less than that observed in the absence of captopril.2. Renal nerve stimulation at low levels, which did not change either renal blood flow or glomerular filtration rate, reduced urine flow, and absolute and fractional sodium excretions by 25, 26 and 23 %, respectively.3. In animals receiving captopril at 0-38 mmol kg-' h-1, low-level nerve stimulation caused small increases in glomerular filtration rate of 7 % and urine flow of 12 %, but did not change either absolute or fractional sodium excretions. At one-fifth the dose of captopril (0-076 mmol kg-' h-'), low-level nerve stimulation did not change renal haemodynamics but decreased urine flow, and absolute and fractional sodium excretions by 10, 10 and 8 %, respectively. 4. These results showed that angiotensin II production was necessary for regulation of glomerular filtration rate in the face of modest neurally induced reductions in renal blood flow and was compatible with an intra-renal site of action of angiotensin II preferentially at the efferent arteriole. They also demonstrated that in the rat the action of the renal nerves to decrease sodium excretion was dependent on angiotensin II.

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“…Thus, the hemodynamic effects of catecholamines are modulated by a complex interaction with the renin angiotensin and PG systems. Hypercapnic acidosis associated with an increase in PCO 2 from 25 to 70 mm Hg activates the RSNA, and renal denervation studies indicate that the neurally mediated renal vasoconstriction is effectively counteracted, at least in part, by enhanced synthesis of vasodilatory PGs [1735] . Inhibition of the RAS partially attenuates the constrictor effects of RNS during cyclooxygenase inhibition [1096,1733] .…”

Section: Neural Interactions With Paracrine Factorsmentioning

confidence: 99%

“…Afferent nerve endings contain the neuropeptides, CGRP, substance P, and vasoactive intestinal peptide [1764][1765][1766] . Two examples of excitatory renorenal reflexes that are initiated by increased renal afferent nerve traffic and affect renal hemodynamics are neurally-mediated ipsilateral vasoconstriction during increased renal venous pressure and contralateral renal vasoconstriction following a unilateral increase in ureteral pressure [474,1664,1696,1707,1735,1762] . Chemoreceptors sense the electrolyte composition of pelvic fluid, in particular potassium concentration and pH, and also are responsive to renal ischemia.…”

Section: Afferent Renal Nervesmentioning

confidence: 99%